1. Correction: miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate cell proliferation and apoptosis in NSCLC
- Author
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Xia, Yang, Wei, Ke, Yang, Feng-Ming, Hu, Liu-Qing, Pan, Chun-Feng, Pan, Xiang-Long, Wu, Wei-Bing, Wang, Jun, Wen, Wei, He, Zhi-Cheng, Xu, Jing, Xu, Xin-Feng, Zhu, Quan, and Chen, Liang
- Subjects
Cancer Research ,Lung Neoplasms ,Immunology ,Correction ,Apoptosis ,Suppressor of Cytokine Signaling Proteins ,Cell Biology ,Transfection ,Up-Regulation ,MicroRNAs ,Proto-Oncogene Proteins c-kit ,Cellular and Molecular Neuroscience ,Mechanisms of disease ,Carcinoma, Non-Small-Cell Lung ,Cell Line, Tumor ,miRNAs ,Humans ,Non-small-cell lung cancer ,YY1 Transcription Factor ,Cell Proliferation ,Signal Transduction - Abstract
Non-small cell lung cancer (NSCLC) is one of the most common aggressive malignancies. miRNAs have been identified as important biomarkers and regulators of NSCLC. However, the functional contributions of miR-1260b to NSCLC cell proliferation and apoptosis have not been studied. In this study, miR-1260b was upregulated in NSCLC plasma, tissues, and cell lines, and its high expression was correlated with tumor size and progression. Functionally, miR-1260b overexpression promoted cell proliferation and cell cycle, conversely inhibited cell apoptosis and senescence. Mechanically, miR-1260b negatively regulated SOCS6 by directly binding to its 3'-UTR. Furthermore, miR-1260b-mediated suppression of SOCS6 activated KIT signaling. Moreover, YY1 was an upstream regulator of miR-1260b. This study is the first to illustrate that miR-1260b, mediated by YY1, activates KIT signaling by targeting SOCS6 to regulate NSCLC cell proliferation and apoptosis, and is a potential biomarker and therapeutic target for NSCLC. In sum, our work provides new insights into the molecular mechanisms of NSCLC involved in cell proliferation and apoptosis.
- Published
- 2020