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LINC01296/miR-141-3p/ZEB1-ZEB2轴通过增强上皮-间质转化过程促进肿瘤转移。

LINC01296/miR-141-3p/ZEB1-ZEB2 axis promotes tumor metastasis via enhancing epithelial-mesenchymal transition process.

作者信息

Sun Zhenqiang, Shao Bo, Liu Zaoqu, Dang Qin, Guo Yaxin, Chen Chen, Guo Yuying, Chen Zhuang, Liu Jinbo, Hu Shengyun, Yuan Weitang, Zhou Quanbo

机构信息

Department of Colorectal Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, China.

Academy of Medical Sciences, Zhengzhou University, Zhengzhou 450052, Henan, China.

出版信息

J Cancer. 2021 Mar 5;12(9):2723-2734. doi: 10.7150/jca.55626. eCollection 2021.

DOI:10.7150/jca.55626
PMID:33854632
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8040730/
Abstract

Tumor metastasis seriously affects the survival of patients. In recent years, some studies confirmed that long non-coding RNA (lncRNA) played an essential role in tumor progression. A few studies reported that LINC01296 acted as an oncogenic regulator of cancer. However, its in-depth specific biological mechanism in tumor metastasis is still unknown. Real-time quantitative PCR (qPCR) was performed to detect the expression of LINC01296 and miR-141-3p in NSCLC, CRC tissues and cell lines, and the dual luciferase report was used to evaluate the relationship between LINC01296, miR-141-3p and ZEB1/ZEB2 relationship. Western blot experiments are used to detect changes in protein levels. Transwell and wound healing measures migration and invasion capabilities. In this study, we used non-small cell lung cancer (NSCLC) and colorectal cancer (CRC) as the research objects, LINC01296 was found to be highly expressed in NSCLC and CRC tissues and positively related to poor prognosis. We also demonstrated LINC01296 regulated NSCLC and CRC invasion and metastasis by modulating epithelial-mesenchymal transition (EMT) by up-regulating ZEB1 and ZEB2. Consequently, LINC01296 acted as a sponge of miR-141-3p, which negatively regulates EMT process. The report revealed a new mechanism by which LINC01296 regulates the EMT process through miR-141-3p/ZEB1-ZEB2 axis and affects cancer metastasis.

摘要

肿瘤转移严重影响患者的生存。近年来,一些研究证实长链非编码RNA(lncRNA)在肿瘤进展中起重要作用。一些研究报道LINC01296作为癌症的致癌调节因子。然而,其在肿瘤转移中深入的具体生物学机制仍不清楚。采用实时定量PCR(qPCR)检测LINC01296和miR-141-3p在非小细胞肺癌(NSCLC)、结直肠癌组织及细胞系中的表达,并利用双荧光素酶报告基因检测评估LINC01296、miR-141-3p与ZEB1/ZEB2之间的关系。通过蛋白质印迹实验检测蛋白质水平的变化。采用Transwell和伤口愈合实验检测迁移和侵袭能力。在本研究中,我们以非小细胞肺癌(NSCLC)和结直肠癌(CRC)为研究对象,发现LINC01296在NSCLC和CRC组织中高表达,且与不良预后呈正相关。我们还证明LINC01296通过上调ZEB1和ZEB2调节上皮-间质转化(EMT),从而调控NSCLC和CRC的侵袭和转移。因此,LINC01296作为miR-141-3p的海绵,负向调节EMT过程。该报告揭示了一种新的机制,即LINC01296通过miR-141-3p/ZEB1-ZEB2轴调节EMT过程并影响癌症转移。

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本文引用的文献

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Up-regulation of long intergenic noncoding RNA 01296 in ovarian cancer impacts invasion, apoptosis and cell cycle distribution via regulating EMT.
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Cell Death Dis. 2024 Dec 18;15(12):895. doi: 10.1038/s41419-024-07259-4.
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