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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 |
| 顯示於類別: | [高齡福祉養生管理系] 期刊論文
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