RPL36A 可激活 ERK 通路并促进结直肠癌的生长。

IF 5 2区医学 Q2 Medicine

Translational Oncology Pub Date : 2024-11-02 DOI:10.1016/j.tranon.2024.102170

Jing Shi , Yebin Yang , Fangci Chen , Linpo Zhou , Haoran Wei , Fanhe Dong , Xiang Wang , Yuqiang Shan , Tianwei Chen

{"title":"RPL36A 可激活 ERK 通路并促进结直肠癌的生长。","authors":"Jing Shi , Yebin Yang , Fangci Chen , Linpo Zhou , Haoran Wei , Fanhe Dong , Xiang Wang , Yuqiang Shan , Tianwei Chen","doi":"10.1016/j.tranon.2024.102170","DOIUrl":null,"url":null,"abstract":"<div><div>Ribosomal protein L36A (RPL36A) was one of the most upregulated proteins in colorectal cancer (CRC), yet its role in colorectal cancer (CRC) remains largely unexplored, with limited studies investigating its expression and biological functions. In this investigation, we confirmed a marked upregulation of RPL36A in CRC tissues, correlating with an adverse prognosis. Silencing RPL36A markedly attenuated CRC cell malignant properties and tumor xenograft growth. Further mechanistic analysis indicated that RPL36A depletion diminished phosphorylated ERK levels, subsequently impacting the expression of c-Myc and ELK1, key downstream effectors in the MAPK/ERK pathway. Notably, the tumor-suppressive effects of RPL36A knockdown could be negated by an ERK activator. Collectively, our findings underscore the oncogenic function of RPL36A in CRC and propose it as a potential target for therapeutic intervention.</div></div>","PeriodicalId":48975,"journal":{"name":"Translational Oncology","volume":"51 ","pages":"Article 102170"},"PeriodicalIF":5.0000,"publicationDate":"2024-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"RPL36A activates ERK pathway and promotes colorectal cancer growth\",\"authors\":\"Jing Shi , Yebin Yang , Fangci Chen , Linpo Zhou , Haoran Wei , Fanhe Dong , Xiang Wang , Yuqiang Shan , Tianwei Chen\",\"doi\":\"10.1016/j.tranon.2024.102170\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div><div>Ribosomal protein L36A (RPL36A) was one of the most upregulated proteins in colorectal cancer (CRC), yet its role in colorectal cancer (CRC) remains largely unexplored, with limited studies investigating its expression and biological functions. In this investigation, we confirmed a marked upregulation of RPL36A in CRC tissues, correlating with an adverse prognosis. Silencing RPL36A markedly attenuated CRC cell malignant properties and tumor xenograft growth. Further mechanistic analysis indicated that RPL36A depletion diminished phosphorylated ERK levels, subsequently impacting the expression of c-Myc and ELK1, key downstream effectors in the MAPK/ERK pathway. Notably, the tumor-suppressive effects of RPL36A knockdown could be negated by an ERK activator. Collectively, our findings underscore the oncogenic function of RPL36A in CRC and propose it as a potential target for therapeutic intervention.</div></div>\",\"PeriodicalId\":48975,\"journal\":{\"name\":\"Translational Oncology\",\"volume\":\"51 \",\"pages\":\"Article 102170\"},\"PeriodicalIF\":5.0000,\"publicationDate\":\"2024-11-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Translational Oncology\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://www.sciencedirect.com/science/article/pii/S1936523324002961\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Translational Oncology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1936523324002961","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"Medicine","Score":null,"Total":0}

引用次数: 0

摘要

核糖体蛋白 L36A（RPL36A）是结直肠癌（CRC）中上调最多的蛋白之一，但其在结直肠癌（CRC）中的作用仍未得到广泛探讨，对其表达和生物学功能的研究也很有限。在这项研究中，我们证实 RPL36A 在 CRC 组织中明显上调，与不良预后相关。抑制 RPL36A 能明显减轻 CRC 细胞的恶性特性和肿瘤异种移植的生长。进一步的机理分析表明，抑制 RPL36A 会降低磷酸化 ERK 水平，进而影响 c-Myc 和 ELK1（MAPK/ERK 通路的关键下游效应物）的表达。值得注意的是，RPL36A基因敲除的肿瘤抑制作用可被ERK激活剂抵消。总之，我们的研究结果强调了 RPL36A 在 CRC 中的致癌功能，并建议将其作为治疗干预的潜在靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

查看原文本刊更多论文

RPL36A activates ERK pathway and promotes colorectal cancer growth

Ribosomal protein L36A (RPL36A) was one of the most upregulated proteins in colorectal cancer (CRC), yet its role in colorectal cancer (CRC) remains largely unexplored, with limited studies investigating its expression and biological functions. In this investigation, we confirmed a marked upregulation of RPL36A in CRC tissues, correlating with an adverse prognosis. Silencing RPL36A markedly attenuated CRC cell malignant properties and tumor xenograft growth. Further mechanistic analysis indicated that RPL36A depletion diminished phosphorylated ERK levels, subsequently impacting the expression of c-Myc and ELK1, key downstream effectors in the MAPK/ERK pathway. Notably, the tumor-suppressive effects of RPL36A knockdown could be negated by an ERK activator. Collectively, our findings underscore the oncogenic function of RPL36A in CRC and propose it as a potential target for therapeutic intervention.

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

Translational Oncology ONCOLOGY-

CiteScore

8.40

自引率

2.00%

发文量

314

审稿时长

54 days

期刊介绍： Translational Oncology publishes the results of novel research investigations which bridge the laboratory and clinical settings including risk assessment, cellular and molecular characterization, prevention, detection, diagnosis and treatment of human cancers with the overall goal of improving the clinical care of oncology patients. Translational Oncology will publish laboratory studies of novel therapeutic interventions as well as clinical trials which evaluate new treatment paradigms for cancer. Peer reviewed manuscript types include Original Reports, Reviews and Editorials.