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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/108182

    Title: CCN3 promotes epithelial-mesenchymal transition in prostate cancer via FAK/Akt/HIF-1α-induced Twist expression
    Authors: 陳?均;Po-Chun Cehn;Huai-Ching T;Huai-Ching Tai;Tien-Huang L;Tien-Huang Lin;Shih-Wei Wan;Shih-Wei Wang;Chih-Yang Li;Chih-Yang Lin;Chia-Chia Ch;Chia-Chia Chao;Hong-Jeng Y;Yu-Chieh Tsa;Yu-Chieh Tsai;Yu-Wei Lai;Chiao-Wen Li;湯智昕;Chih-Hsin Tang
    Contributors: 生物科技學系
    Date: 2017-08
    Issue Date: 2017-10-30 10:43:08 (UTC+8)
    Abstract: Epithelial-mesenchymal transition (EMT) has received considerable attention as a conceptual paradigm for explaining metastatic behavior during cancer progression. NOV/CCN3 is a matrix-associated protein involved in many cellular functions. Previous studies have shown that CCN3 expression is upregulated in prostate cancer (PCa) cells and in PCa patients. In this study, we have provided evidence of tumor promoting effects of CCN3, which includes induction of epithelial-to-mesenchymal transition (EMT) and tumor metastasis. We used an orthotopic in vivo model to demonstrate the prometastatic effects of CCN3. Overexpression or knockdown of CCN3 changed the EMT phenotype in PCa cells. Moreover, treatment with recombinant CCN3 promoted EMT in PCa cells. We also found that CCN3 may promote EMT by activating the FAK/Akt/HIF-1α pathway and this activation is responsible for Twist expression. IHC staining confirmed a positive correlation between the expression of CCN3, Twist, and tumor stage in PCa tissue. Our findings provide insight into the involvement of CCN3 in the EMT regulation of prostate cancer. CCN3 is a promising molecular target that may contribute to a novel therapeutic strategy against metastatic PCa.
    Relation: Oncotarget
    Appears in Collections:[生物科技學系] 期刊論文

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