AICAR induces apoptosis and inhibits migration of prostate cancer cells through an AMPK/mTOR-dependent pathway

Chia Cheng Su, Kun Lin Hsieh, Shu Chi Wang, Hsin Chih Yeh, Shu Pin Huang, Po Len Liu, Shih Hua Fang, Wei Chung Cheng, Kuan Hua Huang, Fang Yen Chiu, I. Ling Lin, Ming Yii Huang, Chia Yang Li

Research output: Contribution to journalArticlepeer-review

Abstract

AICAR (5-aminoimidazole-4-carbox-amide-1-β-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, 22RV1 cells. Cell growth was performed by MTT assay and soft agar assay. Cell apoptosis was examined by Annexin V/PI staining and PARP cleavage Western blot. Cell migration was evaluated by wound-healing assay. The expression of EMT-related protein and the activity of the AMPK/ mTOR-dependent pathway 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, induces apoptosis, attenuates TGF-β-induced cell migration and EMT-related protein expression, and enhances the chemosensitivity to docetaxel through regulating the AMPK/mTOR-dependent pathway. Collectively, these findings support AICAR as a potential therapeutic agent for the treatment of prostate cancer.

Original languageEnglish (US)
JournalUnknown Journal
DOIs
StatePublished - Nov 19 2018
Externally publishedYes

Keywords

  • AICAR
  • AMPK
  • Chemosensitivity
  • Metastasis
  • Prostate cancer

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Agricultural and Biological Sciences(all)
  • Immunology and Microbiology(all)
  • Neuroscience(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

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