hcc

CCL16 is a member of CC chemokine family. CCL16 cDNA encodes a 120 amino acid peptide along with a 23 amino acids signal peptide that is cleaved to generate 97 amino acid protein. CCL16 is distantly related to other CC chemokines, showing less than 30% sequence identity. CCL16 elicits its effects on cells by interacting with cell surface chemokine receptors such as CCR1, CCR2, CCR5 and CCR8. Recombinant CCL16 has been shown to chemoattract human monocytes and THP1 cells but not resting lymphocytes nor neutrophils. CCL16 has potent myelosuppressive activity, suppresses proliferation of myeloid progenitor cells. CCL16ninduces a calcium flux in THP1 cells that can be desensitized by prior exposure to RANTES, suggesting that CCL16 and RANTES share the same receptor in THP1 cells.

MIP-5 Protein, Human, Recombinant (aa 22-113, His) is expressed in E. coli expression system with His tag. The predicted molecular weight is 11.7 kDa and the accession number is Q16663-1.

CCL14 Protein, Human, Recombinant (His) is expressed in E. coli expression system with His tag. The predicted molecular weight is 10.2 kDa and the accession number is Q16627-1.

CCL14 Protein, Human, Recombinant (aa 28-93, His) is expressed in E. coli expression system with His tag. The predicted molecular weight is 9.3 kDa and the accession number is Q16627-1.

MIP-5 Protein, Human, Recombinant (aa 46-113, His) is expressed in E. coli expression system with His tag. The predicted molecular weight is 8.9 kDa and the accession number is Q16663-1.

CCL16, a chemokine poorly characterized at the functional level. Human CCL16 is a member of the CC family, and its gene maps to human chromosome 17q. In the mouse, only a pseudogene has been identified to date. CCL16 is a functional ligand for CCR1, CCR2, CCR5, and CCR8. Recombinant CCL16 demonstrated chemotactic activity on human monocytes and lymphocytes. Based on the ability of human chemokines to exert activity on and bind to murine receptors, the TSA mouse adenocarcinoma cell line was transfected with human CCL16 cDNA and, in comparison with other cytokines, was shown to be the faster inducer of systemic immune response due to massive, prompt infiltration of leukocytes.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy

Myelin protein zero-like protein 1(MPZL1) is encoded by the MPZL1 gene, which is a single-pass type I membrane protein. It is widely expressed with highest levels in heart, placenta, kidney and pancreas. As cell surface receptor, it involved in signal transduction processes. MPZL1 recruits PTPN11/SHP-2 to the cell membrane and subsequently activate/phosphorylate Src kinase at Tyr426, promoting phosphorylation of cortactin and migration of HCC cells. MPZL1also is a major receptor for concanavalin-A (ConA) and involved in cellular signaling induced by ConA, which probably includes Src family tyrosine-protein kinases.

Single nucleotide polymorphism (SNP) of complement component 2 (C2) has been found to be significantly associated with hepatocellular carcinoma (HCC). Significantly lower C2 expression was found at HCC compared to healthy controls, and C2 was associated with TNM stages. Higher C2 expression was significantly associated with better prognosis, and multivariate analysis showed that C2 was also an independent factor for the prognosis of HCC.

Interleukin (IL)-20 is a member of the IL-10 family of cytokines, which has been reported to participate in autoimmune inflammatory diseases. However, the potential role of IL-20 in hepatocellular carcinoma (HCC) progression has not yet been investigated. In addition, IL-20 expression was significantly associated with tumor size, metastasis, TNM stage and poor prognosis in patients with HCC. IL-20 Protein, Mouse, Recombinant (hFc) is expressed in HEK293 mammalian cells with N-hFc tag. The predicted molecular weight is 44.9 kDa and the accession number is Q9JKV9.

chondrolectin (CHODL) is commonly overexpressed in the majority of lung cancers, indicating a possible correlation between CHODL and metastasis of lung cancer cells. the expression of CHODL is significantly decreased in HCC clinical samples and in HCC cell lines. Overexpression of CHODL in SMMC7721 cells with a lentiviral vector increased SMMC7721 cell migration and invasion.

FKBP11 serve as biomarker and/or therapeutic target for Acute aortic dissection (AAD). FKBP11 during the development of HCC and FKBP11 has the potential to be an early marker for HCC.

SET and MYND domain-containing protein 3, also known as Zinc finger MYND domain-containing protein 1, SMYD3, and ZMYND, is a member of the histone-lysine methyltransferase family. SMYD3 contains one MYND-type zinc finger and one SET domain. SMYD3 is a histone H3 lysine-4-specific methyltransferase. It is expressed in skeletal muscles and testis. It is overexpressed in a majority of colorectal carcinoma (CRC) and hepatocellular carcinoma (HCC). SMYD3 plays an important role in transcriptional regulation in human carcinogenesis. It activates the transcription of a set of downstream genes. Of these downstream genes, there are several oncogenes and genes associated with cell adhesion (including those of N-Myc, CrkL, Wnt1b, L-selectin, CD31 and galectin-4), which have been shown to have effects on cell viability, adhesion, migration and metastasis. Increased SMYD3 expression is essential for the proliferation of breast cancer cells. SMYD3 may be a promising new target of therapeutic intervention for the treatment of cancers or other pathological processes associated with cell adhesion and migration.

Alpha-fetoprotein (AFP) is classified as a member of the albuminoid gene superfamily consisting of albumin, AFP, vitaminD (Gc) protein, and alpha-albumin. AFP is a major plasma protein produced by the yolk sac and the liver during fetal development. It is thought to be the fetal form of serum albumin. AFP binds to copper, nickel, fatty acids and bilirubin and is found in monomeric, dimeric and trimeric forms. AFP is one of the several embryo-specific proteins and is adominant serum protein as early in human embryonic life as one month, when albumin and transferrin are present in relatively small amounts. It is first synthesized in the human by the yolk sac and liver (1-2 months) and subsequently predominantly in the liver. A small amount of AFP is produced by the GI tract of the human conceptus. It has been proved that AFP may reappear in the serum in elevated amounts in adult life in association with normal restorative processes and with malignnt growth. Alpha-fetoprotein (AFP) is a specific marker for hepatocellular carcinoma (HCC), teratoblastomas, and neural tube defect (NTD).

Growth Arrest and DNA Damage-Inducible Protein GADD45 β (GADD45B) is a member of the GADD45 family. GADD45B has been shown to interact with MAP3K4, ASK1, MAP2K7, and GADD45GIP1. GADD45B is involved in the regulation of growth and apoptosis. GADD45B reacts to environmental stresses by mediating activation of stress-responsive MTK1/MEKK4 kinase, which is an upstream activator of both p38 and JNK MAPKs. In addition, GADD45B participates in the down-regulation of hepatocellular carcinoma (HCC). It may serve as a possible therapeutic target.

Eukaryotic translation initiation factor 5A2 (EIF5A2) has been demonstrated to be upregulated in numerous types of human cancer and is associated with cancer progression. Silencing of EIF5A2 in the NSCLC cells resulted in the downregulation of the tumorigenic proteins, apoptosis regulator Bcl-2 and myc proto-oncogene protein, and upregulation of E-cadherin, suggesting that EIF5A2 promotes proliferation and metastasis through these proteins. EIF5A2 may therefore serve as a novel therapeutic target for the treatment of NSCLC. EIF5A2 might be a novel therapeutic target for the inhibition of NPC progress. EIF5A2 overexpression may contribute to cancer progression and poor prognosis, it could be a novel potential prognostic marker for FIGO stage I-II cervical cancer. EIF5A2 upregulation plays an important oncogenic role in gastric cancer. EIF5A2 may represent a new predictor for poor survival and is a potential therapeutic target for gastric cancer. The eukaryotic initiation factor 5A2 (EIF5A2) over-expression enhances HCC cell metastasis. EIF5A2, as a target of PI3K/Akt, promotes melanoma cell invasion and may serve as a promising prognostic marker and a potential therapeutic target for melanoma.

Chemokine (C-X-C motif) ligand 17 (CXCL17) is the latest member of the chemokine family. CXCL17 is a potential oncogene and promising therapeutic target, is an independent biomarker of poor prognosis in patients with breast cancer, and can promote proliferation and migration of breast cancer cells in vitro and in vivo. CXCL17 is expressed in a variety of cancers and promotes tumor progression by recruiting myeloid-derived suppressor cells (MDSCs). CXCL17 attenuates IMQ-induced psoriasis-like skin inflammation by recruiting MDSCs and Tregs, which may be important for regulating excessive inflammation in psoriasis skin. CXCL17 production correlated with adverse immune infiltration and might be an important target for anti-HCC therapies. CXCL17 is a major regulator of mucosal inflammatory responses.

Hepatocellular carcinoma (HCC) is a major contributor to cancer-related deaths due to its often late stage diagnosis, and dermcidin (DCD) may have the potential to be used as a serum biomarker for HCC for more timely diagnoses. Human dermcidin (DCD) is an antimicrobial peptide secreted constitutively by sweat glands. And the role of DCD in ischemic heart disease has drawn increasing attention in particular its relationship with insulin secretion and glycemic control, nitric oxide (NO) synthesis and hypertension, platelet aggregation and acute myocardial infarction (AMI).

KIAA11, also known as p15(PAF), is a proliferating cell nuclear antigen-associated factor that interacts with proliferating cell nuclear antigen(PCNA). It was initially isolated in a yeast two-hybrid screen for PCNA binding partners and was shown to bind PCNA competitively with the cell cycle regulator p21(WAF). KIAA11 is localized primarily in the nucleus. It shares the conserved PCNA binding motif with several other PCNA binding proteins including CDK inhibitor p21. KIAA11 is involved in cell proliferation and plays a role in early tumor recurrence (ETR), and prognosis of hepatocellular carcinoma (HCC). KIAA11 is expressed predominantly in the liver, pancreas, and placenta. It cannot be detected in the heart or brain. It is highly expressed in some tumors, especially esophageal tumors, in anaplastic thyroid carcinomas, and non-small-cell lung cancer lines. Overexpression of KIAA11 predicts high stage, early tumor recurrence, and poor prognosis of hepatocellular carcinoma. It also may be involved in the protection of cells from UV-induced cell death.

Angiopoietin-like protein 1 (ANGPTL1) has been reported to suppress migration and invasion in lung and breast cancer, acting as a novel tumor suppressor candidate. Downregulation of tumor suppressor signaling plays an important role in the pathogenesis of hepatocellular carcinoma (HCC).The downregulation of the angiopoietin-like protein ANGPTL1 is associated with vascular invasion, tumor thrombus, metastasis, and poor prognosis in HCC. Ectopic expression of ANGPTL1 in HCC cells effectively decreased their in vitro and in vivotumorigenicity, cell motility, and angiogenesis. shRNA-mediated depletion of ANGPTL1 exerted opposing effects. ANGPTL1 promoted apoptosis via inhibition of the STAT3/Bcl-2-mediated antiapoptotic pathway and decreased cell migration and invasion via downregulation of transcription factors SNAIL and SLUG. Furthermore, ANGPTL1 inhibited angiogenesis by attenuating ERK and AKT signaling and interacted with integrin α1β1 receptor to suppress the downstream FAK/Src-JAK-STAT3 signaling pathway. Taken together, these results suggest ANGPTL1 as a prognostic biomarker and novel therapeutic agent in HCC. ANGPTL1 expression was down-regulated in CRC tissues and inversely correlated with poor survival. ANGPTL1 repressed migration and invasion of CRC cells, and microRNA-138 was involved in this process. Angiopoietin-like protein 1 (ANGPTL1) has been shown to act as a tumor suppressor by inhibiting angiogenesis, cancer invasion, and metastasis.

Thyroid-stimulating hormone (TSH) is secreted by the pituitary gland and promotes thyroid growth and function, with increased TSH levels typically associated with hypothyroidism. Immunohistochemical analysis revealed predominantly nuclei/peri-nuclei localization of TSHR in cancerous tissues but cell membrane localization in non-cancerous parts. Overexpression of TSHR was found in a great majority of HCC tissues and associated with unfavorable prognosis.

Interleukin (IL)-20 is a member of the IL-10 family of cytokines, which has been reported to participate in autoimmune inflammatory diseases. However, the potential role of IL-20 in hepatocellular carcinoma (HCC) progression has not yet been investigated. In addition, IL-20 expression was significantly associated with tumor size, metastasis, TNM stage and poor prognosis in patients with HCC. IL-20 Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with N-His tag. The predicted molecular weight is 19.4 kDa and the accession number is Q9NYY1.

Dysregulation of MST1/STK4, a key kinase component of the Hippo-YAP pathway, is linked to the etiology of many cancers with poor prognosis. STK4/Hippo pathway may have important therapeutic implications for cancer. The tumor suppressor serine/threonine-protein kinase 4 (STK4) differentially regulates TLR3/4/9-mediated inflammatory responses in macrophages and thereby is protective against chronic inflammation-associated Hepatocellular carcinoma (HCC). STK4 has potential as a diagnostic biomarker and therapeutic target for inflammation-induced HCC.

Loss of function mutations in FGG have been associated with fibrinogen deficiency. FGG mRNA was expressed abnormally in HCC and elevated plasma fibrinogen may serve as a useful predictor of clinical progression of HCC patients. Fibrinogen Gamma Chain Protein, Human, Recombinant is expressed in yeast. The predicted molecular weight is 32.2 kDa and the accession number is P02679-1.

Loss of function mutations in FGG have been associated with fibrinogen deficiency. FGG mRNA was expressed abnormally in HCC and elevated plasma fibrinogen may serve as a useful predictor of clinical progression of HCC patients. Fibrinogen Gamma Chain Protein, Mouse, Recombinant is expressed in yeast. The predicted molecular weight is 30.5 kDa and the accession number is Q3UEM7.

Interleukin (IL)-20 is a member of the IL-10 family of cytokines, which has been reported to participate in autoimmune inflammatory diseases. However, the potential role of IL-20 in hepatocellular carcinoma (HCC) progression has not yet been investigated. In addition, IL-20 expression was significantly associated with tumor size, metastasis, TNM stage and poor prognosis in patients with HCC. IL-20 Protein, Human, Recombinant (hFc) is expressed in HEK293 mammalian cells with N-hFc tag. The predicted molecular weight is 44.8 kDa and the accession number is Q9NYY1-1.

Interleukin (IL)-20 is a member of the IL-10 family of cytokines, which has been reported to participate in autoimmune inflammatory diseases. However, the potential role of IL-20 in hepatocellular carcinoma (HCC) progression has not yet been investigated. In addition, IL-20 expression was significantly associated with tumor size, metastasis, TNM stage and poor prognosis in patients with HCC. IL-20 Protein, Mouse, Recombinant (His) is expressed in HEK293 mammalian cells with N-His tag. The predicted molecular weight is 19.5 kDa and the accession number is Q9JKV9.

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.

Artemin (ARTN) is a member of glial cell line-derived neurotrophic factor (GDNF) family of ligands, and its signaling is mediated via a multi-component receptor complex including the glycosylphosphatidylinositol-anchored GDNF family receptors a (GFRa1, GFRa3) and RET receptor tyrosine kinase. The major mechanism of ARTN action is via binding to a non-signaling co-receptor. The major function of ARTN is to drive the molecule to induce migration and axonal projection from sympathetic neurons. It also promotes the survival, proliferation and neurite outgrowth of sympathetic neurons in vitro. ARTN triggers oncogenicity and metastasis by the activation of the AKT signaling pathway. Recent studies have reported that the expression of ARTN in hepatocellular carcinoma is associated with increased tumor size, quick relapse and shorter survival. Furthermore, ARTN promotes drug resistance such as antiestrogens, doxorubicin, fulvestrant, paclitaxel, tamoxifen and trastuzumab. Moreover, ARTN also stimulates the radio-therapeutic resistance. Hypoxia has been reported to regulate the cancer stem cell (CSC) population yet the underlying mechanism is poorly characterized. Artemin (ARTN) is a member of the glial cell derived neurotrophic factor family of ligands, is a hypoxia-responsive factor and is essential for hypoxia-induced CSC expansion in hepatocellular carcinoma (HCC). Clinically, elevated expression of ARTN in HCC was associated with larger tumor size, faster relapse and shorter survival. In vitro, HCC cells with forced expression of ARTN exhibited reduced apoptosis, increased proliferation, epithelial-mesenchymal transition (EMT) and enhanced motility. Additionally, ARTN dramatically increased xenograft tumor size and metastasis in vivo. Moreover, ARTN also enhanced tumorsphere formation and the tumor initiating capacity of HCC cells, consequent to expansion of the CD133+ CSC population. ARTN transcription was directly activated by hypoxia-induced factor-1α (HIF-1α) and hypoxia induced ARTN promoted EMT and increased the CSC population via AKT signaling.