Common genetic variants mapping to two distinct regions of RAD51B, a paralog of RAD51, have been associated with breast cancer risk in genome-wide association studies (GWAS). RAD51B is a plausible candidate gene because of its established role in the homologous recombination (HR) process. How germline genetic variation in RAD51B confers susceptibility to breast cancer is not well understood. Here, we investigate the molecular function of RAD51B in breast cancer cell lines by knocking down RAD51B expression by small interfering RNA and treating cells with DNA-damaging agents, namely cisplatin, hydroxyurea, or methyl-methanesulfonate. Our results show that RAD51B-depleted breast cancer cells have increased sensitivity to DNA damage, reduced efficiency of HR, and altered cell cycle checkpoint responses. The influence of RAD51B on the cell cycle checkpoint is independent of its role in HR and further studies are required to determine whether these functions can explain the RAD51B breast cancer susceptibility alleles.

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The burden of cancer incidence and mortality is rapidly increasing worldwide. The second most frequent cancer in men is prostate cancer which affects 1.41 million people worldwide (WHO statistics). Stevioside is an easily available item and it was observed to significantly inhibit cancer cell growth. Our study aims to analyze Molecular mechanisms underlying the chemopreventive anticancer activity of Stevioside on human prostate cancer cell lines. Prostate cancer cells were treated with Stevioside and the level of Bcl-2, Mcl-1, and Caspase-3 was estimated respectively. Data were expressed as the mean ± SD of 3 individual experiments performed in triplicate. Statistical analysis was performed using one-way ANOVA. In PC-3 cells, the effect of Stevioside extracts on cell viability was analyzed through MTT assay with a significant decrease in the percentage of viable cells with an increase in concentration, while the Mcl-1 gene with a decrease in fold change with a rise in concentration. Caspase 3 with a significant increase in fold change with an increase in concentration indicates effective apoptosis and also inhibits the Bcl-2 gene with a decrease in fold change with a rise in concentration with a significance of p<0.05. According to the results Stevioside extract considerably and strongly (by a significant fold change) suppresses the proliferation of cancer cells. The results imply that Stevioside may be turned into a natural prostate cancer medication and further investigation is necessary to establish the daily intake of Stevia products that is both safe and beneficial to the health of the human body.