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

doi:10.1101/474197

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 journal › Article › peer-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 language	English (US)
Journal	Unknown Journal
DOIs	https://doi.org/10.1101/474197
State	Published - Nov 19 2018
Externally published	Yes

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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10.1101/474197

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AICAR induces apoptosis and inhibits migration of prostate cancer cells through an AMPK/mTOR-dependent pathway. / Su, Chia Cheng; Hsieh, Kun Lin; Wang, Shu Chi; Yeh, Hsin Chih; Huang, Shu Pin; Liu, Po Len; Fang, Shih Hua; Cheng, Wei Chung; Huang, Kuan Hua; Chiu, Fang Yen; Lin, I. Ling; Huang, Ming Yii; Li, Chia Yang.

In: Unknown Journal, 19.11.2018.

Research output: Contribution to journal › Article › peer-review

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

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.",

keywords = "AICAR, AMPK, Chemosensitivity, Metastasis, Prostate cancer",

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

note = "Publisher Copyright: The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license. Copyright: Copyright 2020 Elsevier B.V., All rights reserved.",

year = "2018",

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doi = "10.1101/474197",

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AU - Su, Chia Cheng

AU - Hsieh, Kun Lin

AU - Wang, Shu Chi

AU - Yeh, Hsin Chih

AU - Huang, Shu Pin

AU - Liu, Po Len

AU - Fang, Shih Hua

AU - Cheng, Wei Chung

AU - Huang, Kuan Hua

AU - Chiu, Fang Yen

AU - Lin, I. Ling

AU - Huang, Ming Yii

AU - Li, Chia Yang

N1 - Publisher Copyright: The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license. Copyright: Copyright 2020 Elsevier B.V., All rights reserved.

PY - 2018/11/19

Y1 - 2018/11/19

N2 - 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.

AB - 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.

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