Curcumin enhances ATG3-dependent autophagy and inhibits metastasis in cervical carcinoma.

IF 2.8 4区 生物学 Q3 CELL BIOLOGY Cell Division Pub Date : 2024-11-28 DOI:10.1186/s13008-024-00138-6
Fei Zheng, Jingjing Lu, Chuhan Wang, Huimin Yu, Yanhong Fu, Danli Ma
{"title":"Curcumin enhances ATG3-dependent autophagy and inhibits metastasis in cervical carcinoma.","authors":"Fei Zheng, Jingjing Lu, Chuhan Wang, Huimin Yu, Yanhong Fu, Danli Ma","doi":"10.1186/s13008-024-00138-6","DOIUrl":null,"url":null,"abstract":"<p><p>Cervical carcinoma poses a significant health threat, with traditional treatments proving inadequate in advanced stages. Curcumin, a bioactive compound derived from turmeric, exhibits notable anti-inflammatory, antioxidant, and antineoplastic properties, potentially modulating autophagy, and metastasis in cancer cells. This study examines curcumin's impact on autophagy and metastasis in cervical carcinoma, focusing on its interaction with autophagy-related gene 3 (ATG3). SiHa and HeLa cervical carcinoma cell lines were treated with curcumin, ATG3 knockdown (shATG3), and their combination. Cell migration was evaluated via wound healing assays, while cell proliferation was evaluated with CCK-8 assays. LC3 expression was assessed using immunofluorescence and western blotting. Molecular docking simulations identified curcumin's binding interactions with key proteins. Curcumin and shATG3 significantly inhibited both cell migration and proliferation, with a synergistic effect observed when combined. LC3 expression was enhanced, indicating increased autophagy. Docking studies revealed curcumin's potential binding to MMP2, MMP9, TGF-β, ATG3, LC3, and p62, suggesting modulation of these pathways. The combination of curcumin and ATG3 knockdown significantly inhibited cervical carcinoma cell migration and proliferation, while also enhancing autophagy, supporting the potential of curcumin as a therapeutic agent for cervical carcinoma. Further clinical research is needed to validate these findings.</p>","PeriodicalId":49263,"journal":{"name":"Cell Division","volume":"19 1","pages":"33"},"PeriodicalIF":2.8000,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11606299/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Division","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s13008-024-00138-6","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Cervical carcinoma poses a significant health threat, with traditional treatments proving inadequate in advanced stages. Curcumin, a bioactive compound derived from turmeric, exhibits notable anti-inflammatory, antioxidant, and antineoplastic properties, potentially modulating autophagy, and metastasis in cancer cells. This study examines curcumin's impact on autophagy and metastasis in cervical carcinoma, focusing on its interaction with autophagy-related gene 3 (ATG3). SiHa and HeLa cervical carcinoma cell lines were treated with curcumin, ATG3 knockdown (shATG3), and their combination. Cell migration was evaluated via wound healing assays, while cell proliferation was evaluated with CCK-8 assays. LC3 expression was assessed using immunofluorescence and western blotting. Molecular docking simulations identified curcumin's binding interactions with key proteins. Curcumin and shATG3 significantly inhibited both cell migration and proliferation, with a synergistic effect observed when combined. LC3 expression was enhanced, indicating increased autophagy. Docking studies revealed curcumin's potential binding to MMP2, MMP9, TGF-β, ATG3, LC3, and p62, suggesting modulation of these pathways. The combination of curcumin and ATG3 knockdown significantly inhibited cervical carcinoma cell migration and proliferation, while also enhancing autophagy, supporting the potential of curcumin as a therapeutic agent for cervical carcinoma. Further clinical research is needed to validate these findings.

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
姜黄素增强atg3依赖性自噬并抑制宫颈癌转移。
宫颈癌对健康构成重大威胁,在晚期,传统的治疗方法被证明是不够的。姜黄素是一种从姜黄中提取的生物活性化合物,具有显著的抗炎、抗氧化和抗肿瘤特性,可能调节癌细胞的自噬和转移。本研究探讨姜黄素对宫颈癌自噬和转移的影响,重点研究其与自噬相关基因3 (autophagy-related gene 3, ATG3)的相互作用。姜黄素、ATG3敲除(shATG3)及其联合作用于SiHa和HeLa宫颈癌细胞株。通过伤口愈合试验评估细胞迁移,通过CCK-8试验评估细胞增殖。采用免疫荧光和western blotting检测LC3的表达。分子对接模拟确定了姜黄素与关键蛋白质的结合相互作用。姜黄素和shATG3联合使用可显著抑制细胞迁移和增殖,并具有协同作用。LC3表达增强,表明自噬增加。对接研究显示姜黄素可能与MMP2、MMP9、TGF-β、ATG3、LC3和p62结合,提示这些途径具有调节作用。姜黄素联合ATG3基因敲低可显著抑制宫颈癌细胞的迁移和增殖,同时增强自噬,支持姜黄素作为宫颈癌治疗剂的潜力。需要进一步的临床研究来验证这些发现。
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
Cell Division
Cell Division CELL BIOLOGY-
CiteScore
3.70
自引率
0.00%
发文量
5
审稿时长
>12 weeks
期刊介绍: Cell Division is an open access, peer-reviewed journal that encompasses all the molecular aspects of cell cycle control and cancer, cell growth, proliferation, survival, differentiation, signalling, gene transcription, protein synthesis, genome integrity, chromosome stability, centrosome duplication, DNA damage and DNA repair. Cell Division provides an online forum for the cell-cycle community that aims to publish articles on all exciting aspects of cell-cycle research and to bridge the gap between models of cell cycle regulation, development, and cancer biology. This forum is driven by specialized and timely research articles, reviews and commentaries focused on this fast moving field, providing an invaluable tool for cell-cycle biologists. Cell Division publishes articles in areas which includes, but not limited to: DNA replication, cell fate decisions, cell cycle & development Cell proliferation, mitosis, spindle assembly checkpoint, ubiquitin mediated degradation DNA damage & repair Apoptosis & cell death
期刊最新文献
Maraviroc enhances Bortezomib sensitivity in multiple myeloma by inhibiting M2 macrophage polarization via PI3K/AKT/RhoA signaling pathway in macrophages. Detection of early relapse in multiple myeloma patients. LncRNA-ANRIL regulates CDKN2A to promote malignant proliferation of Kasumi-1 cells. ZNF169 promotes thyroid cancer progression via upregulating FBXW10. Interaction of STIL with FOXM1 regulates SF3A3 transcription in the hepatocellular carcinoma development.
×
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