PSME3 induces radioresistance and enhances aerobic glycolysis in cervical cancer by regulating PARP1

Cervical cancer (CC) ranks the fourth in gynecologic cancers. The incidence and mortality of CC has been decreased due to the cancer screening and early treatments in recent years, but the prognosis of CC patients at advanced stage is still sorrowful. Whether PSME3 exerted a role in the radioresistance of CC cells remains to be investigated. In this study, the expression of PSME3 in mRNA and protein levels was measured by RT-qPCR and western blot analysis, and increased expression of PSME3 in CC tissues and cells was observed. CCK-8 and colony formation assay revealed that the cell viability and proliferation of Hela and CaSki cells treated with different doses of X-ray was reduced due to the depletion of PSME3, indicating that silencing of PSME3 enhanced the radiosensitivity of CC cells. In addition, repair on DNA damage in CC cells was enhanced by PSME3 and the damage was attenuated by PSME3. Besides, the expression of glycolysis-related proteins (GLUT1, PGC-1α, LDHA and HK2) were enhanced by PSME3 but reduced by silencing PSME3 in CC cells. PSME3 restraint attenuated the levels of glucose consumption and lactate production, suggesting PSME3 depletion suppressed abnormal glycolysis of CC cells. Mechanically, PSME3 increased the PARP1 expression via elevating c-myc. Finally, we observed PSME3 attenuation inhibited CC growth in vivo. In conclusion, PSME3 enhanced radioresistance and aerobic glycolysis in CC by regulating PARP1, which might shed a light into the function of PSME3 in CC treatment. •PSME3 level was boosted in CC, and PSME3 reduced the radiosensitivity of CC.•PSME3 elevated DNA damage, restrained damage repair and enhanced abnormal glycolysis of CC cells.•PSME3 increased the PARP1 expression via elevating c-myc.•PSME3 aggravated CC growth in vivo.