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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: OBJECTIVE, METHODS, RESULTS. Meshes: Carcinoma, Non-Small-Cell Lung, Cell Cycle Proteins, Cell Line, Cell Line, Tumor, Cell Proliferation, Disease Progression, Female, Gene Expression Regulation, Neoplastic, Homeodomain Proteins, Humans, Lung Neoplasms, Male, MicroRNAs, Middle Aged, Neoplasm Metastasis, Tissue Inhibitor of Metalloproteinase-2, Tumor Suppressor Proteins, Up-Regulation.
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Does miR-761 promote Progression and Metastasis of Non-Small Cell Lung Cancer by Targeting ING4 and TIMP2? Context: The aim of this study was to investigate the role of microRNA miR-761 in the progression and metastasis of non-small cell lung cancer (NSCLC), and the mechanisms by which miR-761 regulates cell proliferation and metastatic activity of NSCLC cell lines. Quantitative real-time PCR (qRT-PCR) was used to assess miR-761 expression in NSCLC serum and tissue. MTT, wound healing, and transwell assays were performed to examine the role of miR-761 in regulation of cell proliferation and metastatic activity in NSCLC cell lines. In addition, the correlations of miR-761 expression with clinical-pathologic factors were statistically analyzed. Finally, we investigated whether miR-761 promotes proliferation and metastasis in NSCLC cell lines by targeting ING4 (inhibitor of growth family, member 4) and TIMP2 (tissue inhibitor of metalloproteinase 2). MiR-761 was significantly upregulated in both NSCLC serum and tissues as compared to normal participants and paired noncancerous tissues respectively. Ectopic expression of miR-761 promoted cell proliferation and metastasis in H460 cells, while miR-761 inhibitor reduced proliferation rates and metastasis in H23 cells. Furthermore, luciferase reporter assay and functional analyses indicated that miR-761 directly targeted ING4 and TIMP2.
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miR-761 promotes progression and metastasis of NSCLC by targeting ING4 and TIMP2. Final Decision: yes