Irisin inhibits pancreatic cancer cell growth via the AMPK-mTOR pathway

Abstract Irisin, a recently identified myokine that is released from skeletal muscle following exercise, regulates body weight and influences various metabolic diseases such as obesity and diabetes. In this study, human recombinant nonglycosylated P-irisin (expressed in Escherichia coli prokaryote c...

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Autores principales:	Jiayu Liu, Nannan Song, Yibing Huang, Yuxin Chen
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Irisin PC Cell Growth Pancreatic Cancer AMPK-mTOR Pathway Adenosine Monophosphate-activated Protein Kinase (AMPK) Medicine R Science Q
Acceso en línea:	https://doaj.org/article/1af93d718d9b49d4ba9e17c7ccddaf69
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spelling	oai:doaj.org-article:1af93d718d9b49d4ba9e17c7ccddaf692021-12-02T15:08:00ZIrisin inhibits pancreatic cancer cell growth via the AMPK-mTOR pathway10.1038/s41598-018-33229-w2045-2322https://doaj.org/article/1af93d718d9b49d4ba9e17c7ccddaf692018-10-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-33229-whttps://doaj.org/toc/2045-2322Abstract Irisin, a recently identified myokine that is released from skeletal muscle following exercise, regulates body weight and influences various metabolic diseases such as obesity and diabetes. In this study, human recombinant nonglycosylated P-irisin (expressed in Escherichia coli prokaryote cell system) or glycosylated E-irisin (expressed in Pichia pastoris eukaryote cell system) were compared to examine the role of recombinant irisin against pancreatic cancer (PC) cells lines, MIA PaCa-2 and Panc03.27. MTT [3-(4, 5-dimethylthiazol-2-yl)-2, 5-di phenyltetrazolium bromide] and cell colony formation assays revealed that irisin significantly inhibited the growth of MIA PaCa-2 and Panc03.27 in a dose-dependent manner. Irisin also induced G1 arrest in both cell lines. Scratch wound healing and transwell assays revealed that irisin also inhibited the migration of PC cells. Irisin reversed the activity of epithelial–mesenchymal transition (EMT) while increasing E-cadherin expression and reducing vimentin expression. Irisin activated the adenosine monophosphate-activated protein kinase (AMPK) pathway and suppressed the mammalian target of rapamycin (mTOR) signaling. Besides, our results suggest that irisin receptors exist on the surface of human MIA PaCa-2 and Panc03.27 cells. Our results clearly demonstrate that irisin suppressed PC cell growth via the activation of AMPK, thereby downregulating the mTOR pathway and inhibiting EMT of PC cells.Jiayu LiuNannan SongYibing HuangYuxin ChenNature PortfolioarticleIrisinPC Cell GrowthPancreatic CancerAMPK-mTOR PathwayAdenosine Monophosphate-activated Protein Kinase (AMPK)MedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-10 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Irisin PC Cell Growth Pancreatic Cancer AMPK-mTOR Pathway Adenosine Monophosphate-activated Protein Kinase (AMPK) Medicine R Science Q
spellingShingle	Irisin PC Cell Growth Pancreatic Cancer AMPK-mTOR Pathway Adenosine Monophosphate-activated Protein Kinase (AMPK) Medicine R Science Q Jiayu Liu Nannan Song Yibing Huang Yuxin Chen Irisin inhibits pancreatic cancer cell growth via the AMPK-mTOR pathway
description	Abstract Irisin, a recently identified myokine that is released from skeletal muscle following exercise, regulates body weight and influences various metabolic diseases such as obesity and diabetes. In this study, human recombinant nonglycosylated P-irisin (expressed in Escherichia coli prokaryote cell system) or glycosylated E-irisin (expressed in Pichia pastoris eukaryote cell system) were compared to examine the role of recombinant irisin against pancreatic cancer (PC) cells lines, MIA PaCa-2 and Panc03.27. MTT [3-(4, 5-dimethylthiazol-2-yl)-2, 5-di phenyltetrazolium bromide] and cell colony formation assays revealed that irisin significantly inhibited the growth of MIA PaCa-2 and Panc03.27 in a dose-dependent manner. Irisin also induced G1 arrest in both cell lines. Scratch wound healing and transwell assays revealed that irisin also inhibited the migration of PC cells. Irisin reversed the activity of epithelial–mesenchymal transition (EMT) while increasing E-cadherin expression and reducing vimentin expression. Irisin activated the adenosine monophosphate-activated protein kinase (AMPK) pathway and suppressed the mammalian target of rapamycin (mTOR) signaling. Besides, our results suggest that irisin receptors exist on the surface of human MIA PaCa-2 and Panc03.27 cells. Our results clearly demonstrate that irisin suppressed PC cell growth via the activation of AMPK, thereby downregulating the mTOR pathway and inhibiting EMT of PC cells.
format	article
author	Jiayu Liu Nannan Song Yibing Huang Yuxin Chen
author_facet	Jiayu Liu Nannan Song Yibing Huang Yuxin Chen
author_sort	Jiayu Liu
title	Irisin inhibits pancreatic cancer cell growth via the AMPK-mTOR pathway
title_short	Irisin inhibits pancreatic cancer cell growth via the AMPK-mTOR pathway
title_full	Irisin inhibits pancreatic cancer cell growth via the AMPK-mTOR pathway
title_fullStr	Irisin inhibits pancreatic cancer cell growth via the AMPK-mTOR pathway
title_full_unstemmed	Irisin inhibits pancreatic cancer cell growth via the AMPK-mTOR pathway
title_sort	irisin inhibits pancreatic cancer cell growth via the ampk-mtor pathway
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/1af93d718d9b49d4ba9e17c7ccddaf69
work_keys_str_mv	AT jiayuliu irisininhibitspancreaticcancercellgrowthviatheampkmtorpathway AT nannansong irisininhibitspancreaticcancercellgrowthviatheampkmtorpathway AT yibinghuang irisininhibitspancreaticcancercellgrowthviatheampkmtorpathway AT yuxinchen irisininhibitspancreaticcancercellgrowthviatheampkmtorpathway
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Irisin inhibits pancreatic cancer cell growth via the AMPK-mTOR pathway

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