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    標題: AICAR Induces Apoptosis and Inhibits Migration and Invasion in Prostate Cancer Cells Through an AMPK/mTOR-Dependent Pathway
    作者: Chia-Cheng Su(蘇家震)
    Hsieh, Kun-Lin
    Liu, Po-Len
    Yeh, Hsin-Chih
    Huang, Shu-Pin
    Fang, Shih-Hua
    Cheng, Wei-Chung
    Huang, Kuan-Hua
    Chiu, Fang-Yen
    Lin, I-Ling
    Huang, Ming-Yii
    Li, Chia-Yang
    貢獻者: Chi Mei Med Ctr, Div Urol, Dept Surg
    Kaohsiung Med Univ, Grad Inst Med, Coll Med
    Chia Nan Univ Pharm & Sci, Dept Senior Citizen Serv Management
    Kaohsiung Med Univ, Dept Resp Therapy, Coll Med
    Kaohsiung Med Univ, Sch Med, Dept Urol, Coll Med
    Kaohsiung Municipal Tatung Hosp, Dept Urol
    Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Dept Urol
    Natl Taiwan Univ Sport, Inst Athlet
    China Med Univ, Grad Inst Biomed Sci
    China Med Univ, Res Ctr Tumor Med Sci
    Kaohsiung Med Univ, Dept Med Lab Sci & Biotechnol, Coll Hlth Sci
    Kaohsiung Med Univ Hosp, Dept Radiat Oncol
    Kaohsiung Med Univ, Coll Med, Dept Radiat Oncol
    Kaohsiung Med Univ, Ctr Biomarkers & Biotech Drugs
    Kaohsiung Med Univ, Ctr Infect Dis & Canc Res
    關鍵字: AICAR
    AMPK
    prostate cancer
    metastasis
    chemosensitivity
    日期: 2019-04
    上傳時間: 2020-07-29 13:47:29 (UTC+8)
    出版者: MDPI
    摘要: Current clinical challenges of prostate cancer management are to restrict tumor growth and prohibit metastasis. AICAR (5-aminoimidazole-4-carbox-amide-1--d-ribofuranoside), an AMP-activated protein kinase (AMPK) agonist, has demonstrated antitumor activities for several types of cancers. However, the activity of AICAR on the cell growth and metastasis of prostate cancer has not been extensively studied. Herein we examine the effects of AICAR on the cell growth and metastasis of prostate cancer cells. Cell growth was performed by MTT assay and soft agar assay; cell apoptosis was examined by Annexin V/propidium iodide (PI) staining and poly ADP ribose polymerase (PARP) cleavage western blot, while cell migration and invasion were evaluated by wound-healing assay and transwell assay respectively. Epithelial-mesenchymal transition (EMT)-related protein expression and AMPK/mTOR-dependent signaling axis were analyzed by western blot. In addition, we also tested the effect of AICAR on the chemosensitivity to docetaxel using MTT assay. Our results indicated that AICAR inhibits cell growth in prostate cancer cells, but not in non-cancerous prostate cells. In addition, our results demonstrated that AICAR induces apoptosis, attenuates transforming growth factor (TGF)--induced cell migration, invasion and EMT-related protein expression, and enhances the chemosensitivity to docetaxel in prostate cancer cells through regulating the AMPK/mTOR-dependent pathway. These findings support AICAR as a potential therapeutic agent for the treatment of prostate cancer.
    關聯: International Journal of Molecular Sciences, v.20, n.7, 1647
    Appears in Collections:[老人服務事業管理系] 期刊論文

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