MicroRNA-497 inhibits multiple myeloma growth and increases susceptibility to bortezomib by targeting Bcl-2.

Multiple myeloma (MM) is a common severe hematopoietic malignancy occuring in aged population. MicroRNA (miR)‑497 was previously reported to contribute to the apoptosis of other cell types, presumably through targeting B‑cell lymphoma 2 (Bcl‑2). In the present study, miRNA and protein expression levels were detected by reverse transcription‑quantitative polymerase chain reaction and western blot analyses, respectively. The cell proliferation and viability was measured using 3‑(4,5‑dimethylthiazol‑2‑yl)‑2, 5‑diphenyltetrazolium bromide and plate clonality assays, and the cell growth cycle was measured with a flow cytometer. Terminal deoxynucleotidyl transferase (TdT)‑mediated dUTP nick‑end‑labeling, Annexin V and caspase‑3 activity assays were performed to examine the cell apoptotic rates. The results showed that miR‑497 was markedly decreased, whereas Bcl‑2 was enhanced in MM tissues and cell lines. miR‑497 targeted Bcl‑2 and affected its downstream apoptosis‑related genes. The overexpression of miR‑497 promoted MM cell apoptosis through cell cycle arrest, and decreased colony genesis ability and viability. In addition, miR‑497 increased the sensitivity of MM cells to bortezomib. Taken together, miR‑497 suppressed MM cell proliferation and promoted apoptosis by directly targeting Bcl‑2 and altering the expression of downstream apoptosis‑related proteins. The combination of miR‑497 and bortezomib may enhance drug sensitivity, serving as a potentially available therapeutic method for MM.