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Publikasi Scopus 926 artikel (Per 14 Maret 2022)
Publikasi Scopus 926 artikel (Per 14 Maret 2022)
Cancer-associated fibroblast migration in non-small cell lung cancers is modulated by increased integrin α11 expression
2021
Molecular Oncology
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https://www.scopus.com/inward/record.uri?eid=2-s2.0-85103164588&doi=10.1002%2f1878-0261.12937&partnerID=40&md5=b2e053e6ecbd024c8cbcf42081179238
Division of Respiratory Medicine, Juntendo University Faculty of Medicine & Graduate School of Medicine, Tokyo, Japan; Leading Center for the Development and Research of Cancer Medicine, Juntendo University, Tokyo, Japan; Tokyo Metropolitan Institute of Medical Science, Setagaya-ku, Japan; Preventive Medicine and Applied Genomics Unit, RIKEN Center for Integrative Medical Sciences, Yokohama, Japan; RIKEN Preventive Medicine and Diagnosis Innovation Program, Saitama, Japan; Department of Respiratory and Critical Care Medicine, National Center of Gerontology, Beijing Hospital, China; Department of Pulmonology and Respiratory Medicine, Universitas Indonesia Faculty of Medicine, Jakarta, Indonesia; Departments of Molecular Pathogenesis, Graduate School of Medicine, Juntendo University, Tokyo, Japan; Department of Oral Pathobiological Science and Surgery, Tokyo Dental College, Japan; Department of General Thoracic Surgery, Juntendo University School of Medicine, Tokyo, Japan; Faculty of Biology-Oriented Science and Technology, Kindai University, Wakayama, Japan
Cancer-associated fibroblasts (CAFs) regulate cancer progression through the modulation of extracellular matrix (ECM) and cancer cell adhesion. While undergoing a series of phenotypic changes, CAFs control cancer–stroma interactions through integrin receptor signaling. Here, we isolated CAFs from patients with non-small-cell lung cancer (NSCLC) and examined their gene expression profiles. We identified collagen type XI α1 (COL11A1), integrin α11 (ITGA11), and the ITGA11 major ligand collagen type I α1 (COL1A1) among the 390 genes that were significantly enriched in NSCLC-associated CAFs. Increased ITGA11 expression in cancer stroma was correlated with a poor clinical outcome in patients with NSCLC. Increased expression of fibronectin and collagen type I induced ITGA11 expression in CAFs. The cellular migration of CAFs toward collagen type I and fibronectin was promoted via ERK1/2 signaling, independently of the fibronectin receptor integrin α5β1. Additionally, ERK1/2 signaling induced ITGA11 and COL11A1 expression in cancer stroma. We, therefore, propose that targeting ITGA11 and COL11A1 expressing CAFs to block cancer–stroma interactions may serve as a novel, promising anti-tumor strategy. © 2021 The Authors. Molecular Oncology published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.
alpha11 integrin; collagen type 1; collagen type 1 alpha1; collagen type 11; collagen type 11 alpha1; fibronectin; fibronectin receptor; integrin; mitogen activated protein kinase 3; retrovirus vector; small interfering RNA; transforming growth factor beta1; unclassified drug; very late activation antigen 5; adult; aged; Article; cancer associated fibroblast; cancer recurrence; cell interaction; cell migration; chemotaxis; clinical article; clinical outcome; controlled study; DNA modification; enzyme linked immunosorbent assay; female; gene expression profiling; human; human cell; human tissue; immunohistochemistry; in vitro study; lung adenocarcinoma; lung fibroblast; lung parenchyma; male; non small cell lung cancer; priority journal; protein expression; protein expression level; protein
John Wiley and Sons Ltd
15747891
33682233
Article
Q1
2332
1019