USP36 plays an oncogenic role in colorectal cancer cells.

IF 2 4区 医学 Q3 ONCOLOGY Neoplasma Pub Date : 2024-02-01 Epub Date: 2024-01-12 DOI:10.4149/neo_2023_230629N339
Lixiong Luo, Yijiang Li, Rongjie Huang, Ling Li, Chuncai Wu, Qunzhang Zeng
{"title":"USP36 plays an oncogenic role in colorectal cancer cells.","authors":"Lixiong Luo, Yijiang Li, Rongjie Huang, Ling Li, Chuncai Wu, Qunzhang Zeng","doi":"10.4149/neo_2023_230629N339","DOIUrl":null,"url":null,"abstract":"<p><p>Cancer stem cells (CSCs) have emerged as crucial contributors to tumor relapse and chemoresistance, making them promising targets for treating cancers like colorectal cancer (CRC). However, the mechanisms governing CSC maintenance in CRC remain poorly characterized. In this study, we investigated the potential role of ubiquitin-specific protease 36 (USP36) in CRC. Our bioinformatic analysis revealed a significant upregulation of USP36 expression in CRC, and high USP36 levels were associated with poor prognosis in CRC patients. Furthermore, we observed an increase in USP36 expression in CRC cell lines. Knockdown of USP36 resulted in reduced viability, cell cycle arrest, increased apoptosis, and impaired migration and invasion in CRC cells. Additionally, the colony formation and sphere formation ability, as well as the expression of stem cell markers and pluripotent transcription factors, were substantially reduced in USP36-deficient CRC cells. These findings emphasize the role of USP36 as an oncogene in CRC, highlighting its potential as a therapeutic target for the treatment of CRC.</p>","PeriodicalId":19266,"journal":{"name":"Neoplasma","volume":" ","pages":"13-21"},"PeriodicalIF":2.0000,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neoplasma","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.4149/neo_2023_230629N339","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/12 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Cancer stem cells (CSCs) have emerged as crucial contributors to tumor relapse and chemoresistance, making them promising targets for treating cancers like colorectal cancer (CRC). However, the mechanisms governing CSC maintenance in CRC remain poorly characterized. In this study, we investigated the potential role of ubiquitin-specific protease 36 (USP36) in CRC. Our bioinformatic analysis revealed a significant upregulation of USP36 expression in CRC, and high USP36 levels were associated with poor prognosis in CRC patients. Furthermore, we observed an increase in USP36 expression in CRC cell lines. Knockdown of USP36 resulted in reduced viability, cell cycle arrest, increased apoptosis, and impaired migration and invasion in CRC cells. Additionally, the colony formation and sphere formation ability, as well as the expression of stem cell markers and pluripotent transcription factors, were substantially reduced in USP36-deficient CRC cells. These findings emphasize the role of USP36 as an oncogene in CRC, highlighting its potential as a therapeutic target for the treatment of CRC.

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
USP36 在结直肠癌细胞中发挥致癌作用。
癌症干细胞(CSCs)已成为肿瘤复发和化疗耐药性的关键因素,使其成为治疗结直肠癌(CRC)等癌症的有希望的靶点。然而,CSC 在 CRC 中的维持机制仍不甚明了。在本研究中,我们调查了泛素特异性蛋白酶 36(USP36)在 CRC 中的潜在作用。我们的生物信息学分析表明,USP36 在 CRC 中的表达显著上调,高 USP36 水平与 CRC 患者的不良预后相关。此外,我们还观察到 USP36 在 CRC 细胞系中的表达增加。敲除 USP36 会导致 CRC 细胞活力降低、细胞周期停滞、凋亡增加、迁移和侵袭受损。此外,在 USP36 缺失的 CRC 细胞中,集落形成和球形成能力以及干细胞标志物和多能转录因子的表达均大幅降低。这些发现强调了USP36作为癌基因在CRC中的作用,突出了其作为治疗CRC靶点的潜力。
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
Neoplasma
Neoplasma 医学-肿瘤学
CiteScore
5.40
自引率
0.00%
发文量
238
审稿时长
3 months
期刊介绍: The journal Neoplasma publishes articles on experimental and clinical oncology and cancer epidemiology.
期刊最新文献
Six2 regulates the malignant progression and 5-FU resistance of hepatocellular carcinoma through the PI3K/AKT/mTOR pathway and DNMT1/E-cadherin methylation mechanism. Protein level of epithelial membrane protein (EMP) 1, EMP 2, and EMP 3 in carcinoma of unknown primary. The impact of c-Met inhibition on molecular features and metastatic potential of melanoma cells. The real-world comparison of non-small cell lung cancer survival outcomes depending on immunotherapy treatment and PD-L1 expression level. Albumin bound-paclitaxel combined with anlotinib and immunotherapy in the second-line treatment of ES-SCLC: a retrospective cohort study.
×
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