Berberine inhibits the malignant cell phenotype by inactivating PI3K/AKT/mTOR signaling in laryngeal squamous cell carcinoma.

IF 2.5 4区生物学 Q3 CELL BIOLOGY

Histology and histopathology Pub Date : 2024-11-01 Epub Date: 2024-04-23 DOI:10.14670/HH-18-753

Ling Lin, Zhen Chen, Ping Huang, Wei Chen, Zhefei Zou, Yexian Zheng, Chang He, Xiang Gu, Dan Yu, Qiong Zhang

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引用次数: 0

Abstract

Background: Berberine is an active compound found in different herbs used in Chinese medicine and is well-known for its potential anticancer properties. The study aimed to figure out the role of berberine in regulating the malignant behavior of laryngeal squamous cell carcinoma (LSCC) cells.

Methods: LSCC cell lines (SNU-899 and AMC-HN-8) were treated with different concentrations of berberine (0-200 μM) to determine its cytotoxicity. The migration, invasion, and apoptosis of LSCC cells were measured by wound healing assays, Transwell assays, and flow cytometry. Western blot was performed for the quantification of proteins involved in PI3K/AKT/mTOR signaling.

Results: The viability of LSCC cells was dose-dependently reduced by berberine. Berberine dampened LSCC cell migration and invasion while augmenting cell apoptosis, as evidenced by a reduced wound closure rate, a decrease in invaded cell number, and a surge in cell apoptosis in the context of berberine stimulation. Importantly, the effects of berberine on the cancer cell process were enhanced by LY294002 (an inhibitor for PI3K) treatment. Moreover, the protein levels of phosphorylated PI3K, AKT, and mTOR were markedly reduced in response to berberine treatment.

Conclusion: Berberine inhibits cell viability, migration, and invasion but augments cell apoptosis by inactivating PI3K/AKT/mTOR signaling in LSCC.

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小檗碱通过使喉鳞癌中的 PI3K/AKT/mTOR 信号失活来抑制恶性细胞表型。

背景：小檗碱是一种存在于不同中草药中的活性化合物，因其潜在的抗癌特性而闻名。本研究旨在找出小檗碱在调节喉鳞状细胞癌（LSCC）细胞恶性行为中的作用：方法：用不同浓度的小檗碱（0-200 μM）处理喉鳞状细胞癌细胞株（SNU-899 和 AMC-HN-8），以确定其细胞毒性。通过伤口愈合试验、Transwell 试验和流式细胞术检测 LSCC 细胞的迁移、侵袭和凋亡。对参与 PI3K/AKT/mTOR 信号转导的蛋白质进行了 Western 印迹定量：结果：小檗碱可剂量依赖性地降低 LSCC 细胞的活力。小檗碱抑制了 LSCC 细胞的迁移和侵袭，同时促进了细胞凋亡，这表现在小檗碱刺激下伤口闭合率降低、侵袭细胞数量减少以及细胞凋亡激增。重要的是，小檗碱对癌细胞进程的影响在 LY294002（一种 PI3K 抑制剂）处理后得到增强。此外，磷酸化的 PI3K、AKT 和 mTOR 蛋白水平在小檗碱处理后明显降低：结论：小檗碱抑制了 LSCC 中细胞的活力、迁移和侵袭，但通过使 PI3K/AKT/mTOR 信号失活，增加了细胞凋亡。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Histology and histopathology 生物-病理学

CiteScore

3.90

自引率

0.00%

发文量

232

审稿时长

2 months

期刊介绍： HISTOLOGY AND HISTOPATHOLOGY is a peer-reviewed international journal, the purpose of which is to publish original and review articles in all fields of the microscopical morphology, cell biology and tissue engineering; high quality is the overall consideration. Its format is the standard international size of 21 x 27.7 cm. One volume is published every year (more than 1,300 pages, approximately 90 original works and 40 reviews). Each volume consists of 12 numbers published monthly online. The printed version of the journal includes 4 books every year; each of them compiles 3 numbers previously published online.