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Mechanism Underlying Metformin Action and Its Potential to Reduce Gastric Cancer Risk

Diabetes mellitus is associated with a high risk of developing gastric cancer (GC). Metformin, which is conventionally used to treat type 2 diabetes, induces AMP-activated protein kinase signaling and suppresses gluconeogenesis. Recent studies have reported that metformin is associated with benefici...

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Autores principales: Lan, Wen-Hsi, Lin, Ting-Yu, Yeh, Jia-Ai, Feng, Chun-Lung, Hsu, Jun-Te, Lin, Hwai-Jeng, Kuo, Chia-Jung, Lai, Chih-Ho
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9695469/
https://www.ncbi.nlm.nih.gov/pubmed/36430639
http://dx.doi.org/10.3390/ijms232214163
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author Lan, Wen-Hsi
Lin, Ting-Yu
Yeh, Jia-Ai
Feng, Chun-Lung
Hsu, Jun-Te
Lin, Hwai-Jeng
Kuo, Chia-Jung
Lai, Chih-Ho
author_facet Lan, Wen-Hsi
Lin, Ting-Yu
Yeh, Jia-Ai
Feng, Chun-Lung
Hsu, Jun-Te
Lin, Hwai-Jeng
Kuo, Chia-Jung
Lai, Chih-Ho
author_sort Lan, Wen-Hsi
collection PubMed
description Diabetes mellitus is associated with a high risk of developing gastric cancer (GC). Metformin, which is conventionally used to treat type 2 diabetes, induces AMP-activated protein kinase signaling and suppresses gluconeogenesis. Recent studies have reported that metformin is associated with beneficial effects in cancer prevention and treatment owing to its anti-tumor effects. This makes metformin a potential medication for GC therapy. However, contradicting reports have emerged regarding the efficacy of metformin in reducing the risk of GC. This review summarizes the impact of metformin on mitigating GC risk by analyzing clinical databases. The mechanism underlying the anti-tumor effect of metformin on GC is also discussed.
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spelling pubmed-96954692022-11-26 Mechanism Underlying Metformin Action and Its Potential to Reduce Gastric Cancer Risk Lan, Wen-Hsi Lin, Ting-Yu Yeh, Jia-Ai Feng, Chun-Lung Hsu, Jun-Te Lin, Hwai-Jeng Kuo, Chia-Jung Lai, Chih-Ho Int J Mol Sci Review Diabetes mellitus is associated with a high risk of developing gastric cancer (GC). Metformin, which is conventionally used to treat type 2 diabetes, induces AMP-activated protein kinase signaling and suppresses gluconeogenesis. Recent studies have reported that metformin is associated with beneficial effects in cancer prevention and treatment owing to its anti-tumor effects. This makes metformin a potential medication for GC therapy. However, contradicting reports have emerged regarding the efficacy of metformin in reducing the risk of GC. This review summarizes the impact of metformin on mitigating GC risk by analyzing clinical databases. The mechanism underlying the anti-tumor effect of metformin on GC is also discussed. MDPI 2022-11-16 /pmc/articles/PMC9695469/ /pubmed/36430639 http://dx.doi.org/10.3390/ijms232214163 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Lan, Wen-Hsi
Lin, Ting-Yu
Yeh, Jia-Ai
Feng, Chun-Lung
Hsu, Jun-Te
Lin, Hwai-Jeng
Kuo, Chia-Jung
Lai, Chih-Ho
Mechanism Underlying Metformin Action and Its Potential to Reduce Gastric Cancer Risk
title Mechanism Underlying Metformin Action and Its Potential to Reduce Gastric Cancer Risk
title_full Mechanism Underlying Metformin Action and Its Potential to Reduce Gastric Cancer Risk
title_fullStr Mechanism Underlying Metformin Action and Its Potential to Reduce Gastric Cancer Risk
title_full_unstemmed Mechanism Underlying Metformin Action and Its Potential to Reduce Gastric Cancer Risk
title_short Mechanism Underlying Metformin Action and Its Potential to Reduce Gastric Cancer Risk
title_sort mechanism underlying metformin action and its potential to reduce gastric cancer risk
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9695469/
https://www.ncbi.nlm.nih.gov/pubmed/36430639
http://dx.doi.org/10.3390/ijms232214163
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