Long noncoding RNA LINC00152 promotes cell proliferation through competitively binding endogenous miR‐125b with MCL‐1 by regulating mitochondrial apoptosis pathways in ovarian cancer

Abstract

Abstract Recently, an increasing number of studies have focused on the key function of long noncoding RNA s (lnc RNA s) in biological activity. Abnormal lnc RNA expression was found to relate to the development and pathogenesis of multiple cancers. Lnc RNA LINC 00152 served as an oncogene in multiple cancers; however, its role in ovarian cancer remains unknown. In our research study, LINC 00152 was upregulated in ovarian cancer tissues and cell lines. An increasing LINC 00152 level was positively correlated with the histological grade, clinical stage, and poor prognosis of ovarian cancer patients. In addition, knockdown of LINC 00152 reduced cell growth, induced cell apoptosis, and suppressed tumor growth. Moreover, we revealed that LINC 00152 and Myeloid cell leukemia‐1 ( MCL ‐1) were targeted by miR‐125b and had the same miR‐125b combining site. The miR‐125b level was negatively correlated with the expression of LINC 00152, while MCL ‐1 was positively related to the LINC 00152 level. MiR‐125b could affect LINC 00152 levels as evaluated by qRT ‐ PCR . Finally, we affirmed that LINC 00152 mediated cell proliferation by affecting MCL ‐1 expression and MCL ‐1‐mediated mitochondrial apoptosis pathways and by working as a competitive endogenous RNA (ce RNA ) of miR‐125b. In summary, based on ce RNA theory, the combined research on miR‐125b and MCL ‐1, and taking LINC 00152 as a new study point, we provide new insight into the molecular mechanism of reversing cell proliferation in ovarian cancer.