دورية أكاديمية

UBE2N promotes cell viability and glycolysis by promoting Axin1 ubiquitination in prostate cancer cells

التفاصيل البيبلوغرافية
العنوان: UBE2N promotes cell viability and glycolysis by promoting Axin1 ubiquitination in prostate cancer cells
المؤلفون: Bo Yang, Weihua Chen, Tianyi Tao, Jun Zhang, Dehui Kong, Jidong Hao, Chao Yu, Guoqiang Liao, Hua Gong
المصدر: Biology Direct, Vol 19, Iss 1, Pp 1-13 (2024)
بيانات النشر: BMC, 2024.
سنة النشر: 2024
المجموعة: LCC:Biology (General)
مصطلحات موضوعية: Axin1, Glycolysis, Prostate cancer, UBE2N, Ubiquitination, Wnt/β-catenin, Biology (General), QH301-705.5
الوصف: Abstract Background Ubiquitin-conjugating enzyme E2 N (UBE2N) is recognized in the progression of some cancers; however, little research has been conducted to describe its role in prostate cancer. The purpose of this paper is to explore the function and mechanism of UBE2N in prostate cancer cells. Methods UBE2N expression was detected in Cancer Genome Atlas Prostate Adenocarcinoma (TCGA-PRAD) data, prostate cancer tissue microarrays, and prostate cancer cell lines, respectively. UBE2N knockdown or overexpression was used to analyze its role in cell viability and glycolysis of prostate cancer cells and tumor growth. XAV939 or Axin1 overexpression was co-treated with UBE2N overexpression to detect the involvement of the Wnt/β-catenin signaling and Axin1 in the UBE2N function. UBE2N interacting with Axin1 was analyzed by co-immunoprecipitation assay. Results UBE2N was upregulated in prostate cancer and the UBE2N-high expression correlated with the poor prognosis of prostate cancer. UBE2N knockdown inhibited cell viability and glycolysis in prostate cancer cells and restricted tumor formation in tumor-bearing mice. Wnt/β-catenin inhibition and Axin1 overexpression reversed the promoting viability and glycolysis function of UBE2N. UBE2N promoted Axin1 ubiquitination and decreased Axin1 protein level.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1745-6150
Relation: https://doaj.org/toc/1745-6150
DOI: 10.1186/s13062-024-00469-y
URL الوصول: https://doaj.org/article/1f4ac4959fb844659945614b9a9522c8
رقم الأكسشن: edsdoj.1f4ac4959fb844659945614b9a9522c8
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:17456150
DOI:10.1186/s13062-024-00469-y