Numerous studies have confirmed that microRNAs (miRNAs or miRs) have important roles in cancer biogenesis and development including multiple myeloma (MM). MicroRNA‑25‑3p (miR‑25‑3p) has been proven to promote cancer progression, whereas its functions in MM has not yet been reported, at least to the best of our knowledge. Therefore, the present study aimed to investigate the function of miR‑25‑3p in MM and to identify the potential underlying mechanistic pathway. Herein, it was found that miR‑25‑3p expression was significantly increased in MM tissues and cell lines. The upregulation of miR‑25‑3p was closely associated with anemia, renal function impairment international staging system (ISS) staging and Durie‑Salmon (D‑S) staging. A high level of miR‑25‑3p was predictive of a poor prognosis of patients with MM. In vitro, the knockdown of miR‑25‑3p suppressed the proliferation and promoted the apoptosis of RPMI‑8226 and U266 cells, while the overexpression of miR‑25‑3p exerted opposite effects. In addition, phosphatase and tensin homolog deleted on chromosome 10 (PTEN), a well‑known tumor suppressor, was confirmed as a target of miR‑25‑3p in MM cells. Moreover, it was found that the PTEN expression levels were decreased, and inversely correlated with miR‑25‑3p expression levels in MM tissues. Further analyses revealed that the overexpression of PTEN exerted effects similar to those of miR‑25‑3p knockdown, whereas the knockdown of PTEN partially abolished the effects of miR‑25‑3p inhibitor on MM cells. Accompanied by PTEN induction, miR‑25‑3p promoted PI3K/AKT signaling pathway activation in MM cells. Collectively, these findings demonstrate critical roles for miR‑25‑3p in the pathogenesis of MM, and suggest that miR‑25‑3p may serve as a novel prognostic biomarker and therapeutic target of MM.
Keywords: microRNA‑25‑3p; multiple myeloma; phosphatase and tensin homolog deleted on chromosome 10; PI3K/AKT signaling pathway.