Regulation of Butyrate-Induced Resistance through AMPK Signaling Pathway in Human Colon Cancer Cells

Butyrates inhibit cell growth in colon cancer cells by inhibiting histone deacetylases. However, chronic exposure to butyrates induces butyrate resistance in colon cancer cells. The mechanism underlying the acquisition of resistance is not yet fully understood. Here, butyrate-resistant (BR) colon ca...

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Autores principales:	Hee Young Yoo, So Yeon Park, Sun-Young Chang, So Hee Kim
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	butyrate resistance colon cancer AMPK autophagy ACC Akt Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/ad6809eb5c554f9e925b58b9b9ce86be
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spelling	oai:doaj.org-article:ad6809eb5c554f9e925b58b9b9ce86be2021-11-25T16:49:32ZRegulation of Butyrate-Induced Resistance through AMPK Signaling Pathway in Human Colon Cancer Cells10.3390/biomedicines91116042227-9059https://doaj.org/article/ad6809eb5c554f9e925b58b9b9ce86be2021-11-01T00:00:00Zhttps://www.mdpi.com/2227-9059/9/11/1604https://doaj.org/toc/2227-9059Butyrates inhibit cell growth in colon cancer cells by inhibiting histone deacetylases. However, chronic exposure to butyrates induces butyrate resistance in colon cancer cells. The mechanism underlying the acquisition of resistance is not yet fully understood. Here, butyrate-resistant (BR) colon cancer cells were developed in HCT116, HT29, and SW480 human colon cancer cells and were confirmed by the increase in the inhibitory concentrations of cell growth by 50% (IC<sub>50</sub>) compared to their respective parental (PT) cells. Chronic exposure to butyrate induced autophagy via higher expression of Beclin-1 and LC3B-II. The AMP-activated protein kinase (AMPK) was downregulated along with the activation of Akt and mammalian target of rapamycin (mTOR) and decrease in acetyl-CoA carboxylase (ACC) in BR colon cancer cells compared to those in their respective PT cells. Activation of AMPK by AICAR treatment in BR colon cancer cells suppressed cell proliferation by inhibiting Akt and mTOR and activating ACC. Taken together, chronic exposure to butyrate increased butyrate resistance in human colon cancer by inducing protective autophagy through the downregulation of AMPK/ACC and activation of Akt/mTOR signaling. Activation of AMPK restored sensitivity to butyrate by the inhibition of Akt/mTOR, suggesting that AMPK could be a therapeutic target for BR colon cancers.Hee Young YooSo Yeon ParkSun-Young ChangSo Hee KimMDPI AGarticlebutyrate resistancecolon cancerAMPKautophagyACCAktBiology (General)QH301-705.5ENBiomedicines, Vol 9, Iss 1604, p 1604 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	butyrate resistance colon cancer AMPK autophagy ACC Akt Biology (General) QH301-705.5
spellingShingle	butyrate resistance colon cancer AMPK autophagy ACC Akt Biology (General) QH301-705.5 Hee Young Yoo So Yeon Park Sun-Young Chang So Hee Kim Regulation of Butyrate-Induced Resistance through AMPK Signaling Pathway in Human Colon Cancer Cells
description	Butyrates inhibit cell growth in colon cancer cells by inhibiting histone deacetylases. However, chronic exposure to butyrates induces butyrate resistance in colon cancer cells. The mechanism underlying the acquisition of resistance is not yet fully understood. Here, butyrate-resistant (BR) colon cancer cells were developed in HCT116, HT29, and SW480 human colon cancer cells and were confirmed by the increase in the inhibitory concentrations of cell growth by 50% (IC<sub>50</sub>) compared to their respective parental (PT) cells. Chronic exposure to butyrate induced autophagy via higher expression of Beclin-1 and LC3B-II. The AMP-activated protein kinase (AMPK) was downregulated along with the activation of Akt and mammalian target of rapamycin (mTOR) and decrease in acetyl-CoA carboxylase (ACC) in BR colon cancer cells compared to those in their respective PT cells. Activation of AMPK by AICAR treatment in BR colon cancer cells suppressed cell proliferation by inhibiting Akt and mTOR and activating ACC. Taken together, chronic exposure to butyrate increased butyrate resistance in human colon cancer by inducing protective autophagy through the downregulation of AMPK/ACC and activation of Akt/mTOR signaling. Activation of AMPK restored sensitivity to butyrate by the inhibition of Akt/mTOR, suggesting that AMPK could be a therapeutic target for BR colon cancers.
format	article
author	Hee Young Yoo So Yeon Park Sun-Young Chang So Hee Kim
author_facet	Hee Young Yoo So Yeon Park Sun-Young Chang So Hee Kim
author_sort	Hee Young Yoo
title	Regulation of Butyrate-Induced Resistance through AMPK Signaling Pathway in Human Colon Cancer Cells
title_short	Regulation of Butyrate-Induced Resistance through AMPK Signaling Pathway in Human Colon Cancer Cells
title_full	Regulation of Butyrate-Induced Resistance through AMPK Signaling Pathway in Human Colon Cancer Cells
title_fullStr	Regulation of Butyrate-Induced Resistance through AMPK Signaling Pathway in Human Colon Cancer Cells
title_full_unstemmed	Regulation of Butyrate-Induced Resistance through AMPK Signaling Pathway in Human Colon Cancer Cells
title_sort	regulation of butyrate-induced resistance through ampk signaling pathway in human colon cancer cells
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/ad6809eb5c554f9e925b58b9b9ce86be
work_keys_str_mv	AT heeyoungyoo regulationofbutyrateinducedresistancethroughampksignalingpathwayinhumancoloncancercells AT soyeonpark regulationofbutyrateinducedresistancethroughampksignalingpathwayinhumancoloncancercells AT sunyoungchang regulationofbutyrateinducedresistancethroughampksignalingpathwayinhumancoloncancercells AT soheekim regulationofbutyrateinducedresistancethroughampksignalingpathwayinhumancoloncancercells
_version_	1718412915614154752

Regulation of Butyrate-Induced Resistance through AMPK Signaling Pathway in Human Colon Cancer Cells

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