Berberine modulates Keratin 17 to inhibit cervical cancer cell viability and metastasis.

IF 2.6 4区生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Receptors and Signal Transduction Pub Date : 2021-12-01 Epub Date: 2020-10-12 DOI:10.1080/10799893.2020.1830110

Luping Liu, Li Sun, Jing Zheng, Li Cui

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引用次数: 8

Abstract

Aim: Berberine (BBR) acts as a tumor suppressor in different cancer cells. Our paper exerted efforts to discover the effect of BBR on cervical cancer.

Methods: Human cervical cancer cell lines SiHa and Ca Ski were treated with different concentrations of BBR. Cell viability, apoptosis, migration and invasion were detected by MTT assay, flow cytometry, wound healing assay, and Transwell assay, respectively. Expressions of Bcl-2-associated X protein (Bax), Bcl-2, cleaved (C) caspase-3 and epithelial-mesenchymal transition (EMT)-related proteins were measured by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. Keratin 17 (KRT17) expression in cervical cancer was identified by GEPIA2 and qRT-PCR. Rescue assay was then performed to assess the functional interaction between BBR and KRT17.

Results: Human cervical cancer cell viability, migration, and invasion were inhibited by BBR. BBR promoted cell apoptosis by increasing Bax and C caspase-3 expressions and decreasing Bcl-2 expression. Besides, BBR inhibited EMT in cells by decreasing the expressions of MMP-9, N-cadherin and Vimentin and increasing E-cadherin expression. Effects of BBR on cervical cancer cells were in a dose-dependent manner. Higher expression of KRT17 was found in cervical cancer SiHa and Ca Ski cells. BBR rescued the effects of KRT17 on promoting cell viability, metastasis, and the expressions of Bcl-2, MMP-9, N-cadherin and Vimentin, and suppressing apoptosis and the expressions of Bax, C-caspase-3 and E-cadherin.

Conclusion: BBR inhibited cervical cancer cell viability, metastasis and EMT but promoted cell apoptosis via suppressing KRT 17 expression.

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小檗碱调节角蛋白17抑制宫颈癌细胞活力和转移。

目的:小檗碱(Berberine, BBR)在不同的肿瘤细胞中具有抑瘤作用。我们的研究旨在发现BBR对宫颈癌的作用。方法:用不同浓度的BBR处理人宫颈癌细胞株SiHa和Ca Ski。分别采用MTT法、流式细胞术、创面愈合法和Transwell法检测细胞活力、凋亡、迁移和侵袭。采用定量实时聚合酶链式反应(qRT-PCR)和Western blot检测Bcl-2相关X蛋白(Bax)、Bcl-2、cleaved (C) caspase-3和上皮-间质转化(EMT)相关蛋白的表达。应用GEPIA2和qRT-PCR检测宫颈癌组织中Keratin 17 (KRT17)的表达。然后进行拯救实验来评估BBR和KRT17之间的功能相互作用。结果:BBR能抑制人宫颈癌细胞的活力、迁移和侵袭。BBR通过增加Bax和C caspase-3的表达，降低Bcl-2的表达，促进细胞凋亡。此外，BBR通过降低细胞中MMP-9、N-cadherin和Vimentin的表达，增加E-cadherin的表达来抑制细胞中的EMT。BBR对宫颈癌细胞的影响呈剂量依赖性。KRT17在宫颈癌SiHa和Ca Ski细胞中表达较高。BBR恢复了KRT17促进细胞活力、转移和Bcl-2、MMP-9、N-cadherin、Vimentin表达，抑制细胞凋亡和Bax、C-caspase-3、E-cadherin表达的作用。结论:BBR通过抑制krt17的表达，抑制宫颈癌细胞活力、转移和EMT，促进细胞凋亡。

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

Journal of Receptors and Signal Transduction 生物-生化与分子生物学

CiteScore

6.60

自引率

0.00%

发文量

审稿时长

>12 weeks

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