lncRNA MALAT1 sponges miR-124-3p to upregulate PIK3C2A and drive epithelial ovarian cancer progress

Abstract

Epithelial ovarian cancer (EOC) is a highly lethal malignant tumor, with a poor clinical prognosis due to its early peritoneal metastasis. However, the molecular mechanism driving this malignant spread has not been elucidated. In this study, by aggregating the post-transcriptional regulatory network mediated by long non-coding RNAs (lncRNAs), we systematically analyzed the potential regulatory involvement of the MALAT1/miR-124-3p/PIK3C2A axis in the malignant progression of EOC. Through qRT-PCR validation of clinical EOC samples, it was found that MALAT1 and PIK3C2A were significantly upregulated in cancer tissues, while miR-124-3p was significantly down-regulated. Bioinformatics mining of public databases and dual luciferase reporter gene assays supported the interaction between miR-124-3p and PIK3C2A /MALAT1. At the functional level, over-expression of miR-124-3p or knockdown of MALAT1 significantly inhibited the proliferation, invasion, and migration of SKOV3 cells. Mechanistically, long non-coding RNA MALAT1 may function as a competitive endogenous RNA (ceRNA) in post-transcriptional regulation, potentially competing for binding sites with miR-124-3p and thereby contributing to up-regulate the expression of PIK3C2A. In conclusion, this study preliminarily explored that the MALAT1/miR-124-3p/PIK3C2A axis is a potentially relevant signaling pathway associated with the malignant phenotype of EOC, as primarily demonstrated in SKOV3 cells. This finding not only supports an expanded understanding of the regulatory network of non-coding RNAs in EOC metastasis, but also may provide preclinical mechanistic insights into the post-transcriptional regulatory network of non-coding RNAs in EOC metastasis.