tumor growth

Insulin-like growth factor-binding protein 7(IGFBP-7) is a secreted glycosylated protein that contains three protein domain modules. IGFBP7 contains an N-terminal IGFBP domain, followed by a Kazal-type serine proteinase inhibitor domain and a C-terminal immunoglobulin-like C2-type domain. Human and mouse IGFBP7 are highly homologous and share 94% aa sequence identity. It is expressed in many normal tissues and in cancer cells. It is abundantly expressed in high endothelial venules (HEVs) of blood vessels in the secondary lymphoid tissues. It binds IGF and insulin with very low affinity and has been shown to enhance the mitogenic actions of IGF and insulin. IGFBP7 also has IGF/insulin-independent activities. It interacts with heparan sulfate proteoglycans, type IV collagen, and specific chemokines. It supports weak cell adhesion, promotes cell spreading on type IV collagen, and stimulates the production of the potent vasodilator PGI2. It modulates tumor cell growth and has also been implicated in angiogenesis.

Tumor necrosis factor receptor superfamily member 12A(Tnfrsf12a) is a single-pass type I membrane protein and contains 1 TNFR-Cys repeat. It is weak inducer of apoptosis in some cell types.It promotes angiogenesis and it is the proliferation of endothelial cells. It may modulate cellular adhesion to matrix proteins.TNFR binds specifically to tumor necrosis factor (TNF) and blocks its interaction with cell surface TNF receptors. TNF is a naturally occurring cytokine that is involved in normal inflammatory and immune responses. It plays an important role in the inflammatory processes of rheumatoid arthritis (RA), polyarticular-course juvenile rheumatoid arthritis (JRA), and ankylosing spondylitis and the resulting joint pathology. In addition, TNF plays a role in the inflammatory process of plaque psoriasis. Elevated levels of TNF are found in involved tissues and fluids of patients with RA, psoriatic arthritis, ankylosing spondylitis (AS), and plaque psoriasis. Two distinct receptors for TNF (TNFRs), a 55 kilodalton protein (p55) and a 75 kilodalton protein (p75), exist naturally as monomeric molecules on cell surfaces and in soluble forms. Biological activity of TNF is dependent upon binding to either cell surface TNFR.

Tumor Necrosis Factor Ligand Superfamily Member 15 (TNFSF15) is a new member of the tumor necrosis factor family. TNFSF15 is predominantly an endothelial cell-specific gene, and recombinant TNFSF15 is a potent inhibitor of endothelial cell proliferation, angiogenesis and tumor growth. TNFSF15 exerts two activities on endothelial cells: early G1 arrest of G0/G1-cells responding to growth stimuli and programmed cell death of proliferating cells. These activities are highly specific to endothelial cells. TNFSF15 is also able to regulate the expression of several important genes involved in angiogenesis. These findings are consistent with the view that TNFSF15 functions as an autocrine cytokine to inhibit angiogenesis and stabilize the vasculature.

Placental growth factor is a protein that in humans is encoded by the PGF gene. It is a secreted protein and belongs to the PDGF/VEGF growth factor family. Alternate splicing results in at least three human mature PlGF forms containing 131 (PlGF‑1), 152 (PlGF‑2), and 203 (PlGF‑3) amino acids (aa) respectively. PlGF is mainly found as a variably glycosylated, secreted, 55 ‑ 60 kDa disulfide linked homodimer.The protein is a member of the VEGF (vascular endothelial growth factor) sub-family-a key molecule in angiogenesis and vasculogenesis, in particular during embryogenesis. The main source of PGF during pregnancy is the placental trophoblast. PGF is also expressed in many other tissues, including the villous trophoblast. PlGF (especially PlGF‑1) and some forms of VEGF can form dimers that decrease the angiogenic effect of VEGF on VEGF R2. PlGF‑2, like VEGF164/165, shows heparin‑dependent binding of neuropilin (Npn)‑1 and Npn‑2, and can inhibit nerve growth cone collapse. Circulating PlGF often correlates with tumor stage and aggressiveness, and therapeutic PlGF‑2 antibodies are being investigated for their ability to inhibit tumor growth and angiogenesis.

Tumor associated calcium signal transducer 2 (TACSTD2, TROP-2) is a type I cell surface glycoprotein that is highly expressed on human carcinomas. It was originally identified as an antigen present on human gastrointestinal tumors and is the second of two members of this family. Human and mouse TROP-2 share 87% amino acid (aa) similarity. TROP-2 is capable of transducing an intracellular calcium signal and may play a role in tumor growth. It also has adhesive functions. TROP-2 Protein,Human,Recombinant (aa 88-274, hFc） is expressed in HEK293 mammalian cells with C-Fc tag. The predicted molecular weight is 60-80 KDa and the accession number is P09758.

Fibroblast growth factor 7 (FGF7) is a secreted protein which is mainly located in epithelial cells and belongs to the heparin-binding growth factors family. FGF family members possess broad mitogenic and cell survival activities, and are involved in a variety of biological processes, including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion. FGF7 is a potent epithelial cell-specific growth factor, whose mitogenic activity is predominantly exhibited in keratinocytes but not in fibroblasts and endothelial cells. It is possible major paracrine effector of normal epithelial cell proliferation.

Tumor associated calcium signal transducer 2 (TACSTD2, TROP-2) is a type I cell surface glycoprotein that is highly expressed on human carcinomas. It was originally identified as an antigen present on human gastrointestinal tumors and is the second of two members of this family. Human and mouse TROP-2 share 87% amino acid (aa) similarity. TROP-2 is capable of transducing an intracellular calcium signal and may play a role in tumor growth. It also has adhesive functions. TROP-2 Protein, Human, Recombinant (Avi & His), Biotinylated is expressed in HEK293 mammalian cells with C-Avi-6xHis tag. The predicted molecular weight is 40-60 KDa and the accession number is P09758.

Receptor activator of NF-κB(RANK,TNFRSF11A) belongs to one member of tumor necrosis factor receptor family.It is a receptor for TNFSF11/RANKL/TRANCE/OPGL. This gene encodes a type 1 membrane protein with a 30 amino acids (aa) signal peptide, 184 aa extracellular region , a 20 aa transmembrane domain and a 391 aa cytoplasmic region. Human and murine RANK share 81% aa identity in their extracellular domains. RANK is ubiquitous highly expressed in trabecular bone, thymus, small intestine, lung, brain and kidney, but weakly expressed in spleen and bone marrow. After binding its ligand RANKL, RANK can activate signaling pathways such as NF-κB, JNK, ERK, p38, and Akt/PKB, through TRAF protein phosphorylation. RANK/TNFRSF11A signaling is largely considered to be growth promoting and apoptosis reducing such as the effects observed in osteoclasts. RANK/TNFRSF11A was also found to be involved in the regulation of interactions between T-cells and dendritic cells.

Aldehyde dehydrogenase 1 family member A2 (ALDH1A2), also known as retinaldehyde dehydrogenase 2 (RALDH2), belongs to the aldehyde dehydrogenase family which contains two members, the ALDH1 s (ALDH1A1, ALDH1A2 and ALDH1A3) and the 9-cis retinaldehyde dehydrogenase ALDH8 s. ALDH1A2 is key enzyme that catalyzes the synthesis of retinoic acid (RA) from retinaldehyde. RA is a paracrine hormone signaling molecule that functions in developing and adult tissues. ALDH1A2 was also found to regulate normal and tumor cell growth and differentiation. Several studies showed that ALDH1A2 expression is increased after the appearance of AraC resistance in clinical cases which means this protein is effective in AraC resistance.

Insulin-like growth factor I (IGF1) belongs to the family of insulin-like growth factors that are structurally homologous to proinsulin. Mouse IGF-I is synthesized as two precursor isoforms with alternate N- and C-terminal propeptides. These isoforms are differentially expressed by various tissues. Mature mouse IGF-I shares 94% and 99% aa sequence identity with human and rat IGF-I, respectively, and exhibits cross-species activity. It shares 60% aa sequence identity with mature mouse IGF-II. IGF-I induces the proliferation, migration, and differentiation of a wide variety of cell types during development and postnatally. It plays an important role in muscle regeneration and tumor progression. IGF-I binds IGF-I R, IGF-II R, and the insulin receptor. IGF-I association with IGF binding proteins increases its plasma half-life and modulates its interactions with receptors.

Monocyte chemoattractant protein 1 (MCP-1), also called CCL2, is a member of the beta (C-C) subfamily of chemokines that is a chemoattractant for monocytes and basophils but not eosinophils or neutrophils. CCL2 binds the cognate receptor CCR2, and together this signaling pair has been shown to have multiple pro-tumorigenic roles, from mediating tumor growth and angiogenesis to recruiting and usurping host stromal cells to support tumor progression. CCL2 is found in the circulation, where it has been suggested as a diagnostic biomarker of breast cancer and prostate cancer. CCL2 can also induce arachidonic acid release in human monocytes, which has been shown to be involved in adhesion and induction of the chemotactic response, in a pertussis-toxinsensitive manner.

Hyaluronidase-1 (HYAL1) is a secreted lysosomal hyaluronidase that belongs to the glycosyl hydrolase 56 family. HYAL1 contains one EGF-like domain and is highly expressed in the liver, kidney, and heart, but it is weakly expressed in the lung, placenta, and skeletal muscle. HYAL1 is thought to be involved in cell proliferation, migration, and differentiation. It may play a role in promoting tumor progression and blocking the TGFB1-enhanced cell growth. Mutations in HYAL1 are associated with mucopolysaccharidosis type IX, or hyaluronidase deficiency.

Murine PVRIG interacted weakly with poliovirus receptor (PVR) but bound poliovirus receptor-like 2 (PVRL2) strongly, making the latter its principal ligand.PVRIG is an inducible checkpoint receptor and that targeting PVRIG-PVRL2 interactions results in increased CD8+ T-cell function and reduced tumor growth. PVRIG Protein, Mouse, Recombinant (hFc & Avi) is expressed in HEK293 mammalian cells with C-hFc-Avi tag. The predicted molecular weight is 42.70 kDa and the accession number is A0A1B0GS01.

Murine PVRIG interacted weakly with poliovirus receptor (PVR) but bound poliovirus receptor-like 2 (PVRL2) strongly, making the latter its principal ligand.PVRIG is an inducible checkpoint receptor and that targeting PVRIG-PVRL2 interactions results in increased CD8+ T-cell function and reduced tumor growth. PVRIG Protein, Mouse, Recombinant (hFc & Avi), Biotinylated is expressed in HEK293 mammalian cells with C-hFc-Avi tag. The predicted molecular weight is 42.7 kDa and the accession number is A0A1B0GS01.

Plasminogen activator, urokinase (uPA) is a secreted serine protease whose Dysregulation is often accompanied by various cancers. PLAU inhibition could suppress tumor growth. Collectively, PLAU is necessary for tumor progression and can be a diagnostic and prognostic biomarker in HNSCC. PLAU/uPA Protein, Mouse, Recombinant (His & Avi) is expressed in HEK293 mammalian cells with C-His-Avi tag. The predicted molecular weight is 49.00 kDa and the accession number is P06869.

Liver-intestine cadherin (CDH17) has been known to function as a tumor stimulator and diagnostic marker for almost two decades.In vivo studies showed CDH17 knockout resulted in apoptotic PC tumor death through activating caspase-3 activity. Taken together, CDH17 functions as an oncogenic molecule critical to PC growth by regulating tumor apoptosis signaling pathways and CDH17 could be targeted to develop an anti-PC therapeutic approach. CDH17 Protein, Human, Recombinant (His & Avi), Biotinylated is expressed in HEK293 mammalian cells with C-His-Avi tag. The predicted molecular weight is 87.88 kDa and the accession number is Q12864.

Liver-intestine cadherin (CDH17) has been known to function as a tumor stimulator and diagnostic marker for almost two decades.In vivo studies showed CDH17 knockout resulted in apoptotic PC tumor death through activating caspase-3 activity. Taken together, CDH17 functions as an oncogenic molecule critical to PC growth by regulating tumor apoptosis signaling pathways and CDH17 could be targeted to develop an anti-PC therapeutic approach. CDH17 Domain 3 & 4 Protein, Human, Recombinant (mFc) is expressed in HEK293 mammalian cells with C-mFc tag. The predicted molecular weight is 49.16 kDa and the accession number is Q12864.

transforming growth factor beta receptor 1 (TGFBR1), a key stimulator of tumor proliferation and metastasis, was a direct target of miR‑98‑5p. miR‑98‑5p overexpression resulted in the downregulation of TGFBR1 and the suppression of the viability, proliferation, migration and invasion of A549 and H1299 cells. TGFBR1 Protein, Human, Recombinant (mFc & Avi), Biotinylated is expressed in HEK293 mammalian cells with C-mFc-Avi tag. The predicted molecular weight is 38.2 kDa and the accession number is P36897-1.

Nectin-2 is an adhesion molecule that has been reported to play a role in tumor growth, metastasis and tumor angiogenesis. Nectin-2 expression in ovarian cancer may support tumor cell adhesion, leading to growth and lymph node metastasis. Effect of VEGF on Nectin-2 expression as well as permeability was investigated in HUVEC.

transforming growth factor beta receptor 1 (TGFBR1), a key stimulator of tumor proliferation and metastasis, was a direct target of miR‑98‑5p. miR‑98‑5p overexpression resulted in the downregulation of TGFBR1 and the suppression of the viability, proliferation, migration and invasion of A549 and H1299 cells. TGFBR1 Protein, Human, Recombinant (mFc & Avi) is expressed in HEK293 mammalian cells with C-mFc-Avi tag. The predicted molecular weight is 38.2 kDa and the accession number is P36897-1.

IL-20RA was highly expressed in the tumor tissue of CRC and related to the advanced stage.IL-20RA was involved in regulating oncogenic and immune pathways and affecting the expression of genes related to cell proliferation and immune evasion in CRC.Super-enhancer inhibition by JQ-1 or iBET-151 suppressed the growth of tumor cells and inhibited the expression of IL-20RA.

Acts as a regulator of the antiangiogenic activity on endothelial cells. When overexpressed in endothelial cells, leads to inhibition of cell proliferation and migration and an increase in apoptosis. Inhibits melanoma growth When expressed in tumor-associated vasculature. FILIP1L Protein, Human, Recombinant (His) is expressed in E. coli expression system with N-6xHis tag. The predicted molecular weight is 27.6 kDa and the accession number is Q4L180.

Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. Its pro-apoptotic activity is activated via its interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2. However, this activity is inhibited when the interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2 is displaced by PPP1R13L/iASPP. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis and seems to have an effect on cell-cycle regulation. Regulates the circadian clock by repressing CLOCK-ARNTL/BMAL1-mediated transcriptional activation of PER2.

Calcium/calmodulin-dependent myosin light chain kinase implicated in smooth muscle contraction via phosphorylation of myosin light chains (MLC). Also regulates actin-myosin interaction through a non-kinase activity. Phosphorylates PTK2B/PYK2 and myosin light-chains. Involved in the inflammatory response (e.g. apoptosis, vascular permeability, leukocyte diapedesis), cell motility and morphology, airway hyperreactivity and other activities relevant to asthma. Required for tonic airway smooth muscle contraction that is necessary for physiological and asthmatic airway resistance. Necessary for gastrointestinal motility. Implicated in the regulation of endothelial as well as vascular permeability, probably via the regulation of cytoskeletal rearrangements. In the nervous system it has been shown to control the growth initiation of astrocytic processes in culture and to participate in transmitter release at synapses formed between cultured sympathetic ganglion cells. Critical participant in signaling sequences that result in fibroblast apoptosis. Plays a role in the regulation of epithelial cell survival. Required for epithelial wound healing, especially during actomyosin ring contraction during purse-string wound closure. Mediates RhoA-dependent membrane blebbing. Triggers TRPC5 channel activity in a calcium-dependent signaling, by inducing its subcellular localization at the plasma membrane. Promotes cell migration (including tumor cells) and tumor metastasis. PTK2B/PYK2 activation by phosphorylation mediates ITGB2 activation and is thus essential to trigger neutrophil transmigration during acute lung injury (ALI). May regulate optic nerve head astrocyte migration. Probably involved in mitotic cytoskeletal regulation. Regulates tight junction probably by modulating ZO-1 exchange in the perijunctional actomyosin ring. Mediates burn-induced microvascular barrier injury; triggers endothelial contraction in the development of microvascular hyperpermeability by phosphorylating MLC. Essential for intestinal barrier dysfunction. Mediates Giardia spp.-mediated reduced epithelial barrier function during giardiasis intestinal infection via reorganization of cytoskeletal F-actin and tight junctional ZO-1. Necessary for hypotonicity-induced Ca(2+) entry and subsequent activation of volume-sensitive organic osmolyte/anion channels (VSOAC) in cervical cancer cells. Responsible for high proliferative ability of breast cancer cells through anti-apoptosis.

Amine oxidase copper-containing 1 (AOC1; formerly known as amiloride-binding protein 1) is a secreted glycoprotein that catalyzes the degradation of putrescine and histamine. Polyamines and their diamine precursor putrescine are ubiquitous to all organisms and fulfill pivotal functions in cell growth and proliferation. That the Wilms tumor protein, WT1, which is necessary for normal kidney development, activates transcription of the AOC1 gene. Expression of a firefly luciferase reporter under control of the proximal AOC1 promoter was significantly enhanced by co-transfection of a WT1 expression construct. Binding of WT1 protein to a cis-regulatory element in the AOC1 promoter was confirmed by electrophoretic mobility shift assay and chromatin immunoprecipitation. WT1-dependent control of polyamine breakdown, which is mediated by changes in AOC1 expression, has a role in kidney organogenesis.

Platelet-derived growth factor alpha (PDGFA) is frequently upregulated in various cancers and thought to function as a key player in the development and progression of tumor growth by regulating aspects of cell proliferation, angiogenesis and metastasis. The human platelet-derived growth factor A chain gene (PDGFA) on chromosome 7p22 encodes an important mitogen. Within PDGFA lies a complex minisatellite structure that results in partial duplications of exon 4 and the IVS4 splice donor site. PDGFA Protein, Canine, Recombinant (hFc) is expressed in HEK293 mammalian cells with hFc tag. The predicted molecular weight is 41 kDa and the accession number is A0A8C0M6T8.

Acetylcholinesterase, also known as ACHE, is an enzyme that degrades (through its hydrolytic activity) the neurotransmitter acetylcholine, producing choline and an acetate group. Acetylcholinesterase plays a crucial role in nerve impulse transmission at cholinergic synapses by rapid hydrolysis of the neurotransmitter acetylcholine (ACh). ACHE appears to be a potential therapeutic target at muscle injuries including organophosphate myopathy. It is an externally oriented membrane-bound enzyme and its main physiological role is termination of chemical transmission at cholinergic synapses and secretory organs by rapid hydrolysis of the neurotransmitter acetylcholine (ACh). ACHE plays important roles in the cholinergic system, and its dysregulation is involved in a variety of human diseases. ACHE was significantly down-regulated in the cancerous tissues of 69.2% of hepatocellular carcinoma (HCC) patients, and the low ACHE expression in HCC was correlated with tumor aggressiveness, an elevated risk of postoperative recurrence, and a low survival rate. Both the recombinant ACHE protein and the enhanced expression of ACHE significantly inhibited HCC cell growth in vitro and tumorigenicity in vivo. ACHE as a tumor growth suppressor in regulating cell proliferation, the relevant signaling pathways, and the drug sensitivity of HCC cells. Thus, ACHE is a promising independent prognostic predictor for HCC recurrence and the survival of HCC patients. ACHE is responsible for the hydrolysis of acetylcholine in the nervous system. It is inhibited by organophosphate and carbamate pesticides. However, this enzyme is only slightly inhibited by organophosphorothionates.

PFDN1 expression positively correlated with tumor size and tumor invasion. The inhibitory effect of PFDN1 on tumor cell growth and motility was partially due to G2/M cell cycle blockage and cytoskeletal deficiency. PFDN1 was involved in the progression of CRC, and provide new insights into PFDN1 as a potential therapeutic target for colorectal cancer (CRC) treatment. PFDN1 Protein, Mouse, Recombinant (His) is expressed in E. coli expression system with His tag. The predicted molecular weight is 16.5 kDa and the accession number is Q9CQF7.

Tumor necrosis factor (TNF)-alpha-induced protein 8 (TNFAIP8) family is a newly identified protein with vital roles in maintaining immune homeostasis. Tumor necrosis factor-alpha-inducible protein 8 (TNFAIP8) is a TNF-alpha inducible anti-apoptotic protein with multiple roles in tumor growth and survival. by the creation of cellular autophagy events, TNFAIP8 promotes cell survival and drug resistance in prostate cancer cells. TNFAIP8 regulates Hippo pathway through interacting with LATS1 to promote cell proliferation and invasion in lung cancer. TNFAIP8 may serve as a candidate biomarker for poor prognosis and a target for new therapies.

The miR-137 served as a tumor suppressor in non-small cell lung cancer (NSCLC) and its suppressive effect is mediated by repressing TGFA expression. TGFA gene expression was significantly higher in tumor tissues compared to adjacent normal tissue and high TGFA gene expression strongly correlated with poor survival in patients with lung adenocarcinoma, and miR-374a suppresses lung adenocarcinoma cell proliferation and invasion via targeting TGFA gene expression. Transforming growth factor alpha (TGFA) is a well-characterized mammalian growth factor that might contribute to the development of Cleft lip and palate (CL/P).

ADGRD1 (Adhesion G Protein-Coupled Receptor D1, also known as GPR133) is a Protein Coding gene. 4 alternatively spliced human isoforms have been reported. ADGRD1, an orphan member of the adhesion family of G-protein-coupled receptors, is a critical regulator of the response to hypoxia and tumor growth in Glioblastoma (GBM). ADGRD1 represents a novel molecular target in GBM and possibly other malignancies where hypoxia is fundamental to pathogenesis. Variations in the ADGRD1 locus are linked with differences in metabolism, human height, and heart frequency. ADGRD1 is a Gs protein-coupled receptor belonging to the class of adhesion GPCRs. The adhesion G-protein-coupled receptors (GPCRs), including GPR133, are membrane-bound proteins with long N termini containing multiple domains.

FGF19, also known as FGF-19, is a member of the fibroblast growth factor (FGF) family. FGF family members possess broad mitogenic and cell survival activities, and are involved in a variety of biological processes, including embryonic development, cell growth, morphogenesis, tissue repair, tumor growth and invasion. FGF19 interacts with FGFR1, FGFR2, FGFR3 and FGFR4. Affinity between fibroblast growth factors (FGFs) and their receptors is increased by KL, KLB and heparan sulfate glycosaminoglycans that function as coreceptors. It interacts with KL and KLB directly. However, it interacts with FGFR4 in the presence of heparin, KL or KLB. FGF19 is involved in the suppression of bile acid biosynthesis through down-regulation of CYP7A1 expression, following positive regulation of the JNK and ERK1/2 cascades. It also stimulates glucose uptake in adipocytes.

ING5 belongs to the ING family. It contains 1 PHD-type zinc finger and is a component of the HBO1 complex. HBO1 complex has a histone H4-specific acetyltransferase activity, a reduced activity toward histone H3 and is responsible for the bulk of histone H4 acetylation in vivo. HBO1 complex composed at least of ING4 or ING5, KAT7/HBO1, MEAF6, and one of PHF15, PHF16, and PHF17. ING5 also is a component of the MOZ/MORF complex which is composed at least of ING5, KAT6A, KAT6B, MEAF6, and one of BRPF1, BRD1/BRPF2, and BRPF3. It interacts with EP300 and TP53. MOZ/MORF complex has a histone H3 acetyltransferase activity. Through chromatin acetylation, ING5 may regulate DNA replication and may function as a transcriptional coactivator. It interacts with H3K4me3 and to a lesser extent with H3K4me2. ING5 is similar to ING1, a tumor suppressor protein that can interact with TP53, inhibit cell growth, and induce apoptosis. It can bind TP EP300/p300, a component of the histone acetyltransferase complex, suggesting its involvement in the TP53-dependent regulatory pathway.

FGF-13, also known as FGF17, belongs to the fibroblast growth factor (FGF) family. Members of this family show broad mitogenic and cell survival activities, and play a role in a variety of biological processes including embryonic development cell growth, morphogenesis, tissue repair, tumor growth and invasion. FGF-13 is preferentially expressed in the embryonic brain. It interacts with FGFR3 and FGFR4. FGF-13 plays an important role in the regulation of embryonic development and as signaling molecule in the induction and patterning of the embryonic brain. It is also required for normal brain development.

Tumor protein, also known as TPT1, is a highly conserved protein among many eukaryotic organisms. Tumor protein is involved in a variety of cellular activities, including microtubule stabilization, calcium-binding activities, and apoptosis. The Mammalian translationally controlled tumour protein (TPT1) (or P23) is a protein that has been found to be preferentially synthesised in cells during the early growth phase of some types of tumour, but which is also expressed in normal cells. It was first identified as a histamine-releasing factor, acting in IgE +-dependent allergic reactions. In addition, TPT1 has been shown to bind to tubulin in the cytoskeleton, has a high affinity for calcium, is the binding target for the antimalarial compound artemisinin, and is induced in vitamin D-dependent apoptosis. TPT1 production is thought to be controlled at the translational as well as the transcriptional level.

Platelet-derived growth factor-B (PDGFB) is necessary for normal cardiovascular development. The administration of PDGFB alone normalized tumor vasculature by increasing periendothelial coverage and vascular functionality. Interestingly, this effect exerted by PDGFB was also observed in the presence of DAPT. So PDGFB is able to improve tumor vascularity and allows the anticancer action of DAPT in the tumor. PDGFB Protein, Mouse, Recombinant (His) is expressed in yeast with His tag. The predicted molecular weight is 14.2 kDa and the accession number is Q8R3X9.

Human VEGF121, also known as Vascular endothelial growth factor A, VEGFA, Vascular permeability factor, VPF and VEGF, is a homodimeric, heparin-binding glycoprotein which belongs to the platelet-derived growth factor (PDGF) vascular endothelial growth factor (VEGF) family. VEGF-A is a glycosylated mitogen that specifically acts on endothelial cells and has various effects, including mediating increased vascular permeability, inducing angiogenesis, vasculogenesis, permeabilization of blood vessels and endothelial cell growth, increasing microvascular permeability, promoting cell migration and inhibiting apoptosis. Alternatively spliced transcript variants of VEGF-A encod either secreted or cell-associated isoforms. The lymphangiogenesis may be promoted by upregulation of VEGF121, which may in turn act in part via induction of VEGF-C. It binds to the FLT1 VEGFR1 and KDR VEGFR2 receptors, heparan sulfate and heparin. NRP1 Neuropilin-1 binds isoforms VEGF-165 and VEGF-145. Isoform VEGF165B binds to KDR but does not activate downstream signaling pathways, does not activate angiogenesis and inhibits tumor growth.

Hepatoma-Derived Growth Factor is a original member of the HDGF family. HDGF is a cytoplasmic protein and contains one PWWP domain. HDGF expression levels are high in the nucleus and cytoplasm of smooth muscle and endothelial cells. HDGF has proliferative, angiogenic and neurotrophic activity. HDGF was initially characterized as a secreted mitogen from the Huh-7 human hepatoma cell line. As a heparin-binding protein, which is highly expressed in tumor cells where it stimulates proliferation. HDGF has mitogenic activity for fibroblasts and acts as a transcriptional repressor. It has been shown that HDGF is linked with tumorigenesis and the growth of cancer.

C-Kit/SCF R is a type 3 transmembrane receptor for MGF (mast cell growth factor, also known as stem cell factor). c-Kit contains 5 Ig-like C2-type (immunoglobulin-like) domains and 1 protein kinase domain. It belongs to the protein kinase superfamily and CSF-1/PDGF receptor subfamily. SCF R expression on mast cells enables them to infiltrate SCF-secreting tumors where they promote tumor growth and induce local immune suppression. SCF R is up-regulated on dendritic cells by Th2-orTh17-biasing stimuli, and it is required for subsequent dendritic cell induction of Th2 and Th17 responses. SCF R protects vascular smooth muscle cells from apoptosis and assists in the recovery of cardiac function following myocardial infarction.

Activin Receptor-Like Kinase 1 (ALK-1) is a type I cell-surface receptor for the TGF-β superfamily of ligands, which mediates signaling of BMP9 (bone morphogenetic protein) and BMP10. ALK1 signaling is necessary for angiogenesis during embryogenesis, wound healing, and tumor growth. ALK-1 has a high degree of similarity in serine-threonine kinase subdomains, a glycine and serine rich region preceding the kinase-domain, and a C-terminal tail with other activin receptor-like kinase proteins. ALK-1 is mainly expressed in endothelial cells regulating proliferation and migration in vitro and angiogenesis in vivo. Mutations in ALK-1 as well as in endoglin are associated with hereditary hemorrhagic telangiectasia (HHT), suggesting ALK-1 plays a critical role for in the control of blood vessel development or repair.

Wnt Inhibitory Factor 1 (WIF1) is a secreted protein, which binds WNT proteins and inhibits their activities. WNT proteins are extracellular signaling molecules involved in the control of embryonic development. WIF1 contains a WNT inhibitory factor (WIF) domain and 5 epidermal growth factor (EGF)-like domains. is found to be present in fish, amphibia and mammals. WIF1 is a recurrent target in human salivary gland oncogenesis.WIF1 may be involved in mesoderm segmentation. WIF1 is a tumor suppressor, specifically in nonfunctioning pituitary tumors.

Galectin-3(LGALS3) is also known as Galactose-specific lectin 3, Mac-2 antigen, Carbohydrate-binding protein 35, Laminin-binding protein and Galactoside-binding protein. LGALS3 is highly expressed in early stages of papillary carcinoma, and lowly during tumor progression. LGALS3 is probably forms homo- or heterodimers and secreted by a non-classical secretory pathway and associates with the cell surface. LGALS3 plays an important role during the acquisition of vasculogenic mimicry and angiogenic properties. LGLAS3 takes part in an immune regulator to inhibit T-cell immune responses and promote tumor growth, as a result providing a new mechanism for tumor immune tolerance.

Serine Protease Inhibitor Kazal-Type 1 (SPINK1) is a trypsin inhibitor that prevent the trypsin-catalyzed premature activation of zymogens within the pancreas. Defects in SPINK1 are a cause of pancreatitis (PCTT). A disease characterized by the presence of calculi in pancreatic ducts. It causes severe abdominal pain attacks. Defects in SPINK1 are the cause of susceptibility to tropical calcific pancreatitis (TCP). Recombinant SPINK1 protein (rSPINK1) stimulated cell proliferation in benign RWPE as well as cancerous prostate cells. The research result indicated that the potential of SPINK1 as an extracellular therapeutic target in prostate cancer. In contrast, knockdown of SPINK1 in 22RV1 cells inhibited cell proliferation, cell invasion, and tumor growth in xenograft assays.

Plasminogen activator, urokinase (uPA) is a secreted serine protease whose Dysregulation is often accompanied by various cancers. PLAU inhibition could suppress tumor growth. Collectively, PLAU is necessary for tumor progression and can be a diagnostic and prognostic biomarker in HNSCC. PLAU/uPA Protein (active form), Human, Recombinant (His & Avi), Biotinylated is expressed in HEK293 mammalian cells with C-His-Avi tag. The predicted molecular weight is 49.3 kDa and the accession number is P00749-1.

Claudin-4 (CLDN4) is a key component of tight junctions (TJs) in epithelial cells. CLDN4 is overexpressed in many epithelial malignancies and correlates with cancer progression. Changes in CLDN4 expression have been associated with epigenetic factors (such as hypomethylation of promoter DNA), inflammation associated with infection and cytokines, and growth factor signaling. CLDN4 helps to maintain the tumor microenvironment by forming TJs and acts as a barrier to the entry of anticancer drugs into tumors.

The interplay between glioma stem cells (GSCs) and the tumor microenvironment plays crucial roles in promoting malignant growth of glioblastoma (GBM), the most lethal brain tumor. WISP1 is preferentially expressed and secreted by GSCs. Silencing WISP1 markedly disrupts GSC maintenance, reduces tumor-supportive TAMs (M2), and potently inhibits GBM growth. WISP1 signals through Integrin α6β1-Akt to maintain GSCs by an autocrine mechanism and M2 TAMs through a paracrine manner.

Liver-intestine cadherin (CDH17) has been known to function as a tumor stimulator and diagnostic marker for almost two decades.In vivo studies showed CDH17 knockout resulted in apoptotic PC tumor death through activating caspase-3 activity. Taken together, CDH17 functions as an oncogenic molecule critical to PC growth by regulating tumor apoptosis signaling pathways and CDH17 could be targeted to develop an anti-PC therapeutic approach. CDH17 Domain 6-7 Protein, Human, Recombinant (mFc) is expressed in HEK293 mammalian cells with C-mFc tag. The predicted molecular weight is 50.18 kDa and the accession number is Q12864.

Oncostatin M (OSM) is a glycoprotein belonging to the interleukin-6 family of cytokines that includes leukemia-inhibitory factor, granulocyte colony-stimulating factor, and interleukin 6. OSM encodes a growth regulator, which Inhibits the proliferation of a number of tumor cell lines. It stimulates proliferation of AIDS-KS cells. OSM regulates cytokine production, including IL-6, G-CSF and GM-CSF from endothelial cells. OSM is considered as a pleiotropic cytokine that initiates its biological activities through specific cell surface receptors. The low affinity LIF receptor that shares the similarity of containing protein gp130 has now been identified to be a component of a high- affinity OSM receptor that will transduce OSM signals. OSM has also been shown to play a role in both pro and anti-inflammatory actions. OSM may also be involved in many biometabolism processes including liver development, haematopoeisis, inflammation, bone formation and destruction and possibly CNS development.

Acts as a tumor suppressor in many tumor types; induces growth arrest or apoptosis depending on the physiological circumstances and cell type. Involved in cell cycle regulation as a trans-activator that acts to negatively regulate cell division by controlling a set of genes required for this process. One of the activated genes is an inhibitor of cyclin-dependent kinases. Apoptosis induction seems to be mediated either by stimulation of BAX and FAS antigen expression, or by repression of Bcl-2 expression. Its pro-apoptotic activity is activated via its interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2. However, this activity is inhibited when the interaction with PPP1R13B/ASPP1 or TP53BP2/ASPP2 is displaced by PPP1R13L/iASPP. In cooperation with mitochondrial PPIF is involved in activating oxidative stress-induced necrosis; the function is largely independent of transcription. Prevents CDK7 kinase activity when associated to CAK complex in response to DNA damage, thus stopping cell cycle progression. Induces the transcription of long intergenic non-coding RNA p21 (lincRNA-p21) and lincRNA-Mkln1. LincRNA-p21 participates in TP53-dependent transcriptional repression leading to apoptosis, but seems to have to effect on cell-cycle regulation. Regulates the circadian clock by repressing CLOCK-ARNTL/BMAL1-mediated transcriptional activation of PER2.

Growth factor that plays an essential role in the regulation of embryonic development, cell proliferation, cell migration, survival and chemotaxis. Potent mitogen for cells of mesenchymal origin. Plays an important role in wound healing. Has oncogenic potential and can induce tumor formation. Induces macrophage recruitment, increased interstitial pressure, and blood vessel maturation during angiogenesis. Can initiate events that lead to a mesangial proliferative glomerulonephritis, including influx of monocytes and macrophages and production of extracellular matrix.