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    標題: COL11A1 activates cancer-associated fibroblasts by modulating TGF-beta 3 through the NF-kappa B/IGFBP2 axis in ovarian cancer cells
    作者: Wu, Yi-Hui
    Huang, Yu-Fang
    Chang, Tzu-Hao
    Chen, Chien-Chin
    Wu, Pei-Ying
    Huang, Soon-Cen
    Chou, Cheng-Yang
    貢獻者: Chi Mei Med Ctr, Dept Med Res
    Natl Cheng Kung Univ, Natl Cheng Kung Univ Hosp, Coll Med, Dept Obstet & Gynecol
    Taipei Med Univ, Grad Inst Biomed Informat
    Chia Yi Christian Hosp, Dept Pathol, Ditmanson Med Fdn
    Chia Nan Univ Pharm & Sci, Dept Cosmet Sci
    Chi Mei Med Ctr, Dept Obstet & Gynecol
    關鍵字: NF-KAPPA-B
    TGF-BETA
    BREAST-CANCER
    CARCINOMA
    GROWTH
    EXPRESSION
    IL-6
    CHEMORESISTANCE
    SIGNATURE
    SURVIVAL
    日期: 2021
    上傳時間: 2023-11-11 11:50:23 (UTC+8)
    出版者: SPRINGERNATURE
    摘要: Ovarian cancer has a unique tumor microenvironment (TME) that enables cancer-associated fibroblasts (CAFs) to interact with cellular and matrix constituents and influence tumor development and migration into the peritoneal cavity. Collagen type XI alpha 1 (COL11A1) is overexpressed in CAFs; therefore this study examines its role during CAF activation in epithelial ovarian cancer (EOC). Coculturing human ovarian fibroblasts (HOFs) with high COL11A1-expressing EOC cells or exposure to the conditioned medium of these cells prompted the expression of COL11A1 and CAF phenotypes. Conversely, coculturing HOFs with low COL11A1-expressing EOC cells or COL11A1-knockdown abrogated COL11A1 overexpression and secretion, in addition to CAF activation. Increased p-SP1 expression attributed to COL11A1-mediated extracellular signal-regulated kinase activation (ERK) induced p65 translocation into the nucleus and augmented its binding to the insulin-like growth factor binding protein 2 (IGFBP2) promoter, ultimately inducing TGF-beta 3 activation. The CAF-cancer cell crosstalk triggered interleukin-6 release, which in turn promoted EOC cell proliferation and invasiveness. These in vitro results were confirmed by in vivo findings in a mouse model, showing that COL11A1 overexpression in EOC cells promoted tumor formation and CAF activation, which was inhibited by TGF-beta 3 antibody. Human tumors with high TGF-beta 3 levels showed elevated expression of COL11A1 and IGFBP2, which was associated with poor survival. Our findings suggest the possibility that anti-TGF-beta 3 treatment strategy may be effective in targeting CAFs in COL11A1-positive ovarian tumors.
    關聯: ONCOGENE, v.40, n.26, pp.4503-4519
    顯示於類別:[化妝品應用與管理系(所)] 期刊論文

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