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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Cell Cycle, Cell Line, Tumor, Cell Proliferation, Gene Expression Regulation, Neoplastic, Humans, Jurkat Cells, MicroRNAs, Microfilament Proteins, Nuclear Proteins, Precursor Cell Lymphoblastic Leukemia-Lymphoma.
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Does microRNA-144 regulate cancer cell proliferation and cell-cycle transition in acute lymphoblastic leukemia through the interaction of FMN2? Context: In this study, we explored the functional roles of microRNA-144 (miR-144) upregulation and downregulation in human acute lymphoblastic leukemia (ALL). Gene expression of miR-144 was examined by qRT-PCR in both ALL cell lines and T-leukemic cells of ALL patients. In ALL cell lines Molt-3 and Jurkat cells, miR-144 was either upregulated or downregulated through lentiviral transduction. The subsequent effects of miR-144 upregulation or downregulation on ALL proliferation, cell-cycle transition, and in vivo xenograft were assessed. Possible downstream target of miR-144, human formin-2 (FMN2), was assessed by dual-luciferase activity assay, qRT-PCR and western blot. FMN2 was then overexpressed in miR-144-upregulated Molt-3 and Jurkat cells to assess its effect on miR-144 induced tumor suppression on ALL proliferation and cell-cycle transition. MiR-144 was significantly downregulated in both ALL cell lines and T-leukemic cells of ALL patients. Lentiviral transfection successfully induced miR-144 upregulation or downregulation in Molt-3 and Jurkat cells without affecting cell viability. Functional assays demonstrated that miR-144 upregulation suppressed ALL proliferation and cell-cycle transition in vitro, and growth of Jurkat xenograft in vivo, whereas miR-144 downregulation had no functional effect on ALL development. Multiple approaches confirmed that FMN2 was the downstream target of miR-144 in ALL. Finally, overexpressing FMN2 reversed the inhibitory effects of miR-144-upregulation on ALL proliferation and cell-cycle transition.
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MiR-144 is functioning as a tumor suppressor in ALL, very likely through the inverse regulation of its target gene FMN2. Final Decision: yes