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利多卡因通过 SIRT5 介导的琥珀酰化作用降低 HIST1H2BL 水平来抑制肺癌进展。

Lidocaine inhibits the lung cancer progression through decreasing the HIST1H2BL levels via SIRT5 mediated succinylation.

机构信息

Department of Oncology, Jiangxi Provincial Chest Hospital, Nanchang, China.

Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Enze Hospital, Taizhou Enze Medical Center (Group), No.1, Tongyang Road, Luqiao District, Taizhou City, 318020, Zhejiang Province, China.

出版信息

Sci Rep. 2024 Oct 7;14(1):23310. doi: 10.1038/s41598-024-73966-9.

DOI:10.1038/s41598-024-73966-9
PMID:39375419
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11458836/
Abstract

Lung cancer is a malignant tumor originating from the bronchial mucosa or gland of the lung. Recently, lidocaine, a widely used amide local anesthetic, was demonstrated to inhibit many cancer progression. This research was performed to explore the specific mechanism of lidocaine in the lung cancer progression. The human normal lung epithelial cells (BEAS-2B), and NSCLC cell lines (A549 and H1299) were used and treated with lidocaine in this study. The cell biological behaviors were detected by CCK-8, wound healing and transwell assay. Besides, the mRNA and protein levels of related genes were detected by western blot. The results showed that lidocaine treatment significantly decreased the cell viability and migration of the A549 and H1299 cells. Furthermore, the lidocaine treatment significantly decreased the succinylation and protein levels of HIST1H2BL, which was reversed after SIRT5 knockdown. Additionally, HIST1H2BL knockdown decreased the cell viability and migration of the A549 and H1299 cells, while HIST1H2BL overexpression reversed the effects of lidocaine on the cell viability and migration of the A549 and H1299 cells. In conclusion, lidocaine treatment might inhibited the lung cancer progression through decreasing the SIRT5 mediated succinylation of HIST1H2BL.

摘要

肺癌是一种起源于支气管黏膜或肺腺的恶性肿瘤。最近，一种广泛应用的酰胺类局部麻醉药——利多卡因，被证实能够抑制多种癌症的进展。本研究旨在探索利多卡因在肺癌进展中的具体作用机制。本研究使用人正常肺上皮细胞（BEAS-2B）和非小细胞肺癌细胞系（A549 和 H1299），并给予利多卡因处理。通过 CCK-8 法、划痕愈合实验和 Transwell 实验检测细胞的生物学行为，Western blot 检测相关基因的 mRNA 和蛋白水平。结果表明，利多卡因处理显著降低了 A549 和 H1299 细胞的活力和迁移能力。此外，利多卡因处理显著降低了 HIST1H2BL 的琥珀酰化和蛋白水平，而 SIRT5 敲低后这种作用被逆转。此外，HIST1H2BL 敲低降低了 A549 和 H1299 细胞的活力和迁移能力，而过表达 HIST1H2BL 则逆转了利多卡因对 A549 和 H1299 细胞活力和迁移能力的影响。总之，利多卡因处理可能通过降低 SIRT5 介导的 HIST1H2BL 琥珀酰化来抑制肺癌的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d41/11458836/30cf86528198/41598_2024_73966_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d41/11458836/9155d0f48047/41598_2024_73966_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d41/11458836/1c46664f367b/41598_2024_73966_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d41/11458836/824bbf712244/41598_2024_73966_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d41/11458836/334373276e91/41598_2024_73966_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d41/11458836/30cf86528198/41598_2024_73966_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d41/11458836/9155d0f48047/41598_2024_73966_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d41/11458836/1c46664f367b/41598_2024_73966_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d41/11458836/824bbf712244/41598_2024_73966_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d41/11458836/334373276e91/41598_2024_73966_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7d41/11458836/30cf86528198/41598_2024_73966_Fig5_HTML.jpg

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