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.
Highlights
Lung cancer is one of the most common malignancies in the world[1]
Results miR-1260b was increased in the plasma of Non-small cell lung cancer (NSCLC) patients At first, the data of gene expression microarray (GSE68951)[13] were downloaded from Gene Expression Omnibus (GEO) database and the peripheral blood profiles of patients with NSCLC and controls were obtained
By targeting SOCS6, miR-1260b mediated by YY1, regulates p38 and ERK expression involved in KIT signaling
Summary
Lung cancer is one of the most common malignancies in the world[1]. In China, there were 733,000 lung cancer cases and 61,000 lung cancer deaths in 2015, which ranks first in the incidence and death of all malignant tumors[3]. Lung cancer has become a major public health problem that threatens the lives and health of people in our country and even the world. Of. Cancer is a type of disease that involves multiple genetic alterations, resulting in the continued proliferation of cells. In the development of tumors, changes in various regulatory factors, including the activation of oncogenes and the inactivation of tumor suppressor genes, are currently important anti-tumor targets. Abnormal expression of Cyclins family is one type of the important regulatory factors of tumor cell proliferation[4].
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