MicroRNA-143 increases cell apoptosis in myelodysplastic syndrome through the Fas/FasL pathway both in vitro and in vivo

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.