Abstract
Whilst the role of microRNA‑143 (miR‑143) in myelodysplastic syndrome (MDS) remains unclear, abnormally expressed microRNA‑143 has been detected in many types of cancer tissues. In this study, we describe a cohort study for the verification of miR‑143 expression, as well as the investigation of the molecular mechanisms of miR‑143 in MDS/acute myeloid leukaemia (AML). In a series of experiments, miR‑143 recombinant lentiviral vectors transformed into SKM‑1 cells were either overexpressed or knocked down, and the results illustrated that the overexpression of miR‑143 inhibited SKM‑1 cell growth, arrested the SKM‑1 cells in the G0/G1 phase, interfered with cell proliferation and induced cell apoptosis via the Fas/FasL pathway. Conversely, miR‑143 knockdown induced a decrease in the apoptosis and promoted the proliferation of SKM‑1 cells. Moreover, miR‑143 was shown to suppress MLLT3/AF9 expression by binding to its 3'‑UTR. Taken together, the findings of this study indicate that miR‑143 may be a critical regulator of MDS/AML cell carcinogenesis, acting as a potent antitumour molecular target for the diagnosis or treatment of cancers associated with the abnormal expression of MLLT3/AF9, hence facilitating the development of potential therapeutics against MDS/AML.