Catechin hydrate inhibits proliferation and mediates apoptosis of SiHa human cervical cancer cells

► Dose- and time-dependent induction of apoptosis were observed when SiHa cells were treated with CH. ► CH exhibits anticancer effects by inducing apoptosis in SiHa cells. ► Apoptosis was confirmed by TUNEL Assay. ► qRT–PCR revealed, apoptosis in part by modulating tp53 and caspase-3, -8, and -9 expressions. Catechin hydrate (CH), one of the chemical compounds in green tea, has been shown to inhibit tumor growth. Green tea possesses anticancer potential and is one of the most commonly used herbal medicines worldwide. In this study, we sought to characterize the DNA damage and downstream genes targeted by CH extracts using SiHa human cervical cancer cells. The efficacy of CH in killing cervical cancer cells in vitro was investigated in this study to determine whether CH possesses anticancer potential and could be developed as a therapeutic agent for cervical cancer upon further investigation. To scientifically validate the anticancer activities of CH on cervical cancer, CH was tested for its cytotoxic and growth-inhibition properties, specifically the induction of apoptosis in SiHa cervical cancer cells. CH showed a 50% inhibition of SiHa human cervical cancer cells at a concentration of 196.07μg/mL at 24h. CH induced the several folds increase of caspase-3, -8, and -9 after 24h and 48h; the increase of these genes may be involved in the induction of apoptosis. The analysis of apoptosis by DeadEnd terminal transferase-mediated dUTP-digoxigenin-end labeling (TUNEL) assay was used to further confirm that CH induced apoptosis. The results suggested that CH has the potential to benefit cervical cancer prevention. This is the first report that shows the possible mechanism of the anti-proliferative effects of CH in the prevention of cervical cancer in cell culture models. CH, either in its original form or in combination with other anticancer drugs, could potentially be an alternative medicine for cervical cancer. Further study may increase our understanding of the mechanism by which CH has an effect on cervical cancer therapy.