LINC00941 is a diagnostic biomarker for lung adenocarcinoma and promotes tumorigenesis through cell autophagy

IF 5.3
Qin Yang, Xi Yong, Xiaoli Chen, Rong Huang, Xiaolin Wang, Zhengmin Xu, Wei Chen
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引用次数: 0

Abstract

Non-small cell lung cancer (NSCLC) is a lethal malignancy. There is mounting evidence indicating that lncRNAs are crucial players with dual roles as both biomarkers and regulators across various cancers. It was reported that LINC00941 plays a cancer-promoting role in NSCLC. However, its impact on tumour autophagy remains poorly understood. In this study, we developed a risk assessment model and identified an autophagy-related lncRNA LINC00941, which has independent predictive and early diagnostic potential. Using RT-qPCR analysis, we confirmed the upregulation of LINC00941 in tumour tissues and cell lines of human lung adenocarcinoma (LUAD). Functional assays, such as CCK8, colony formation and xenograft models, demonstrated the cancer-promoting activity of LINC00941 both in vitro and in vivo. Further analysis using Western blotting analysis, mRFP-GFP-LC3 double fluorescence lentivirus vector and transmission electron microscopy (TEM) confirmed that the knockdown of LINC00941 triggered autophagy. These results indicate that knockdown of LINC00941 induces autophagy and impairs the proliferation of LUAD. Therefore, we propose LINC00941 as an independent biomarker for early diagnosis as well as a therapeutic target in LUAD.

LINC00941 是肺腺癌的诊断生物标志物,通过细胞自噬促进肿瘤发生。
非小细胞肺癌(NSCLC)是一种致命的恶性肿瘤。越来越多的证据表明,lncRNAs 在各种癌症中扮演着生物标志物和调控因子的双重角色。据报道,LINC00941 在 NSCLC 中起着促癌作用。然而,人们对其对肿瘤自噬的影响仍知之甚少。在这项研究中,我们建立了一个风险评估模型,并确定了与自噬相关的lncRNA LINC00941,它具有独立的预测和早期诊断潜力。通过 RT-qPCR 分析,我们证实了 LINC00941 在人类肺腺癌(LUAD)的肿瘤组织和细胞系中的上调。CCK8、集落形成和异种移植模型等功能测试证明了 LINC00941 在体外和体内的促癌活性。利用 Western 印迹分析、mRFP-GFP-LC3 双荧光慢病毒载体和透射电子显微镜(TEM)进行的进一步分析证实,敲除 LINC00941 会引发自噬。这些结果表明,敲除 LINC00941 会诱导自噬并损害 LUAD 的增殖。因此,我们建议将 LINC00941 作为 LUAD 早期诊断的独立生物标记物和治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
11.50
自引率
0.00%
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期刊介绍: The Journal of Cellular and Molecular Medicine serves as a bridge between physiology and cellular medicine, as well as molecular biology and molecular therapeutics. With a 20-year history, the journal adopts an interdisciplinary approach to showcase innovative discoveries. It publishes research aimed at advancing the collective understanding of the cellular and molecular mechanisms underlying diseases. The journal emphasizes translational studies that translate this knowledge into therapeutic strategies. Being fully open access, the journal is accessible to all readers.
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