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被E3连接酶PRKN泛素化并降解的DYNLL1调节肺腺癌细胞的细胞周期停滞和凋亡。

DYNLL1 ubiquitinated and degraded by E3 ligase PRKN regulates cell cycle arrest and apoptosis in lung adenocarcinoma cells.

作者信息

Tang Hongjie, Wei Changjiang

机构信息

Department of Surgery, The Fifth People's Hospital of Suzhou/The Affiliated Infectious Hospital of Soochou University, No. 10 Guangqian Road, Suzhou, 215131, Jiangsu, China.

出版信息

Discov Oncol. 2024 Dec 18;15(1):806. doi: 10.1007/s12672-024-01686-7.

DOI:10.1007/s12672-024-01686-7
PMID:39692845
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11655802/
Abstract

This study was intended to investigate the role of DYNLL1 in lung adenocarcinoma (LUAD) and reveal the relevant molecular mechanism. To this end, we manipulated the expression of DYNLL1 and PRKN with shRNA and/or overexpression to assess their effects on A549 cell phenotypes including cell proliferation, cycle arrest and apoptosis using CCK-8 assay, EdU staining, colony formation assay, flow cytometry, TUNEL and western blot. DYNLL1 is a carcinogenic factor in LUAD since it is highly expressed and DYNLL1 upregulation is associated with the low overall survival rate of LUAD patients. Silencing DYNLL1 inhibited the proliferation of LUAD cells while accelerating cell cycle arrest and apoptosis. The regulatory effects of silencing DYNLL1 were counteracted by PRKN deficiency, indicating a functional connection between DYNLL1 and PRKN, which could be attributed to the ubiquitination of DYNLL1 by PRKN. This study could help identify the role of DYNLL1 in LUAD pathogenies and develop reliable therapeutic targets for LUAD improvement.

摘要

本研究旨在探讨DYNLL1在肺腺癌（LUAD）中的作用，并揭示相关分子机制。为此，我们利用短发夹RNA（shRNA）和/或过表达来调控DYNLL1和PRKN的表达，通过CCK-8检测、EdU染色、集落形成实验、流式细胞术、TUNEL和蛋白质免疫印迹法评估它们对A549细胞表型的影响，包括细胞增殖、细胞周期阻滞和凋亡。DYNLL1是LUAD中的致癌因子，因为它高表达，且DYNLL1上调与LUAD患者的低总生存率相关。沉默DYNLL1可抑制LUAD细胞增殖，同时加速细胞周期阻滞和凋亡。PRKN缺陷可抵消沉默DYNLL1的调节作用，表明DYNLL1与PRKN之间存在功能联系，这可能归因于PRKN对DYNLL1的泛素化作用。本研究有助于明确DYNLL1在LUAD发病机制中的作用，并为改善LUAD开发可靠的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17d8/11655802/ae9b2a0a08ca/12672_2024_1686_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17d8/11655802/cefaa192bd51/12672_2024_1686_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17d8/11655802/e48ca235de7a/12672_2024_1686_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17d8/11655802/afb5bf23dc44/12672_2024_1686_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17d8/11655802/c6a2377474cd/12672_2024_1686_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17d8/11655802/068ea558ea62/12672_2024_1686_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17d8/11655802/ae9b2a0a08ca/12672_2024_1686_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17d8/11655802/cefaa192bd51/12672_2024_1686_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17d8/11655802/e48ca235de7a/12672_2024_1686_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17d8/11655802/afb5bf23dc44/12672_2024_1686_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17d8/11655802/c6a2377474cd/12672_2024_1686_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17d8/11655802/068ea558ea62/12672_2024_1686_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/17d8/11655802/ae9b2a0a08ca/12672_2024_1686_Fig6_HTML.jpg

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本文引用的文献

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2
DYNLL1 accelerates cell cycle via ILF2/CDK4 axis to promote hepatocellular carcinoma development and palbociclib sensitivity.DYNLL1 通过 ILF2/CDK4 轴加速细胞周期进程，促进肝细胞癌的发展和帕博西尼敏感性。
Br J Cancer. 2024 Jul;131(2):243-257. doi: 10.1038/s41416-024-02719-2. Epub 2024 Jun 1.
3
USP26 promotes colorectal cancer tumorigenesis by restraining PRKN-mediated mitophagy.
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Oncogene. 2024 May;43(21):1581-1593. doi: 10.1038/s41388-024-03009-0. Epub 2024 Apr 2.
4
Parkin inhibits proliferation and migration of bladder cancer via ubiquitinating Catalase.Parkin 通过泛素化 Catalase 抑制膀胱癌的增殖和迁移。
Commun Biol. 2024 Feb 29;7(1):245. doi: 10.1038/s42003-024-05935-x.
5
ACAT2 may be a novel predictive biomarker and therapeutic target in lung adenocarcinoma.ACAT2 可能是肺腺癌的一种新的预测性生物标志物和治疗靶点。
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6
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7
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