دورية أكاديمية

GINS1 promotes the initiation and progression of bladder cancer by activating the AKT/mTOR/c-Myc signaling pathway.

التفاصيل البيبلوغرافية
العنوان: GINS1 promotes the initiation and progression of bladder cancer by activating the AKT/mTOR/c-Myc signaling pathway.
المؤلفون: Fu Q; Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China. Electronic address: fqq15279210670@163.com., Zheng H; Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China. Electronic address: zh-urology@whu.edu.cn., Wang X; Department of Public Health, Wuhan University Hospital, Wuhan University, Wuhan, China. Electronic address: wxask1981@126.com., Tang F; Department of Urology, Jingzhou Central Hospital, Jingzhou, China. Electronic address: tangfeng0013@163.com., Yu H; Department of Plastic Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China. Electronic address: wudayuhua@whu.edu.cn., Wang H; Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China. Electronic address: whswx126yx@126.com., Wan Z; Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China. Electronic address: 592135672@qq.com., Zheng Z; Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China. Electronic address: whuzzj1025@163.com., Yang Z; Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China. Electronic address: yangzhonghua@whu.edu.cn., Liu T; Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China. Electronic address: liutaozaiwuda@whu.edu.cn., Peng J; Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China. Electronic address: pengjianping@whu.edu.cn.
المصدر: Experimental cell research [Exp Cell Res] 2024 Jul 01; Vol. 440 (1), pp. 114125. Date of Electronic Publication: 2024 Jun 15.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Academic Press Country of Publication: United States NLM ID: 0373226 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1090-2422 (Electronic) Linking ISSN: 00144827 NLM ISO Abbreviation: Exp Cell Res Subsets: MEDLINE
أسماء مطبوعة: Publication: Orlando Fl : Academic Press
Original Publication: New York, Academic Press.
مواضيع طبية MeSH: Urinary Bladder Neoplasms*/pathology , Urinary Bladder Neoplasms*/genetics , Urinary Bladder Neoplasms*/metabolism , Proto-Oncogene Proteins c-akt*/metabolism , Proto-Oncogene Proteins c-akt*/genetics , TOR Serine-Threonine Kinases*/metabolism , TOR Serine-Threonine Kinases*/genetics , Chromosomal Proteins, Non-Histone*/metabolism , Chromosomal Proteins, Non-Histone*/genetics , Signal Transduction* , Cell Proliferation*/genetics, Humans ; Animals ; Cell Line, Tumor ; Proto-Oncogene Proteins c-myc/metabolism ; Proto-Oncogene Proteins c-myc/genetics ; Gene Expression Regulation, Neoplastic ; Mice ; Disease Progression ; Mice, Nude ; Male ; Female ; Prognosis ; Mice, Inbred BALB C ; DNA-Binding Proteins
مستخلص: Bladder cancer(BC) is one of the most prevalent cancers in the urinary tract, with high recurrence and fatality rates. Research indicates that go-ichi-ni-san complex subunit 1 (GINS1) crucially influences cancer progression by regulating DNA replication through cell cycle modulation. Thus, suppressing the active proliferation of cells in tumor tissues may require silencing GINS1. However, the consequences of GINS1 in bladder cancer aren't to be determined. In this paper, we examine the role and mechanism of GINS1 in the development of bladder cancer. GINS1 expression levels and prognostic relevance in bladder cancer were validated using Western blotting, immunohistochemistry, and Kaplan-Meier survival analysis. The influence of GINS1 on bladder cancer was investigated using a variety of approaches, including cell transfection, cell counts, transwell migrations, colony formation, and flow cytometry. Immunohistochemistry studies demonstrate that GINS1 expression is increased in bladder cancer tissues. GINS1 silencing resulted in an arrest of the cell cycle at the phase of G0/G1, which inhibited BC cell growth both in vitro and in vivo. GINS1 knockdown also hindered the AKT/mTOR pathway. Furthermore, increased GINS1 expression affects the cell cycle and stimulates the AKT/mTOR pathway, allowing BC to develop more quickly. Consequently, GINS1 occurs as a latent therapeutic target, particularly for individuals with BC.
Competing Interests: Declaration of competing interest The authors have no conflict of interest to declare.
(Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)
فهرسة مساهمة: Keywords: AKT/mTOR pathway; Bladder cancer; Cell cycle; GINS1; c-Myc
المشرفين على المادة: EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
EC 2.7.11.1 (TOR Serine-Threonine Kinases)
0 (Chromosomal Proteins, Non-Histone)
EC 2.7.1.1 (MTOR protein, human)
0 (GINS1 protein, human)
0 (Proto-Oncogene Proteins c-myc)
0 (MYC protein, human)
0 (DNA-Binding Proteins)
تواريخ الأحداث: Date Created: 20240616 Date Completed: 20240627 Latest Revision: 20240719
رمز التحديث: 20240719
DOI: 10.1016/j.yexcr.2024.114125
PMID: 38880324
قاعدة البيانات: MEDLINE
الوصف
تدمد:1090-2422
DOI:10.1016/j.yexcr.2024.114125