SCYL1-mediated regulation of the mTORC1 signaling pathway inhibits autophagy and promotes gastric cancer metastasis.

IF 2.7 3区医学 Q3 ONCOLOGY Journal of Cancer Research and Clinical Oncology Pub Date : 2024-10-12 DOI:10.1007/s00432-024-05938-5

Zihao Zhao, Jinlong Liu, Xian Gao, Zhuzheng Chen, Yilin Hu, Junjie Chen, Weijie Zang, Wanjiang Xue

{"title":"SCYL1-mediated regulation of the mTORC1 signaling pathway inhibits autophagy and promotes gastric cancer metastasis.","authors":"Zihao Zhao, Jinlong Liu, Xian Gao, Zhuzheng Chen, Yilin Hu, Junjie Chen, Weijie Zang, Wanjiang Xue","doi":"10.1007/s00432-024-05938-5","DOIUrl":null,"url":null,"abstract":"Background: The SCY1-like (SCYL) family has been reported to be closely related to cancer metastasis, but it has not been reported in gastric cancer (GC), and its specific mechanism is not clear.Methods: We utilized databases like Deepmap, TCGA, and GEO to identify SCYL1's role in GC. Clinical samples were analyzed for SCYL1 expression and its correlation with patient prognosis. In vitro and in vivo experiments were conducted to assess SCYL1's function in GC cell migration, invasion, and autophagy.Results: SCYL1 showed an increased expression in GC tissues, which correlated with a negative prognosis. In vitro experiments demonstrated that SCYL1 promotes GC cell migration and invasion and inhibits autophagy. GSEA indicated an inverse relationship between SCYL1 and autophagy, while a direct relationship was observed with the mTORC1 signaling pathway. Knockdown of SCYL1 enhanced autophagy, while activation of mTORC1 reversed this effect.Conclusions: SCYL1 is a significant contributor to GC progression, promoting metastasis by activating the mTORC1 signaling pathway and inhibiting autophagy. These findings suggest SCYL1 as a potential therapeutic target for GC treatment.","PeriodicalId":15118,"journal":{"name":"Journal of Cancer Research and Clinical Oncology","volume":null,"pages":null},"PeriodicalIF":2.7000,"publicationDate":"2024-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11469978/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Cancer Research and Clinical Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s00432-024-05938-5","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Background: The SCY1-like (SCYL) family has been reported to be closely related to cancer metastasis, but it has not been reported in gastric cancer (GC), and its specific mechanism is not clear.

Methods: We utilized databases like Deepmap, TCGA, and GEO to identify SCYL1's role in GC. Clinical samples were analyzed for SCYL1 expression and its correlation with patient prognosis. In vitro and in vivo experiments were conducted to assess SCYL1's function in GC cell migration, invasion, and autophagy.

Results: SCYL1 showed an increased expression in GC tissues, which correlated with a negative prognosis. In vitro experiments demonstrated that SCYL1 promotes GC cell migration and invasion and inhibits autophagy. GSEA indicated an inverse relationship between SCYL1 and autophagy, while a direct relationship was observed with the mTORC1 signaling pathway. Knockdown of SCYL1 enhanced autophagy, while activation of mTORC1 reversed this effect.

Conclusions: SCYL1 is a significant contributor to GC progression, promoting metastasis by activating the mTORC1 signaling pathway and inhibiting autophagy. These findings suggest SCYL1 as a potential therapeutic target for GC treatment.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

SCYL1 介导的 mTORC1 信号通路调节抑制自噬并促进胃癌转移。

背景：据报道，SCY1-like（SCYL）家族与癌症转移密切相关，但在胃癌（GC）中尚未见报道，其具体机制也不清楚：据报道，SCY1-like（SCYL）家族与癌症转移密切相关，但在胃癌（GC）中尚未见报道，其具体机制也不清楚：我们利用 Deepmap、TCGA 和 GEO 等数据库确定 SCYL1 在 GC 中的作用。分析了临床样本中 SCYL1 的表达及其与患者预后的相关性。体外和体内实验评估了 SCYL1 在 GC 细胞迁移、侵袭和自噬中的功能：结果：SCYL1在GC组织中的表达增加，这与预后不良有关。体外实验表明，SCYL1 可促进 GC 细胞的迁移和侵袭，并抑制自噬。GSEA表明SCYL1与自噬之间存在反向关系，而与mTORC1信号通路之间存在直接关系。敲除 SCYL1 会增强自噬，而激活 mTORC1 则会逆转这种影响：结论：SCYL1 是 GC 进展的一个重要因素，它通过激活 mTORC1 信号通路和抑制自噬促进转移。这些发现表明 SCYL1 是治疗 GC 的潜在治疗靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

Journal of Cancer Research and Clinical Oncology 医学-肿瘤学

CiteScore

4.00

自引率

2.80%

发文量

577

审稿时长

2 months

期刊介绍： The "Journal of Cancer Research and Clinical Oncology" publishes significant and up-to-date articles within the fields of experimental and clinical oncology. The journal, which is chiefly devoted to Original papers, also includes Reviews as well as Editorials and Guest editorials on current, controversial topics. The section Letters to the editors provides a forum for a rapid exchange of comments and information concerning previously published papers and topics of current interest. Meeting reports provide current information on the latest results presented at important congresses. The following fields are covered: carcinogenesis - etiology, mechanisms; molecular biology; recent developments in tumor therapy; general diagnosis; laboratory diagnosis; diagnostic and experimental pathology; oncologic surgery; and epidemiology.