AICAR Induces Apoptosis and Inhibits Migration and Invasion in Prostate Cancer Cells Through an AMPK/mTOR-Dependent Pathway

doi:10.3390/ijms20071647

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Title:	AICAR Induces Apoptosis and Inhibits Migration and Invasion in Prostate Cancer Cells Through an AMPK/mTOR-Dependent Pathway
Authors:	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
Contributors:	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
Keywords:	AICAR AMPK prostate cancer metastasis chemosensitivity
Date:	2019-04
Issue Date:	2020-07-29 13:47:29 (UTC+8)
Publisher:	MDPI
Abstract:	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.
Relation:	International Journal of Molecular Sciences, v.20, n.7, 1647
Appears in Collections:	[Dept. of Senior Service and Health Management] Periodical Articles

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