CBX8 Promotes Epithelial-mesenchymal Transition, Migration, and Invasion of Lung Cancer through Wnt/β-catenin Signaling Pathway.

IF 1.9 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Current protein & peptide science Pub Date : 2024-01-01 DOI:10.2174/0113892037273375231204080906
Xiaoping Cai, Yuankai Lv, Jiongwei Pan, Zhuo Cao, Junzhi Zhang, Yuling Li, Hao Zheng
{"title":"CBX8 Promotes Epithelial-mesenchymal Transition, Migration, and Invasion of Lung Cancer through Wnt/β-catenin Signaling Pathway.","authors":"Xiaoping Cai, Yuankai Lv, Jiongwei Pan, Zhuo Cao, Junzhi Zhang, Yuling Li, Hao Zheng","doi":"10.2174/0113892037273375231204080906","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Lung cancer (LC) is primarily responsible for cancer-related deaths worldwide. Epithelial-mesenchymal transition (EMT) is a process in which epithelial cells acquire mesenchymal features and is associated with the development of tumors. CBX8, a member of the PcG protein family, plays a critical role in various cancers, containing LC. However, specific regulatory mechanisms of CBX8 in LC progression are not fully understood. This study aimed to investigate the regulatory role of CBX8 in LC progression.</p><p><strong>Methods: </strong>Bioinformatics was used to analyze the relationship between CBX8 level and tumor and the enrichment pathway of CBX8 enrichment. qRT-PCR was used to detect the differential expression of CBX8 in LC cells and normal lung epithelial cells. The effects of knockdown or overexpression of CBX8 on the proliferation, migration and invasion of LC cells were evaluated by CCK- -8 assay and Transwell assay, and the levels of proteins associated with the EMT pathway and Wnt/ β-catenin signaling pathway were detected by western blot.</p><p><strong>Results: </strong>Bioinformatics analysis revealed that CBX8 was highly expressed in LC and enriched on the Wnt/β-catenin signaling pathway. The expression level of CBX8 was significantly elevated in LC cells. Knockdown of CBX8 significantly inhibited cell proliferation, migration and invasion, and decreased the expression levels of EMT-related proteins and Wnt/β-catenin pathway-related proteins. Conversely, overexpression of CBX8 promoted cell proliferation, migration and invasion, and increased the expression levels of EMT-related proteins and Wnt/β-catenin pathway-related proteins. The Wnt inhibitor IWP-4 alleviated the effects produced by overexpression of CBX8.</p><p><strong>Conclusion: </strong>Collectively, these data demonstrated that CBX8 induced EMT through Wnt/β-- catenin signaling, driving migration and invasion of LC cells.</p>","PeriodicalId":10859,"journal":{"name":"Current protein & peptide science","volume":" ","pages":"386-393"},"PeriodicalIF":1.9000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current protein & peptide science","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.2174/0113892037273375231204080906","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Background: Lung cancer (LC) is primarily responsible for cancer-related deaths worldwide. Epithelial-mesenchymal transition (EMT) is a process in which epithelial cells acquire mesenchymal features and is associated with the development of tumors. CBX8, a member of the PcG protein family, plays a critical role in various cancers, containing LC. However, specific regulatory mechanisms of CBX8 in LC progression are not fully understood. This study aimed to investigate the regulatory role of CBX8 in LC progression.

Methods: Bioinformatics was used to analyze the relationship between CBX8 level and tumor and the enrichment pathway of CBX8 enrichment. qRT-PCR was used to detect the differential expression of CBX8 in LC cells and normal lung epithelial cells. The effects of knockdown or overexpression of CBX8 on the proliferation, migration and invasion of LC cells were evaluated by CCK- -8 assay and Transwell assay, and the levels of proteins associated with the EMT pathway and Wnt/ β-catenin signaling pathway were detected by western blot.

Results: Bioinformatics analysis revealed that CBX8 was highly expressed in LC and enriched on the Wnt/β-catenin signaling pathway. The expression level of CBX8 was significantly elevated in LC cells. Knockdown of CBX8 significantly inhibited cell proliferation, migration and invasion, and decreased the expression levels of EMT-related proteins and Wnt/β-catenin pathway-related proteins. Conversely, overexpression of CBX8 promoted cell proliferation, migration and invasion, and increased the expression levels of EMT-related proteins and Wnt/β-catenin pathway-related proteins. The Wnt inhibitor IWP-4 alleviated the effects produced by overexpression of CBX8.

Conclusion: Collectively, these data demonstrated that CBX8 induced EMT through Wnt/β-- catenin signaling, driving migration and invasion of LC cells.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
CBX8通过Wnt/β-catenin信号通路促进肺癌的上皮-间质转化、迁移和侵袭
背景:肺癌是全球癌症相关死亡的主要原因。上皮-间质转化(EMT)是上皮细胞获得间质特征的过程,与肿瘤的发展有关。CBX8 是 PcG 蛋白家族的成员,在多种癌症(包括 LC)中发挥着关键作用。然而,CBX8 在 LC 进展过程中的具体调控机制尚不完全清楚。本研究旨在探讨 CBX8 在 LC 进展中的调控作用:方法:采用生物信息学方法分析 CBX8 水平与肿瘤的关系以及 CBX8 的富集途径;采用 qRT-PCR 方法检测 CBX8 在 LC 细胞和正常肺上皮细胞中的差异表达。通过CCK-8试验和Transwell试验评估了敲除或过表达CBX8对LC细胞增殖、迁移和侵袭的影响,并通过Western blot检测了EMT通路和Wnt/β-catenin信号通路相关蛋白的水平:生物信息学分析表明,CBX8在LC中高表达,并富集于Wnt/β-catenin信号通路。CBX8 在 LC 细胞中的表达水平明显升高。敲除 CBX8 能明显抑制细胞增殖、迁移和侵袭,降低 EMT 相关蛋白和 Wnt/β-catenin 通路相关蛋白的表达水平。相反,过表达 CBX8 会促进细胞增殖、迁移和侵袭,并提高 EMT 相关蛋白和 Wnt/β-catenin 通路相关蛋白的表达水平。Wnt 抑制剂 IWP-4 可减轻过表达 CBX8 所产生的影响:总之,这些数据表明,CBX8 通过 Wnt/β-catenin 信号传导诱导 EMT,推动 LC 细胞的迁移和侵袭。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Current protein & peptide science
Current protein & peptide science 生物-生化与分子生物学
CiteScore
5.20
自引率
0.00%
发文量
73
审稿时长
6 months
期刊介绍: Current Protein & Peptide Science publishes full-length/mini review articles on specific aspects involving proteins, peptides, and interactions between the enzymes, the binding interactions of hormones and their receptors; the properties of transcription factors and other molecules that regulate gene expression; the reactions leading to the immune response; the process of signal transduction; the structure and function of proteins involved in the cytoskeleton and molecular motors; the properties of membrane channels and transporters; and the generation and storage of metabolic energy. In addition, reviews of experimental studies of protein folding and design are given special emphasis. Manuscripts submitted to Current Protein and Peptide Science should cover a field by discussing research from the leading laboratories in a field and should pose questions for future studies. Original papers, research articles and letter articles/short communications are not considered for publication in Current Protein & Peptide Science.
期刊最新文献
Comparative Proteomic Analysis of Cell Wall Proteins of Aminoglycosides Resistant and Sensitive Mycobacterium tuberculosis Clinical Isolates. Myotoxicity of Crotoxin on C2C12 Myoblasts and its Inhibition by Crotalus Neutralizing Factor versus Enhanced Resistance in Myotubes: Exploring Toxicity and Membrane Potential. Insights into the Binding of Metadoxine with Bovine Serum Albumin: A Multi-Spectroscopic Investigation Combined with Molecular Docking. A Study on the Rationality of Baicalein in the Treatment of Osteoporosis: A Narrative Review. Effects of the Amyotrophic Lateral Sclerosis-related Q108P Mutation on the Structural Ensemble Characteristics of CHCHD10.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1