文化大學機構典藏 CCUR:Item 987654321/49504
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    题名: MicroRNA-362 negatively and positively regulates SMAD4 expression in TGF-beta/SMAD signaling to suppress cell migration and invasion
    作者: Cheng, HP (Cheng, Han Ping)
    Huang, CJ (Huang, Chiu-Jung)
    Tsai, ML (Tsai, Ming-Long)
    Ong, HT (Ong, Hooi Tin)
    Cheong, SK (Cheong, Soon Keng)
    Choo, KB (Choo, Kong Bung)
    Chiou, SH (Chiou, Shih-Hwa)
    贡献者: 動科系
    关键词: microRNA-362
    EMT/MET
    SMAD4
    TGF-beta/SMAD signaling pathway
    cell migration/invasion
    metastasis
    日期: 2021
    上传时间: 2021-04-22 11:02:33 (UTC+8)
    摘要: Cell migration and invasion are modulated by epithelial-to-mesenchymal transition (EMT) and the reverse MET process. Despite the detection of microRNA-362 (miR- 362, both the miR-362-5p and -3p species) in cancers, none of the identified miR-362 targets is a mesenchymal or epithelial factor to link miR-362 with EMT/MET and metastasis. Focusing on the TGF-beta/SMAD signaling pathway in this work, luciferase assays and western blot data showed that miR-362 targeted and negatively regulated expression of SMAD4 and E-cadherin, but not SNAI1, which is regulated by SMAD4. However, miR-362 knockdown also down-regulated SMAD4 and SNAI1, but up-regulated E-cadherin expression. Wound-healing and transwell assays further showed that miR-362 knockdown suppressed cell migration and invasion, effects which were reversed by over-expressing SMAD4 or SNAI1, or by knocking down E-cadherin in the miR-362 knockdown cells. In orthotopic mice, miR-362 knockdown inhibited metastasis, and displayed the same SMAD4 and E-cadherin expression profiles in the tumors as in the in vitro studies. A scheme is proposed to integrate miR-362 negative regulation via SMAD4, and to explain miR-362 positive regulation of SMAD4 via miR-362 targeting of known SMAD4 suppressors, BRK and DACH1, which would have resulted in SMAD4 depletion and annulment of subsequent involvement in TGF-beta signaling actions. Hence, miR-362 both negatively and positively regulates SMAD4 expression in TGF-beta/SMAD signaling pathway to suppress cell motility and invasiveness and metastasis, and may explain the reported clinical association of anti-miR-362 with suppressed metastasis in various cancers. MiR-362 knockdown in miR-362-positive cancer cells may be used as a therapeutic strategy to suppress metastasis.
    關聯: INTERNATIONAL JOURNAL OF MEDICAL SCIENCES 卷冊: 18 期: 8 頁數: 1798-1809
    显示于类别:[動物科學系 ] 期刊論文

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