دورية أكاديمية

Collagen XVII promotes dormancy of colorectal cancer cells by activating mTORC2 signaling.

التفاصيل البيبلوغرافية
العنوان: Collagen XVII promotes dormancy of colorectal cancer cells by activating mTORC2 signaling.
المؤلفون: Lin J; State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou 510060, PR China., Zou B; State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou 510060, PR China., Li H; Department of Musculoskeletal Oncology, the First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China., Wang J; Department of Anesthesiology, Sun Yat-sen University Cancer Center, Guangzhou 510060, China., Li S; Department of Medical Oncology, Affiliated Cancer Hospital of Zhengzhou University, Henan Cancer Hospital, Zhengzhou 450008, China., Cao J; State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou 510060, PR China., Xie D; State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou 510060, PR China; Department of Pathology, Sun Yat-sen University Cancer Center, Guangzhou 510060, China. Electronic address: xiedan@sysucc.org.cn., Wang F; State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-sen University Cancer Center, Guangzhou 510060, PR China. Electronic address: wangfengw@sysucc.org.cn.
المصدر: Cellular signalling [Cell Signal] 2024 Aug; Vol. 120, pp. 111234. Date of Electronic Publication: 2024 May 23.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Elsevier Science Ltd Country of Publication: England NLM ID: 8904683 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-3913 (Electronic) Linking ISSN: 08986568 NLM ISO Abbreviation: Cell Signal Subsets: MEDLINE
أسماء مطبوعة: Publication: Oxford : Elsevier Science Ltd
Original Publication: Oxford ; New York : Pergamon Press, 1988-
مواضيع طبية MeSH: Colorectal Neoplasms*/metabolism , Colorectal Neoplasms*/pathology , Colorectal Neoplasms*/genetics , Mechanistic Target of Rapamycin Complex 2*/metabolism , Signal Transduction* , Non-Fibrillar Collagens*/metabolism , Non-Fibrillar Collagens*/genetics , Collagen Type XVII*, Humans ; Cell Line, Tumor ; Animals ; Proto-Oncogene Proteins c-akt/metabolism ; Autoantigens/metabolism ; Mice ; Mice, Nude ; Cell Proliferation ; Mice, Inbred BALB C
مستخلص: Tumor dormancy is the underpinning for cancer relapse and chemoresistance, leading to massive cancer-related death in colorectal cancer (CRC). However, our comprehension of the mechanisms dictating tumor dormancy and strategies for eliminating dormant tumor cells remains restricted. In this study, we identified that collagen XVII (COL17A1), a hemidesmosomal transmembrane protein, can promote the dormancy of CRC cells. The upregulation of COL17A1 was observed to prolong quiescence periods and diminish drug susceptibility of CRC cells. Mechanistically, COL17A1 acts as a scaffold, enhancing the crosstalk between mTORC2 and Akt, thereby instigating the mTORC2-mediated dormant signaling. Notably, the activation of mTORC2 is contingent upon the intracellular domain of COL17A1, regardless of its ectodomain shedding. Our findings underscore a pivotal role of the COL17A1-mTORC2 axis in CRC dormancy, suggesting that mTORC2-specific inhibitors may hold therapeutic prospects for the eradication of dormant tumor cells.
Competing Interests: Declaration of competing interest The authors have no conflict of interest.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
فهرسة مساهمة: Keywords: COL17A1; CRC; Dormancy; Scaffold; mTORC2
المشرفين على المادة: EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 2)
0 (Non-Fibrillar Collagens)
0 (Collagen Type XVII)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
0 (Autoantigens)
تواريخ الأحداث: Date Created: 20240525 Date Completed: 20240611 Latest Revision: 20240621
رمز التحديث: 20240621
DOI: 10.1016/j.cellsig.2024.111234
PMID: 38795810
قاعدة البيانات: MEDLINE
الوصف
تدمد:1873-3913
DOI:10.1016/j.cellsig.2024.111234