Copyright (c) 2023 Yongjun Deng, Huimin Li, Chao x Chao Liu, Xiuqiong Xia, Yanhua Lv, Dandan Zhang, Jianping Liang
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.Long-non-coding RNA AK001058: A genetic biomarker in cisplatin sensitivity of non-small-cell lung carcinoma
Corresponding Author(s) : Jianping Liang
Cellular and Molecular Biology,
Vol. 69 No. 14: Cancer molecular biology: Diagnosis and treatment
Abstract
Previous evidences have shown that lncRNA AK001058 serves as an oncogene. This study aims to elucidate the expression characteristic of AK001058 in NSCLC samples, and its potential influence on the malignant progression and cisplatin resistance of NSCLC. Relative levels of AK001058 and IGF2 in NSCLC and non-tumoral tissues were detected by qRT-PCR. Proliferation inhibition rate and migratory rate in DDP-induced SPC-A1 and A549 cells were examined by CCK-8 and Transwell assay, respectively. Subsequently, DDP-resistant SPC-A1 and A549 cell lines were generated, and the role of AK001058 in affecting their cell phenotypes was determined. Using dual-luciferase reporter assay, the binding relationship between AK001058 and IGF2 was verified. Their co-regulation on DDP-resistant NSCLC cells was finally explored via rescue experiments. AK001058 was upregulated in NSCLC samples. The proliferative rate was dose-dependently and time-dependently declined in DDP-induced SPC-A1 and A549 cells. Cisplatin induction upregulated AK001058 in NSCLC cells, and attenuated migratory potential. Transfection of sh-AK001058 reduced proliferative and migratory rates in SPC-A1/DDP and A549/DDP cells. IGF2 was the downstream target binding AK001058, which was lowly expressed in NSCLC samples. AK001058 upregulation in NSCLC reduces cisplatin sensitivity and promotes malignant progression by negatively regulating IGF2, leading to cisplatin resistance.
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