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AMP‐activated protein kinase β1 or β2 deletion enhances colon cancer cell growth and tumorigenesis: Effects of AMPKβ1 or β2 deletion in colon cancer
Abnormal metabolism is a major hallmark of cancer and has been validated as a therapeutic target. Adenine monophosphate‐activated protein kinase (AMPK), an αβγ heterotrimer, performs essential functions in cancer progression due to its central role in maintaining the homeostasis of cellular energy....
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9828713/ https://www.ncbi.nlm.nih.gov/pubmed/35880569 http://dx.doi.org/10.3724/abbs.2022086 |
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author | Shi, Fuli Tang, Zhimin Jiang, Shanshan Xiong, Zhijuan Zhang, Wansi Li, Yuanjun Lin, Hui Luo, Zhijun Ying, Ying |
author_facet | Shi, Fuli Tang, Zhimin Jiang, Shanshan Xiong, Zhijuan Zhang, Wansi Li, Yuanjun Lin, Hui Luo, Zhijun Ying, Ying |
author_sort | Shi, Fuli |
collection | PubMed |
description | Abnormal metabolism is a major hallmark of cancer and has been validated as a therapeutic target. Adenine monophosphate‐activated protein kinase (AMPK), an αβγ heterotrimer, performs essential functions in cancer progression due to its central role in maintaining the homeostasis of cellular energy. While the contributions of AMPKα and AMPKγ subunits to cancer development have been established, specific roles of AMPKβ1 and AMPKβ2 isoforms in cancer development are poorly understood. Here, we show the functions of AMPKβ1 and AMPKβ2 in colon cancer. Specifically, deletion of AMPKβ1 or AMPKβ2 leads to increased cell proliferation, colony formation, migration, and tumorigenesis in HCT116 and HT29 colon cancer cells. Interestingly, the AMPKβ1 and AMPKβ2 isoforms have slightly different effects on regulating cancer metabolism, as colon cancer cells with AMPKβ1 knockout showed decreased rates of glycolysis-related oxygen consumption, while AMPKβ2 deletion led to enhanced rates of oxygen consumption due to oxidative phosphorylation. These results demonstrate that functional AMPKβ1 and AMPKβ2 inhibit growth and tumorigenesis in colon cancer cells, suggesting their potential as effective targets for colon cancer therapy. |
format | Online Article Text |
id | pubmed-9828713 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-98287132023-02-10 AMP‐activated protein kinase β1 or β2 deletion enhances colon cancer cell growth and tumorigenesis: Effects of AMPKβ1 or β2 deletion in colon cancer Shi, Fuli Tang, Zhimin Jiang, Shanshan Xiong, Zhijuan Zhang, Wansi Li, Yuanjun Lin, Hui Luo, Zhijun Ying, Ying Acta Biochim Biophys Sin (Shanghai) Research Article Abnormal metabolism is a major hallmark of cancer and has been validated as a therapeutic target. Adenine monophosphate‐activated protein kinase (AMPK), an αβγ heterotrimer, performs essential functions in cancer progression due to its central role in maintaining the homeostasis of cellular energy. While the contributions of AMPKα and AMPKγ subunits to cancer development have been established, specific roles of AMPKβ1 and AMPKβ2 isoforms in cancer development are poorly understood. Here, we show the functions of AMPKβ1 and AMPKβ2 in colon cancer. Specifically, deletion of AMPKβ1 or AMPKβ2 leads to increased cell proliferation, colony formation, migration, and tumorigenesis in HCT116 and HT29 colon cancer cells. Interestingly, the AMPKβ1 and AMPKβ2 isoforms have slightly different effects on regulating cancer metabolism, as colon cancer cells with AMPKβ1 knockout showed decreased rates of glycolysis-related oxygen consumption, while AMPKβ2 deletion led to enhanced rates of oxygen consumption due to oxidative phosphorylation. These results demonstrate that functional AMPKβ1 and AMPKβ2 inhibit growth and tumorigenesis in colon cancer cells, suggesting their potential as effective targets for colon cancer therapy. Oxford University Press 2022-07-12 /pmc/articles/PMC9828713/ /pubmed/35880569 http://dx.doi.org/10.3724/abbs.2022086 Text en © The Author(s) 2021. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Research Article Shi, Fuli Tang, Zhimin Jiang, Shanshan Xiong, Zhijuan Zhang, Wansi Li, Yuanjun Lin, Hui Luo, Zhijun Ying, Ying AMP‐activated protein kinase β1 or β2 deletion enhances colon cancer cell growth and tumorigenesis: Effects of AMPKβ1 or β2 deletion in colon cancer |
title | AMP‐activated protein kinase β1 or β2 deletion enhances colon cancer cell growth and tumorigenesis: Effects of AMPKβ1 or β2 deletion in colon cancer |
title_full | AMP‐activated protein kinase β1 or β2 deletion enhances colon cancer cell growth and tumorigenesis: Effects of AMPKβ1 or β2 deletion in colon cancer |
title_fullStr | AMP‐activated protein kinase β1 or β2 deletion enhances colon cancer cell growth and tumorigenesis: Effects of AMPKβ1 or β2 deletion in colon cancer |
title_full_unstemmed | AMP‐activated protein kinase β1 or β2 deletion enhances colon cancer cell growth and tumorigenesis: Effects of AMPKβ1 or β2 deletion in colon cancer |
title_short | AMP‐activated protein kinase β1 or β2 deletion enhances colon cancer cell growth and tumorigenesis: Effects of AMPKβ1 or β2 deletion in colon cancer |
title_sort | amp‐activated protein kinase β1 or β2 deletion enhances colon cancer cell growth and tumorigenesis: effects of ampkβ1 or β2 deletion in colon cancer |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9828713/ https://www.ncbi.nlm.nih.gov/pubmed/35880569 http://dx.doi.org/10.3724/abbs.2022086 |
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