MiR-93-5p inhibits ovarian cancer through SLC7A11-mediated-ferroptosis

Abstract

AimOvarian cancer (OC) is the most lethal gynecological malignancy, which seriously affects the prognosis and life quality of female patients. Therefore, new therapeutic targets and treatments are urgently needed. MethodsExpression levels of miR-93-5p and SLC7A11 and ferroptosis status in paracancerous and tumor tissues were examined and compared. The effect of the miR-93-5p-SLC7A11 regulatory loop on the malignant phenotype as well as the ferroptosis phenotype of SKOV3 cells was assessed. Furthermore, the interaction between miR-93-5p and SLC7A11 was confirmed via rescue experiment. ResultsIn this study, we found that miR-93-5p was lowly expressed in cancer tissues, and suggested that overexpression of miR-93-5p could target SLC7A11 to reduce its expression and promote ferroptosis, thereby inhibiting the malignant biological behaviors such as proliferation, invasion and migration, while knockdown of miR-93-5p restrained ferroptosis and promoting tumor growth. Besides, erastin, as a specific inhibitor of SLC7A11, could target down the expression of SLC7A11, induce the occurrence of ferroptosis, and reverse the effect of knockdown of miR-93-5p. ConclusionsTaken together, our findings disclosed that miR-93-5p increased the level of ferroptosis and inhibited the progression of OC by targeting and inhibiting the expression level of SLC7A11, which was a potential treatment in OC.