Galectin-1 通过 NRP-1/c-JUN/Wee1 通路促进胃癌进展和顺铂抗性

IF 3.2 4区 医学 Q2 GASTROENTEROLOGY & HEPATOLOGY
Zhengyang Pan, Guoxi Xu, Yan Zhang, Meiling Wu, Jiahui Yu, Xujun He, Wei Zhang, Junfeng Hu
{"title":"Galectin-1 通过 NRP-1/c-JUN/Wee1 通路促进胃癌进展和顺铂抗性","authors":"Zhengyang Pan, Guoxi Xu, Yan Zhang, Meiling Wu, Jiahui Yu, Xujun He, Wei Zhang, Junfeng Hu","doi":"10.5230/jgc.2024.24.e25","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose: </strong>Gastric cancer (GC) is among the deadliest malignancies and the third leading cause of cancer-related deaths worldwide. Galectin-1 (Gal-1) is a primary protein secreted by cancer-associated fibroblasts (CAFs); however, its role and mechanisms of action of Gal-1 in GC remain unclear. In this study, we stimulated GC cells with exogenous human recombinant galectin-1 protein (rhGal-1) to investigate its effects on the proliferation, migration, and resistance to cisplatin.</p><p><strong>Materials and methods: </strong>We used simulated rhGal-1 protein as a paracrine factor produced by CAFs to induce GC cells and investigated its promotional effects and mechanisms in GC progression and cisplatin resistance. Immunohistochemical (IHC) assay confirmed that Gal-1 expression was associated with clinicopathological parameters and correlated with the expression of neuropilin-1 (NRP-1), c-JUN, and Wee1.</p><p><strong>Results: </strong>Our study reveals Gal-1 expression was significantly associated with poor outcomes. Gal-1 boosts the proliferation and metastasis of GC cells by activating the NRP-1/C-JUN/Wee1 pathway. Gal-1 notably increases GC cell resistance to cisplatin The NRP-1 inhibitor, EG00229, effectively counteracts these effects.</p><p><strong>Conclusions: </strong>These findings revealed a potential mechanism by which Gal-1 promotes GC growth and contributes to chemoresistance, offering new therapeutic targets for the treatment of GC.</p>","PeriodicalId":56072,"journal":{"name":"Journal of Gastric Cancer","volume":"24 3","pages":"300-315"},"PeriodicalIF":3.2000,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11224716/pdf/","citationCount":"0","resultStr":"{\"title\":\"Galectin-1 Promotes Gastric Carcinoma Progression and Cisplatin Resistance Through the NRP-1/c-JUN/Wee1 Pathway.\",\"authors\":\"Zhengyang Pan, Guoxi Xu, Yan Zhang, Meiling Wu, Jiahui Yu, Xujun He, Wei Zhang, Junfeng Hu\",\"doi\":\"10.5230/jgc.2024.24.e25\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose: </strong>Gastric cancer (GC) is among the deadliest malignancies and the third leading cause of cancer-related deaths worldwide. Galectin-1 (Gal-1) is a primary protein secreted by cancer-associated fibroblasts (CAFs); however, its role and mechanisms of action of Gal-1 in GC remain unclear. In this study, we stimulated GC cells with exogenous human recombinant galectin-1 protein (rhGal-1) to investigate its effects on the proliferation, migration, and resistance to cisplatin.</p><p><strong>Materials and methods: </strong>We used simulated rhGal-1 protein as a paracrine factor produced by CAFs to induce GC cells and investigated its promotional effects and mechanisms in GC progression and cisplatin resistance. Immunohistochemical (IHC) assay confirmed that Gal-1 expression was associated with clinicopathological parameters and correlated with the expression of neuropilin-1 (NRP-1), c-JUN, and Wee1.</p><p><strong>Results: </strong>Our study reveals Gal-1 expression was significantly associated with poor outcomes. Gal-1 boosts the proliferation and metastasis of GC cells by activating the NRP-1/C-JUN/Wee1 pathway. Gal-1 notably increases GC cell resistance to cisplatin The NRP-1 inhibitor, EG00229, effectively counteracts these effects.</p><p><strong>Conclusions: </strong>These findings revealed a potential mechanism by which Gal-1 promotes GC growth and contributes to chemoresistance, offering new therapeutic targets for the treatment of GC.</p>\",\"PeriodicalId\":56072,\"journal\":{\"name\":\"Journal of Gastric Cancer\",\"volume\":\"24 3\",\"pages\":\"300-315\"},\"PeriodicalIF\":3.2000,\"publicationDate\":\"2024-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11224716/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Gastric Cancer\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.5230/jgc.2024.24.e25\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"GASTROENTEROLOGY & HEPATOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Gastric Cancer","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5230/jgc.2024.24.e25","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"GASTROENTEROLOGY & HEPATOLOGY","Score":null,"Total":0}
引用次数: 0

摘要

目的:胃癌(GC)是最致命的恶性肿瘤之一,也是全球癌症相关死亡的第三大原因。Galectin-1(Gal-1)是癌症相关成纤维细胞(CAFs)分泌的一种主要蛋白质;然而,Gal-1在胃癌中的作用和作用机制仍不清楚。在本研究中,我们用外源性人重组 galectin-1 蛋白(rhGal-1)刺激 GC 细胞,研究其对细胞增殖、迁移和顺铂抗性的影响:我们利用模拟的rhGal-1蛋白作为CAFs产生的旁分泌因子诱导GC细胞,并研究其在GC进展和顺铂抗性中的促进作用和机制。免疫组化(IHC)检测证实,Gal-1的表达与临床病理参数相关,并与神经蛋白-1(NRP-1)、c-JUN和Wee1的表达相关:结果:我们的研究显示,Gal-1的表达与不良预后显著相关。Gal-1通过激活NRP-1/C-JUN/Wee1通路促进GC细胞的增殖和转移。NRP-1抑制剂EG00229能有效抵消这些影响:这些发现揭示了 Gal-1 促进 GC 生长并导致化疗耐药性的潜在机制,为治疗 GC 提供了新的治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Galectin-1 Promotes Gastric Carcinoma Progression and Cisplatin Resistance Through the NRP-1/c-JUN/Wee1 Pathway.

Purpose: Gastric cancer (GC) is among the deadliest malignancies and the third leading cause of cancer-related deaths worldwide. Galectin-1 (Gal-1) is a primary protein secreted by cancer-associated fibroblasts (CAFs); however, its role and mechanisms of action of Gal-1 in GC remain unclear. In this study, we stimulated GC cells with exogenous human recombinant galectin-1 protein (rhGal-1) to investigate its effects on the proliferation, migration, and resistance to cisplatin.

Materials and methods: We used simulated rhGal-1 protein as a paracrine factor produced by CAFs to induce GC cells and investigated its promotional effects and mechanisms in GC progression and cisplatin resistance. Immunohistochemical (IHC) assay confirmed that Gal-1 expression was associated with clinicopathological parameters and correlated with the expression of neuropilin-1 (NRP-1), c-JUN, and Wee1.

Results: Our study reveals Gal-1 expression was significantly associated with poor outcomes. Gal-1 boosts the proliferation and metastasis of GC cells by activating the NRP-1/C-JUN/Wee1 pathway. Gal-1 notably increases GC cell resistance to cisplatin The NRP-1 inhibitor, EG00229, effectively counteracts these effects.

Conclusions: These findings revealed a potential mechanism by which Gal-1 promotes GC growth and contributes to chemoresistance, offering new therapeutic targets for the treatment of GC.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Journal of Gastric Cancer
Journal of Gastric Cancer Biochemistry, Genetics and Molecular Biology-Cancer Research
CiteScore
4.30
自引率
12.00%
发文量
36
期刊介绍: The Journal of Gastric Cancer (J Gastric Cancer) is an international peer-reviewed journal. Each issue carries high quality clinical and translational researches on gastric neoplasms. Editorial Board of J Gastric Cancer publishes original articles on pathophysiology, molecular oncology, diagnosis, treatment, and prevention of gastric cancer as well as articles on dietary control and improving the quality of life for gastric cancer patients. J Gastric Cancer includes case reports, review articles, how I do it articles, editorials, and letters to the editor.
×
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
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
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 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信