IGF2BP3 is upregulated in endometrial cancer and tightly regulates the growth of drug-resistant endometrial cancer cells via HMGA1.

IF 2.6 4区综合性期刊 Q2 MULTIDISCIPLINARY SCIENCES Science Progress Pub Date : 2025-01-01 DOI:10.1177/00368504251315008

Yiwei Zhang, Yanlai Xiao, Xiangzhai Zhao, Jie Xu, Huan Zhao, Zhaojun Guo, Jun Zhao, Yajing Zhang, Ruoxi Wang, Jian Wang

{"title":"IGF2BP3 is upregulated in endometrial cancer and tightly regulates the growth of drug-resistant endometrial cancer cells via HMGA1.","authors":"Yiwei Zhang, Yanlai Xiao, Xiangzhai Zhao, Jie Xu, Huan Zhao, Zhaojun Guo, Jun Zhao, Yajing Zhang, Ruoxi Wang, Jian Wang","doi":"10.1177/00368504251315008","DOIUrl":null,"url":null,"abstract":"Objective: Endometrial cancer (EC) is a malignant tumor with various histological subtypes and molecular phenotypes. The evaluation of drug resistance is important for cancer treatment. Progesterone resistance is the major challenge in EC. Knowledge of drug resistance in EC is important in the development of novel therapies.Methods: In this study, ten paracancerous and ten tumor tissues were collected to measure the expression of insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) and high-mobility group protein 1 (HMGA1). AN3CA and Ishikawa cells were used to explore the effects of IGF2BP3 on EC.Results: The expression levels of IGF2BP3 and HMGA1 were higher in EC tumor tissues than in paracancerous tissues. IGF2BP3 and HMGA1 are highly expressed in cisplatin-resistant EC cells. IGF2BP3 knockdown decreased the growth of cisplatin-resistant EC cells. Knockdown of IGF2BP3 decreased the level of HMGA1 protein. HMGA1 knockdown decreased the growth of cisplatin-resistant EC cells.Discuss and conclusions: The findings demonstrate that IGF2BP3 is upregulated in EC and closely regulates the growth of drug-resistant EC cells via HMGA1. The findings will inform the development of novel therapies for EC.","PeriodicalId":56061,"journal":{"name":"Science Progress","volume":"108 1","pages":"368504251315008"},"PeriodicalIF":2.6000,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11775961/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Science Progress","FirstCategoryId":"103","ListUrlMain":"https://doi.org/10.1177/00368504251315008","RegionNum":4,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MULTIDISCIPLINARY SCIENCES","Score":null,"Total":0}

引用次数: 0

Abstract

Objective: Endometrial cancer (EC) is a malignant tumor with various histological subtypes and molecular phenotypes. The evaluation of drug resistance is important for cancer treatment. Progesterone resistance is the major challenge in EC. Knowledge of drug resistance in EC is important in the development of novel therapies.

Methods: In this study, ten paracancerous and ten tumor tissues were collected to measure the expression of insulin-like growth factor 2 mRNA binding protein 3 (IGF2BP3) and high-mobility group protein 1 (HMGA1). AN3CA and Ishikawa cells were used to explore the effects of IGF2BP3 on EC.

Results: The expression levels of IGF2BP3 and HMGA1 were higher in EC tumor tissues than in paracancerous tissues. IGF2BP3 and HMGA1 are highly expressed in cisplatin-resistant EC cells. IGF2BP3 knockdown decreased the growth of cisplatin-resistant EC cells. Knockdown of IGF2BP3 decreased the level of HMGA1 protein. HMGA1 knockdown decreased the growth of cisplatin-resistant EC cells.

Discuss and conclusions: The findings demonstrate that IGF2BP3 is upregulated in EC and closely regulates the growth of drug-resistant EC cells via HMGA1. The findings will inform the development of novel therapies for EC.

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

求助全文

约1分钟内获得全文去求助

来源期刊

Science Progress Multidisciplinary-Multidisciplinary

CiteScore

3.80

自引率

0.00%

发文量

119

期刊介绍： Science Progress has for over 100 years been a highly regarded review publication in science, technology and medicine. Its objective is to excite the readers'' interest in areas with which they may not be fully familiar but which could facilitate their interest, or even activity, in a cognate field.