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本文引用的文献

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BECN2 (beclin 2)-mediated non-canonical autophagy in innate immune signaling and tumor development.BECN2（自噬相关蛋白 Beclin 2）调控的非经典自噬在固有免疫信号转导和肿瘤发生中的作用。
Autophagy. 2020 Dec;16(12):2310-2312. doi: 10.1080/15548627.2020.1839277. Epub 2020 Oct 29.
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Coronavirus interactions with the cellular autophagy machinery.冠状病毒与细胞自噬机制的相互作用。
Autophagy. 2020 Dec;16(12):2131-2139. doi: 10.1080/15548627.2020.1817280. Epub 2020 Sep 23.
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ACTA2-AS1 suppresses lung adenocarcinoma progression via sequestering miR-378a-3p and miR-4428 to elevate SOX7 expression.ACTA2-AS1 通过海绵吸附 miR-378a-3p 和 miR-4428 来抑制肺腺癌进展，从而提高 SOX7 表达。
Cell Biol Int. 2020 Dec;44(12):2438-2449. doi: 10.1002/cbin.11451. Epub 2020 Oct 7.
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EZH2: a novel target for cancer treatment.EZH2：癌症治疗的新靶点。
J Hematol Oncol. 2020 Jul 28;13(1):104. doi: 10.1186/s13045-020-00937-8.
5
Epigenetic Landscape in Pancreatic Ductal Adenocarcinoma: On the Way to Overcoming Drug Resistance?胰腺导管腺癌中的表观遗传学景观：是否有望克服耐药性？
Int J Mol Sci. 2020 Jun 8;21(11):4091. doi: 10.3390/ijms21114091.
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lncRNA CCAT1 Acts as a MicroRNA-218 Sponge to Increase Gefitinib Resistance in NSCLC by Targeting HOXA1.长链非编码RNA CCAT1通过靶向HOXA1充当微小RNA-218的海绵，从而增加非小细胞肺癌对吉非替尼的耐药性。
Mol Ther Nucleic Acids. 2020 Mar 6;19:1266-1275. doi: 10.1016/j.omtn.2020.01.006. Epub 2020 Jan 17.
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lncRNA UCA1 Promotes Gefitinib Resistance as a ceRNA to Target FOSL2 by Sponging miR-143 in Non-small Cell Lung Cancer.长链非编码RNA UCA1通过在非小细胞肺癌中海绵化miR-143作为竞争性内源RNA靶向FOSL2来促进吉非替尼耐药
Mol Ther Nucleic Acids. 2020 Mar 6;19:643-653. doi: 10.1016/j.omtn.2019.10.047. Epub 2019 Nov 29.
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Long Non-Coding RNA in Drug Resistance of Non-Small Cell Lung Cancer: A Mini Review.长链非编码RNA在非小细胞肺癌耐药中的研究进展：一篇综述
Front Pharmacol. 2019 Dec 18;10:1457. doi: 10.3389/fphar.2019.01457. eCollection 2019.
9
Long Noncoding RNA LINC01116 Contributes to Gefitinib Resistance in Non-small Cell Lung Cancer through Regulating IFI44.长链非编码RNA LINC01116通过调控IFI44促进非小细胞肺癌对吉非替尼的耐药性。
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10
Long non-coding RNA MALAT1 enhances the apoptosis of cardiomyocytes through autophagy inhibition by regulating TSC2-mTOR signaling.长链非编码 RNA MALAT1 通过调节 TSC2-mTOR 信号通路抑制自噬增强心肌细胞凋亡。
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长链非编码 RNA ACTA2-AS1 通过抑制 TSC2 抑制自噬来抑制非小细胞肺癌细胞对顺铂的耐药性。

Long non-coding RNA ACTA2-AS1 inhibits the cisplatin resistance of non-small cell lung cancer cells through inhibiting autophagy by suppressing TSC2.

机构信息

Department of Pharmacy, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

出版信息

Cell Cycle. 2022 Feb;21(4):368-378. doi: 10.1080/15384101.2021.2020433. Epub 2022 Jan 5.

DOI:10.1080/15384101.2021.2020433
PMID:34985374
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8855873/
Abstract

Long non-coding RNA (lncRNA) ACTA2-AS1 has been reported to play an important role in the progression of multiple human malignancies. The article aims to explore the role of ACTA2-AS1 on the cisplatin resistance of non-small cell lung cancer (NSCLC). RT-qPCR was performed to investigate the expression of ACTA2-AS1 in cisplatin-resistant NSCLC cell lines. Western blot was used to investigate the effects of ACTA2-AS1 on autophagy-related protein expression. RIP assay and RNA pull down were used to analyze the combination of ACTA2-AS1 and enhancer of zeste homolog 2 (EZH2), and CHIP was used to analyze the combination of tuberous sclerosis complex-2 (TSC2) gene promoter and Lys-27 of histone H3 (H3K27me3). In this study, ACTA2-AS1 was downregulated in cisplatin-resistant NSCLC cell lines. ACTA2-AS1 negatively regulated the cell viability and positively regulated the cell apoptosis of cisplatin-resistant NSCLC cell lines. Furthermore, our results demonstrated that ACTA2-AS1 promoted cisplatin-resistant NSCLC cells apoptosis through inhibiting autophagy. The regulation of ACTA2-AS1 to the cisplatin-resistant NSCLC cell autophagy was reversed by TSC2 increasing. Importantly, our results displayed that ACTA2-AS1 bound with EZH2, and TSC2 gene promoter combined with H3k27me3. The inhibition of ACTA2-AS1 to TSC2 expression was recused by EZH2 silencing. In conclusion, ACTA2-AS1 inhibited the cisplatin resistances of NSCLC cell lines through suppressing TSC2 expressing by recruiting EZH2 to TSC2 gene promoter.

摘要

长链非编码 RNA (lncRNA) ACTA2-AS1 已被报道在多种人类恶性肿瘤的进展中发挥重要作用。本文旨在探讨 ACTA2-AS1 在非小细胞肺癌 (NSCLC) 顺铂耐药中的作用。通过 RT-qPCR 检测顺铂耐药 NSCLC 细胞系中 ACTA2-AS1 的表达。通过 Western blot 检测 ACTA2-AS1 对自噬相关蛋白表达的影响。RIP 测定和 RNA 下拉实验分析 ACTA2-AS1 与增强子的结合锌指蛋白 2 (EZH2)，CHIP 分析结节性硬化复合物-2 (TSC2) 基因启动子和组蛋白 H3 的赖氨酸 27 (H3K27me3) 的结合。在本研究中，ACTA2-AS1 在顺铂耐药 NSCLC 细胞系中下调。ACTA2-AS1 负调控顺铂耐药 NSCLC 细胞系的细胞活力，正调控顺铂耐药 NSCLC 细胞系的细胞凋亡。此外，我们的结果表明，ACTA2-AS1 通过抑制自噬促进顺铂耐药 NSCLC 细胞凋亡。TSC2 的增加逆转了 ACTA2-AS1 对顺铂耐药 NSCLC 细胞自噬的调节。重要的是，我们的结果显示，ACTA2-AS1 与 EZH2 结合，TSC2 基因启动子与 H3k27me3 结合。EZH2 沉默可挽救 ACTA2-AS1 对 TSC2 表达的抑制作用。综上所述，ACTA2-AS1 通过募集 EZH2 到 TSC2 基因启动子，抑制 TSC2 的表达，从而抑制 NSCLC 细胞系的顺铂耐药。