Long non‑coding RNA MCM3AP‑AS1 drives ovarian cancer progression via the microRNA‑143‑3p/TAK1 axis.

Abstract

The long non-coding RNA (lncRNA) MCM3AP antisense 1 (MCM3AP-AS1) has previously been shown to be a key regulator of multiple types of cancer; however whether it is important in the context of ovarian cancer (OC) is uncertain. The present study determined that MCM3AP-AS1 expression in samples from patients with OC was significantly increased, and was associated with tumor stage, presence of lymph node metastases and poorer overall survival. The role of this lncRNA was investigated in vitro, and it was observed that knockdown of MCM3AP-AS1 impaired OC cell proliferation, migration and colony formation. Similarly, it disrupted tumor growth in vivo. The present study further determined that MCM3AP-AS1 was able to directly interact with microRNA (miRNA or miR)-143-3p as a competing endogenous (ce)RNA for this miRNA, thereby regulating the expression of transforming growth factor-β-activated kinase 1 (TAK1), a known target of miR-143-3p in OC. Consistent with this, inhibition of miR-143-3p was sufficient to partially reverse the effects of MCM3AP-AS1-knockdown, which inhibited the proliferation, migration and invasion of OC cells. Together, these results indicate that MCM3AP-AS1 serves as an oncogenic lncRNA in OC by binding to miR-143-3p and thereby promoting TAK1 expression, and suggest that this lncRNA may be a possible target for therapy in OC.