Tanshinone IIA mediates the apoptosis and proliferation of endometrial cancer through the CK2/DBC1/SIRT1/P53 pathway

Abstract The pathogenesis of endometrial cancer (EC) remains unclear. Currently, there is a lack of available drugs that specifically target EC. Here, we demonstrated that both DBC1 and SIRT1 as oncogenic factors were involved in the development and progression of EC and associated with histological grade, lymph node metastasis, depth of myometrial invasion and FIGO stage, the protein interaction ability of DBC1 and SIRT1 in cancer group decreased compared with the control group, and tanshinone IIA promoted apoptosis and inhibited proliferation of Ishikawa cells through P53-Cleaved caspase-3 pathway and Bcl-2 pathway, a process possibly regulated by CK2/DBC1/SIRT1/P53 signaling pathway. In the xenograft model of Ishikawa origin, high-concentration tanshinone IIA also down-regulated the expression of DBC1 and SIRT1, and inhibited the growth of tumors. Our results indicate that DBC1 and SIRT1 may serve as novel molecular targets and tanshinone IIA may play a role in the treatment of EC.