Paclitaxel (Taxol) is a natural product and a microtubule polymer stabilizer. Paclitaxel has anti-tumor activity and causes cell death by inducing mitotic arrest, apoptosis, and cell autophagy.

METHODS: Human T-cell lymphoblastic leukemia cells CCRF-HSB-2 were treated with Paclitaxel (0.01-1 µM) for 48 h. Cell growth inhibition was detected by MTT.
RESULTS: Paclitaxel dose-dependently inhibited the growth of CCRF-HSB-2 cells with an IC50 of 0.25 µM.[1]
METHODS: Human gastric cancer cells AGS were treated with Paclitaxel (10-160 nM) for 24-48 h. The expression levels of target proteins were detected by Western Blot.
RESULTS: Paclitaxel induced the up-regulation of the expression of cleaved caspase-3 and cleaved PARP, which are apoptosis-related proteins. [2]
METHODS: Canine mammary tumor cells CHMm were treated with Paclitaxel (0.01-1 μM) for 24 h. Apoptosis was detected using Flow Cytometry.
RESULTS: Paclitaxel dose-dependently induced apoptosis in CHMm cells. [3]

METHODS: To investigate the effect of low-dose Paclitaxel on tumor invasion, Paclitaxel (2.6 mg/kg) was administered intraperitoneally to SCID mice bearing cholangiocarcinoma tumor EGI-1 once daily for two weeks.
RESULTS: Low-dose Paclitaxel treatment reduced the pulmonary spread of EGI-1 cells without significantly affecting their local tumor growth. [4]
METHODS: To develop a preclinical model of Paclitaxel alcohol-induced negative affective symptoms, Paclitaxel (2-8 mg/kg in 1 volume ethanol+1 volume Emulphor-620 +18 volumes distilled water) was injected intraperitoneally into C57BL/6J mice every four injections were given to C57BL/6J mice once every two days.
RESULTS: 8 mg/kg Paclitaxel treatment resulted in the development and maintenance of mechanical and cold abnormalities of pain. Paclitaxel also induced anxiety-like and depressive-like behaviors. Paclitaxel produced behavioral changes in the mouse affective state modeling assay, whereas the increase in injurious responses lasted longer. [5]

To determine which caspases are involved in apoptosis induced by taxol, caspase-3 inhibitor (DEVD-CHO), caspase-6 inhibitor (Z-VEID-FMK), caspase-8 inhibitor (Z-IETD-FMK or IETD-CHO), caspase-9 inhibitors (Z-LEHD-FMK or LEHD-CHO), and caspase-10 inhibitor (Z-AEVD-FMK) are used. These caspase inhibitors are dissolved in dimethyl sulfoxide (Me2SO); the final concentration of Me2SO is 0.1%. Cells (5×105) are preincubated in the presence or absence of 100 μM?each of these inhibitors for 3 h at 37°C then treated with or without 0.1, 0.5, and 1 μM?Paclitaxel for 48 h and processed for annexin V binding assay [1].

1×10^4 cells are plated in 100 μL of the growth medium in the presence or absence of increasing concentrations (0.1-1 μM) of taxol in 96-well plates and cultured at 37°C in 5% CO2 for 12-48 h. The cells are then incubated with 25 μL of MTT (5 mg/mL) at 37°C for 4 h. After dissolving the crystals with 0.04 N HCl in isopropanol, the plates are read in a microplate reader at 570 nm [1].

Adult (250-320 g) male Sprague-Dawley rats are used for all experiments. One week following the DiI injection, rats are anesthetized with isofluorane and injected into the tail vein with 2 mg/kg paclitaxel or its vehicle (1:1:23, cremophor EL:ethanol:0.9% saline). The tail vein injection is repeated three more times every other day for a total of four injections [4].