Protein kinase C β inhibits autophagy and sensitizes cervical cancer Hela cells to cisplatin

Recently, autophagy has been indicated to play an essential role in various biological events, such as the response of cervical cancer cells to chemotherapy. However, the exact signalling mechanism that regulates autophagy during chemotherapy remains unclear. In the present study, we investigated the regulation by cisplatin on protein kinase C beta (PKC beta), on B-cell lymphoma 2 (Bcl-2) and on apoptosis in cervical cancer Hela cells. And then we examined the regulation by cisplatin on autophagy and the role of autophagy on the chemotherapy in Hela cells. In addition, the regulation of the PKC beta on the autophagy was also investigated. Our results indicated that cisplatin promoted PKC beta in Hela cells. The PKC beta inhibitor reduced the cisplatin-induced apoptosis, whereas increased the cisplatin-induced autophagy in Hela cells. On the other side, the PKC beta overexpression aggravated the cisplatin-induced apoptosis, whereas down-regulated the cisplatin-induced autophagy. Taken together, our study firstly recognized the involvement of PKC beta in the cytotoxicity of cisplatin via inhibiting autophagy in cervical cancer cells. We propose that PKC beta would sensitize cervical cancer cells to chemotherapy via reducing the chemotherapy induced autophagy in cancer cells.