Abstract: Objective To explore the affection of overexpression MIPU1 on DOX-mediated apoptosis and the mechanisms underlying, we hope that our studies would provide novel insight into the biological functions of Mipu1, and provide a new clue for preventing the side-effects of DOX during anticancer implication. Methods Apoptosis was induced by Doxorubicin in this experiment. The eukaryotic expression plasmid pEGFP-MIPU1 was constructed previously and delivered into the cells to increase the expression of MIPU1. Firstly, MTT assay was used to estimate the cells viability. Then apoptosis was assessed by using Hoechst staining and flow cytometry (FCM). Thirdly, Western blot and RT-PCR were performed to detect the expression of Bax, P53 and Bcl-2 at the mRNA and protein levels respectively. Results After transfected with pEGFP-MIPU1, the overexpression of MIPU1 significantly attenuated the mortality rate induced by DOX (P<0.05 VS pEGFP+DOX), and markedly decreased the cellular apoptosis treated with DOX (P<0.01 VS pEGFP+DOX ); The overexpression MIPU1 inhibited the increase of P53 and Bax induced by DOX (P<0.05 VS pEGFP+DOX), while reversed the decrease of Bcl-2 expression in DOX-induced HEK293 cells (P<0.05 VS pEGFP+DOX). Conclution Overexpression MIPU1 inhibited apoptosis in HEK293 cells induced by DOX, and the possible mechanism is that MIPU1 decreased the expression of P53 and Bax, and promoted the expression of Bcl-2 in DOX-induced HEK293 cells.

Key words: Key words: apoptosis, Doxorubicin, MIPU1, Bax, Bcl-2