Deciphering the role of SAMHD1 in endometrial cancer progression.

IF 5.7 2区生物学 Q1 BIOLOGY

Biology Direct Pub Date : 2024-10-11 DOI:10.1186/s13062-024-00525-7

Ping Qiang, Ying Chen, Yang Shao, Qicheng Deng, Songyuan Xu, Weipei Zhu

{"title":"Deciphering the role of SAMHD1 in endometrial cancer progression.","authors":"Ping Qiang, Ying Chen, Yang Shao, Qicheng Deng, Songyuan Xu, Weipei Zhu","doi":"10.1186/s13062-024-00525-7","DOIUrl":null,"url":null,"abstract":"Background: Endometrial cancer (EC) presents significant clinical challenges due to its heterogeneity and complex pathophysiology. SAMHD1, known for its role as a deoxynucleotide triphosphate triphosphohydrolase, has been implicated in the progression of various cancers, including EC. This study focuses on elucidating the role of SAMHD1 in EC through its impact on TRIM27-mediated PTEN ubiquitination.Results: Utilizing a combination of bioinformatics and cellular biology techniques, we investigated the interactions among SAMHD1, TRIM27, and PTEN. Our findings reveal that SAMHD1 modulates PTEN ubiquitination via TRIM27, impacting key pathways involved in EC pathogenesis. These interactions suggest a critical mechanism by which SAMHD1 could influence tumor behavior and progression in EC.Conclusions: The results from this study underscore the potential of targeting the SAMHD1-TRIM27-PTEN axis as a therapeutic strategy in EC. By providing new insights into the molecular mechanisms underlying EC progression, our research supports the development of novel therapeutic approaches that could contribute to improve treatment strategies for patients with EC.","PeriodicalId":9164,"journal":{"name":"Biology Direct","volume":"19 1","pages":"89"},"PeriodicalIF":5.7000,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11468744/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biology Direct","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1186/s13062-024-00525-7","RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Background: Endometrial cancer (EC) presents significant clinical challenges due to its heterogeneity and complex pathophysiology. SAMHD1, known for its role as a deoxynucleotide triphosphate triphosphohydrolase, has been implicated in the progression of various cancers, including EC. This study focuses on elucidating the role of SAMHD1 in EC through its impact on TRIM27-mediated PTEN ubiquitination.

Results: Utilizing a combination of bioinformatics and cellular biology techniques, we investigated the interactions among SAMHD1, TRIM27, and PTEN. Our findings reveal that SAMHD1 modulates PTEN ubiquitination via TRIM27, impacting key pathways involved in EC pathogenesis. These interactions suggest a critical mechanism by which SAMHD1 could influence tumor behavior and progression in EC.

Conclusions: The results from this study underscore the potential of targeting the SAMHD1-TRIM27-PTEN axis as a therapeutic strategy in EC. By providing new insights into the molecular mechanisms underlying EC progression, our research supports the development of novel therapeutic approaches that could contribute to improve treatment strategies for patients with EC.

查看原文本刊更多论文

破解 SAMHD1 在子宫内膜癌进展中的作用。

背景：子宫内膜癌（EC）因其异质性和复杂的病理生理学而给临床带来了巨大挑战。SAMHD1是一种脱氧核苷酸三磷酸三磷酸水解酶，与包括子宫内膜癌在内的多种癌症的进展有关。本研究的重点是通过SAMHD1对TRIM27介导的PTEN泛素化的影响，阐明其在EC中的作用：结果：我们结合生物信息学和细胞生物学技术，研究了SAMHD1、TRIM27和PTEN之间的相互作用。我们的研究结果表明，SAMHD1通过TRIM27调节PTEN的泛素化，从而影响涉及EC发病机制的关键通路。这些相互作用表明，SAMHD1是影响EC肿瘤行为和进展的关键机制：本研究结果强调了靶向 SAMHD1-TRIM27-PTEN 轴作为 EC 治疗策略的潜力。我们的研究为了解EC进展的分子机制提供了新的视角，有助于开发新的治疗方法，从而改善EC患者的治疗策略。

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分钟内获得全文求助全文

来源期刊

Biology Direct 生物-生物学

CiteScore

6.40

自引率

10.90%

发文量

审稿时长

7 months

期刊介绍： Biology Direct serves the life science research community as an open access, peer-reviewed online journal, providing authors and readers with an alternative to the traditional model of peer review. Biology Direct considers original research articles, hypotheses, comments, discovery notes and reviews in subject areas currently identified as those most conducive to the open review approach, primarily those with a significant non-experimental component.