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

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cris.lastimport.scopus2026-02-26T16:02:14Z
dc.creatorSu, Chia-Cheng
dc.creatorHsieh, Kun-Lin
dc.creatorLiu, Po-Len
dc.creatorYeh, Hsin-Chih
dc.creatorHuang, Shu-Pin
dc.creatorFang, Shih-Hua
dc.creatorCheng, Wei-Chung
dc.creatorHuang, Kuan-Hua
dc.creatorChiu, Fang-Yen
dc.creatorLin, I-Ling
dc.creatorHuang, Ming-Yii
dc.creatorLi, Chia-Yang
dc.date2019-04
dc.date.accessioned2021-11-11T07:02:13Z
dc.date.accessioned2025-07-27T15:03:22Z
dc.date.available2021-11-11T07:02:13Z
dc.date.issued2021-11-11T07:02:13Z
dc.description.abstractCurrent 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.
dc.format.extent104 bytes
dc.format.mimetypetext/html
dc.identifier.doi10.3390/ijms20071647
dc.identifier.issn1422-0067
dc.identifier.urihttps://ir.ntus.edu.tw/handle/987654321/64483
dc.languageen_US
dc.publisherBASEL, SWITZERLAND: MDPI
dc.relationINTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 20(7)
dc.subjectAICAR
dc.subjectAMPK
dc.subjectprostate cancer
dc.subjectmetastasis
dc.subjectchemosensitivity
dc.titleAICAR Induces Apoptosis and Inhibits Migration and Invasion in Prostate Cancer Cells Through an AMPK/mTOR-Dependent Pathway
dc.typearticle
dspace.entity.typePublication

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