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长链非编码RNA与肺癌中不断演变的耐药性

Long non-coding RNA and Evolving drug resistance in lung cancer.

作者信息

Wang Meibin, Fu Yujie, Zhong Chuyue, Gacche Rajesh N, Wu Peiliang

机构信息

The Dingli Clinical college of Wenzhou Medical University, Wenzhou 325000, PR China.

Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, PR China.

出版信息

Heliyon. 2023 Nov 24;9(12):e22591. doi: 10.1016/j.heliyon.2023.e22591. eCollection 2023 Dec.

DOI:10.1016/j.heliyon.2023.e22591
PMID:38089985
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10711135/
Abstract

Non-small cell lung cancer (NSCLC) is one of the most devastating cancers with a high incidence and mortality rates of all cancers. Locally advanced or metastatic NSCLC patients can benefit from platinum-based chemotherapy and targeted therapy drugs. Nevertheless, primary or acquired drug resistance will result in ineffective treatment, leading to tumor progression. The detailed mechanism underlying drug resistance to NSCLC are complicated and result from various factor. Among them, long noncoding RNAs (lncRNAs) have been found to be critically involved in NSCLC development and play a vital role in mediating therapy resistance. In this review, we attempt to systematically summarize the mechanisms underlying the lncRNA-mediated resistance to chemotherapy agents and targeted therapy drugs against lung cancer.

摘要

非小细胞肺癌(NSCLC)是最具毁灭性的癌症之一,在所有癌症中发病率和死亡率都很高。局部晚期或转移性NSCLC患者可从铂类化疗和靶向治疗药物中获益。然而,原发性或获得性耐药会导致治疗无效,从而导致肿瘤进展。NSCLC耐药的详细机制很复杂,是由多种因素造成的。其中,长链非编码RNA(lncRNA)已被发现与NSCLC的发展密切相关,并在介导治疗耐药中发挥重要作用。在这篇综述中,我们试图系统地总结lncRNA介导的肺癌化疗药物和靶向治疗药物耐药的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da1/10711135/8ae96a89887c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da1/10711135/6cd563b32e9a/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da1/10711135/8ae96a89887c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da1/10711135/6cd563b32e9a/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2da1/10711135/8ae96a89887c/gr2.jpg

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本文引用的文献

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MARCKSL1-2 reverses docetaxel-resistance of lung adenocarcinoma cells by recruiting SUZ12 to suppress HDAC1 and elevate miR-200b.MARCKSL1-2 通过招募 SUZ12 抑制 HDAC1 并上调 miR-200b 逆转肺腺癌细胞对多西紫杉醇的耐药性。
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LINC00323 knockdown suppresses the proliferation, migration, and vascular mimicry of non-small cell lung cancer cells by promoting ubiquitinated degradation of AKAP1.LINC00323基因敲低通过促进AKAP1的泛素化降解来抑制非小细胞肺癌细胞的增殖、迁移和血管拟态形成。
Noncoding RNA Res. 2024 Dec 14;11:131-140. doi: 10.1016/j.ncrna.2024.12.006. eCollection 2025 Apr.
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