Tannic acid, an inhibitor of poly(ADP-ribose) glycohydrolase, sensitizes ovarian carcinoma cells to cisplatin.

Tannic acid (TA) has been associated with anticancer functions in multiple tumor types both in vitro and in vivo. However, its effect on ovarian carcinoma cells has not been investigated, and its underlying anticancer mechanism(s) remain unclear. In this study, the effects of TA alone and in combination with cisplatin were evaluated using ovarian carcinoma cell lines. Combined treatment with TA and cisplatin was found to induce apoptosis and increase DNA damage in the cisplatin-resistant (SKOV-3 CDDP/R) and cisplatin-sensitive (SKOV-3) human ovarian carcinoma cell lines, respectively. TA was also found to enhance the toxicity of cisplatin in ovarian carcinoma cells associated with the inhibition of poly(ADP-ribose) glycohydrolase (PARG) expression, increase the accumulation of poly(ADP-ribose) (pADPr), following the release of apoptosis-inducing factor, and the activation of caspase-3. In conclusion, as a PARG inhibitor, TA showed anticancer activity and increased the sensitivity of SKOV-3 cells and SKOV-3 CDDP/R cell lines to cisplatin.