Association between RECQL5 genetic polymorphisms and susceptibility to breast cancer.

Previous studies indicated that the RECQL5 gene polymorphism was associated with human cancers. However, the association of RECQL5 gene polymorphism with breast cancer remains unclear. In the present study, we investigated the association between polymorphisms of the RECQL gene and breast cancer in a Chinese population. We selected four polymorphisms of the RECQL5 gene (rs820186, rs820196, rs820200, and rs4789223) for the present study. The genotyping was performed using the TaqMan method in 510 patients with breast cancer and 510 age- and sex-matched non-cancer controls. We found that rs820196 and rs828200 polymorphisms of RECQL5 were associated with breast cancer. For rs820196, the CC genotype (16.7 vs 9.4 %, P < 0.001) and C allele (42.5 vs 34.3 %, P < 0.001) were common in the breast cancer patients than in the control subjects, respectively. For rs828200, the GG genotype (23.7 vs 18.0 %, P < 0.001) and G allele (52.7 vs 43.8 %, P < 0.001) were common in the breast cancer patients than in the control subjects, respectively. Haplotype analysis showed that C-G (odds ratio (OR) = 2.247, 95 % confidence interval (CI) 1.854∼2.722; P < 0.001) was associated with increased risk for breast cancer. However, the C-T (OR = 0.175, 95 % CI 0.110∼0.278; P < 0.001) and T-G (OR = 0.544; 95 % CI 0.428∼0.692; P < 0.001) were associated with decreased risk for breast cancer, respectively. The present study indicated that the RECQL5 genetic polymorphism and haplotypes were associated with breast cancer in a Chinese population.

Inhibitory effect of caffeic acid phenethyl ester on the growth of SW480 colorectal tumor cells involves beta-catenin associated signaling pathway down-regulation.

AIM: To study the anti-tumor effect of caffeic acid phenethyl ester (CAPE) and the influence of CAPE on beta-catenin associated signaling pathway in SW480 colorectal cancer (CRC) cells. METHODS: SW480 cells were treated with CAPE at serial concentrations. The proliferative status of cells was measured by methabenzthiazuron (MTT) assay. Cell cycle and cell apoptosis were analyzed using flow cytometry (FCM). Western blotting assay was used to evaluate the protein level of beta-catenin, c-myc and cyclinD1. Beta-catenin localization was determined by indirect immunofluorescence. RESULTS: CAPE displayed a strong inhibitory effect in a significant dose- and time-dependent manner on SW480 cell growth. FCM analysis showed that the ratio of G0/G1 phase cells increased, S phase ratio decreased and apoptosis rate increased after SW480 cells were exposed to CAPE for 24 h. Pretreatment of SW480 cells with CAPE significantly suppressed beta-catenin, c-myc and cyclinD1 protein expression. CAPE treatment was associated with decreased accumulation of beta-catenin protein in nucleus and cytoplasm, and concurrently increased its accumulation on the surface of cell membrane. CONCLUSION: CAPE can inhibit SW480 cell proliferation by inducing cell cycle arrest and apoptosis. Decreased beta-catenin and the associated signaling pathway target gene expression may mediate the anti-tumor effects of CAPE.