MicroRNA­143 increases cell apoptosis in myelodysplastic syndrome through the Fas/FasL pathway both in vitro and in vivo.

ABSTRACT

Whilst the role of microRNA­143 (miR­143) in myelodysplastic syndrome (MDS) remains unclear, abnormally expressed microRNA­143 has been detected in many types of cancer tissues. In this study, we describe a cohort study for the verification of miR­143 expression, as well as the investigation of the molecular mechanisms of miR­143 in MDS/acute myeloid leukaemia (AML). In a series of experiments, miR­143 recombinant lentiviral vectors transformed into SKM­1 cells were either overexpressed or knocked down, and the results illustrated that the overexpression of miR­143 inhibited SKM­1 cell growth, arrested the SKM­1 cells in the G0/G1 phase, interfered with cell proliferation and induced cell apoptosis via the Fas/FasL pathway. Conversely, miR­143 knockdown induced a decrease in the apoptosis and promoted the proliferation of SKM­1 cells. Moreover, miR­143 was shown to suppress MLLT3/AF9 expression by binding to its 3'­UTR. Taken together, the findings of this study indicate that miR­143 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.