[RITA combined with temozolomide inhibits the proliferation of human glioblastoma U87 cells].

OBJECTIVE: To observe the effect of RITA, a small molecule that targets p53, combined with temozolomide (TMZ) on proliferation, colony formation and apoptosis of human glioblastoma U87 cells and explore the underlying mechanism. METHODS: Cultured U87 cells were treated with RITA (1, 5, 10, 20 µmol/L), TMZ, or RITA+TMZ (half dose) for 24, 48 or 72 h. MTS assay were used to detect the cell proliferation, and the cell proliferation rate and inhibitory rate were calculated. The effect of combined treatments was evaluated by the q value. The expressions of p53, p21 and other apoptosis-associated genes were detected by qRT-PCR and Western blotting; cell apoptosis was assayed using flow cytometry with Annexin V/PI double staining; colony formation of the cells was detected with crystal violet staining. RESULTS: MTS assay showed that RITA at the 4 doses more potently inhibited U87 cell viability than TMZ at 72 h (P=0.000) with inhibitory rates of 25.94%-41.38% and 3.84%-8.20%, respectively. RITA combined with TMZ caused a more significant inhibition of U87 cells (29.21%-52.11%) than RITA (P<0.01) and TMZ (P=0.000) alone. At the doses above 5 µmol/L, the combined treatments with RITA+TMZ for 48 h resulted in q values exceeding 1.2 and showed an obvious synergistic effect of the drugs. Both RITA and TMZ, especially the latter, significantly increased the expressions of p53, p21, puma, and other apoptosis-associated genes to accelerate apoptosis and inhibit the growth and colony formation of U87 cells, and the effect was more obvious with a combined treatment. CONCLUSION: RITA inhibits the growth of human glioblastoma cells and enhance their sensitivity to TMZ by up-regulating p53 expression, and when combined, RITA and TMZ show a synergistic effect to cause a stronger cell inhibition.

Association between green tea and colorectal cancer risk: a meta-analysis of 13 case-control studies.

OBJECTIVE: Experimental studies have suggested green tea to be a chemopreventive agent for colorectal cancer, and many studies have examined possible associations. However, the conclusions were inconsistent or even contradictory, so we performed a meta-analysis based on published case-control studies to explore if green tea is indeed a protective factor. METHODS: PubMed was searched up to May 10th, 2012 for relevant studies, and references of included studies were manually searched. Finally 13 eligible studies, involving 12,636 cases and 38,419 controls were identified. After data extraction, a meta-analysis was performed using CMA v2 software. RESULTS: The results indicated there may be a weak but not statistically significant reduced risk of colorectal cancer with high dose of green tea intake (OR=0.95, 95% CI:0.81-1.11, p=0.490.69-0.98). This protective effect was also found in all subgroups, except in American and European populations. Sensitivity analysis indicated the result to be robust. Publication bias was not detected by either funnel plot or Egger tests. CONCLUSION: The results of this meta-analysis indicate a weak lower tendency for colorectal cancer development with green tea consumption, but available epidemiologic data are insufficient to conclude that green tea may protect against colorectal cancer in humans.