Copyright (c) 2023 Wenfei Liu, Surong Fang, Zhenhua Yang, Jiyong Ma, Yan Tan, Yubao Chen, Kai Zhang, Kai Liu, Wei Gu
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.ITGA9-AS1 up-regulates ITGA9 by targeting miR-4765 and recruiting HNRNPU to affect the proliferation and apoptosis of non-small cell lung cancer cells
Corresponding Author(s) : Wei Gu
Cellular and Molecular Biology,
Vol. 69 No. 14: Cancer molecular biology: Diagnosis and treatment
Abstract
Long non-coding RNAs (lncRNAs) have been regarded as promising biomarkers in the regulation of various biological and pathological processes of non-small cell lung cancer (NSCLC). LncRNAITGA9-AS1 has been reported to be down-regulated in elderly patients with lung cancer, but how it may influence NSCLC remains to be identified. Therefore, we aim to explore the specific mechanism involving ITGA9-AS1 and ITGA9 in NSCLC. A functional assay was conducted to verify ITGA9-AS1's proliferative effects on NSCLC cells. Mechanism experiments with bioinformatics predictions were performed to explore the interaction of ITGA9-AS1 and ITGA9 in NSCLC cells. ITGA9-AS1 inhibited NSCLC cell proliferation while enhancing cell apoptosis. It up-regulated ITGA9 by competitively sponging miR-4765, and it stabilizedITGA9 mRNA by recruiting a RNA-binding protein (RBP)-HNRNPU (heterogeneous nuclear ribonucleoprotein U) in NSCLC cells. ITGA9-AS1 suppressed NSCLC progression by the up-regulation of ITGA9 via targeting miR-4765 and recruiting HNRNPU.
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