{"title":"Evaluation of autophagy related ATG4B gene, protein and miR-655-3p expression levels in endometrial cancer and hyperplasia.","authors":"Elmira Mahdinia, Rahim Rostami, Azadeh Rezaei, Parvin Ghaderi, Sahar Yarahmadi, Soudabeh Fallah","doi":"10.3802/jgo.2025.36.e33","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>The pathogenesis of endometrial cancer (EC) and hyperplasia is complex and poorly understood. Autophagy has emerged as a crucial aspect of this process.</p><p><strong>Methods: </strong>This study examines the role of autophagy in the pathogenesis of EC and hyperplasia by investigating the expression of the autophagy-related 4B cysteine peptidase (ATG4B) gene, protein, and miR-665-3p levels in patients compared to a control group. This cross-sectional case control study analyzed 90 endometrial tissues, including 30 tumors, 30 normal controls, and 30 hyperplasia, using quantitative reverse transcription polymerase chain reaction and Western blot to assess ATG4B gene and protein levels.</p><p><strong>Results: </strong>Higher ATG4B gene expression levels were found in the endometrial tissue of EC patients than in hyperplasia patients and controls. Furthermore, protein levels of ATG4B were also higher in EC and hyperplasia patients than in controls. ATG4B gene expression and protein levels were positively correlated in EC patients. However, in EC patients, miR-655-3p showed a significant negative correlation with the ATG4B gene and protein levels.</p><p><strong>Conclusion: </strong>ATG4B gene and protein expression is elevated in EC tissue, suggesting their role as a tumor promoter. Evaluating their levels could serve as markers for monitoring EC progression and prognosis.</p>","PeriodicalId":15868,"journal":{"name":"Journal of Gynecologic Oncology","volume":null,"pages":null},"PeriodicalIF":3.4000,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Gynecologic Oncology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3802/jgo.2025.36.e33","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"OBSTETRICS & GYNECOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: The pathogenesis of endometrial cancer (EC) and hyperplasia is complex and poorly understood. Autophagy has emerged as a crucial aspect of this process.
Methods: This study examines the role of autophagy in the pathogenesis of EC and hyperplasia by investigating the expression of the autophagy-related 4B cysteine peptidase (ATG4B) gene, protein, and miR-665-3p levels in patients compared to a control group. This cross-sectional case control study analyzed 90 endometrial tissues, including 30 tumors, 30 normal controls, and 30 hyperplasia, using quantitative reverse transcription polymerase chain reaction and Western blot to assess ATG4B gene and protein levels.
Results: Higher ATG4B gene expression levels were found in the endometrial tissue of EC patients than in hyperplasia patients and controls. Furthermore, protein levels of ATG4B were also higher in EC and hyperplasia patients than in controls. ATG4B gene expression and protein levels were positively correlated in EC patients. However, in EC patients, miR-655-3p showed a significant negative correlation with the ATG4B gene and protein levels.
Conclusion: ATG4B gene and protein expression is elevated in EC tissue, suggesting their role as a tumor promoter. Evaluating their levels could serve as markers for monitoring EC progression and prognosis.
期刊介绍:
The Journal of Gynecologic Oncology (JGO) is an official publication of the Asian Society of Gynecologic Oncology. Abbreviated title is ''J Gynecol Oncol''. It was launched in 1990. The JGO''s aim is to publish the highest quality manuscripts dedicated to the advancement of care of the patients with gynecologic cancer. It is an international peer-reviewed periodical journal that is published bimonthly (January, March, May, July, September, and November). Supplement numbers are at times published. The journal publishes editorials, original and review articles, correspondence, book review, etc.