LINC01342 promotes the progression of ovarian cancer by absorbing microRNA‐30c‐2‐3p to upregulate HIF3A

Ovarian cancer (OC) is a highly prevalent gynecologic malignancy and its mortality is extremely high. Therefore, the development of novel therapeutic approaches for OC is of great significance. In this study, LINC01342 was upregulated in OC tissue in the GSE38666 microarray and in tumor tissue samples collected in our center. The silencing of LINC01342 suppressed the proliferative and metastatic capacities of A2780 and HO8910 cells. Subcellular distribution assays showed that LINC01342 was mainly enriched in the cytoplasm. Subsequently, the downregulation of microRNA‐30c‐2‐3p was proven to be the target of LINC01342. The silencing of microRNA‐30c‐2‐3p enhanced the clonality and migratory capacity of OC cells. Moreover, the silencing of microRNA‐30c‐2‐3p could reverse the inhibited migration and clonality in OC cells caused by LINC01342 knockdown. In addition, hypoxia‐inducible factor 3 subunit α (HIF3A) was proven to be the target gene of microRNA‐30c‐2‐3p, which was upregulated. HIF3A was negatively regulated by microRNA‐30c‐2‐3p but positively regulated by LINC01342 in OC cells. An RNA binding protein immunoprecipitation assay showed that microRNA‐30c‐2‐3p, LINC01342, and HIF3A could bind to argonaute RISC catalytic component 2. The overexpression of HIF3A reversed the inhibited migration and clonality in OC cells with LINC01342 knockdown. By analyzing the follow‐up data from the enrolled OC patients, the LINC01342 and HIF3A levels were negatively correlated with prognosis, while the microRNA‐30c‐2‐3p level was positively correlated with the same. In short, the upregulated LINC01342 in OC absorbs microRNA‐30c‐2‐3p to release HIF3A. Thus, upregulated HIF3A expression accelerates the progression of OC.