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Potential Therapies Targeting the Metabolic Reprogramming of Diabetes-Associated Breast Cancer

In recent years, diabetes-associated breast cancer has become a significant clinical challenge. Diabetes is not only a risk factor for breast cancer but also worsens its prognosis. Patients with diabetes usually show hyperglycemia and hyperinsulinemia, which are accompanied by different glucose, pro...

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Autores principales: Shum, Hang Chee Erin, Wu, Ke, Vadgama, Jaydutt, Wu, Yong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9861470/
https://www.ncbi.nlm.nih.gov/pubmed/36675817
http://dx.doi.org/10.3390/jpm13010157
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author Shum, Hang Chee Erin
Wu, Ke
Vadgama, Jaydutt
Wu, Yong
author_facet Shum, Hang Chee Erin
Wu, Ke
Vadgama, Jaydutt
Wu, Yong
author_sort Shum, Hang Chee Erin
collection PubMed
description In recent years, diabetes-associated breast cancer has become a significant clinical challenge. Diabetes is not only a risk factor for breast cancer but also worsens its prognosis. Patients with diabetes usually show hyperglycemia and hyperinsulinemia, which are accompanied by different glucose, protein, and lipid metabolism disorders. Metabolic abnormalities observed in diabetes can induce the occurrence and development of breast cancer. The changes in substrate availability and hormone environment not only create a favorable metabolic environment for tumorigenesis but also induce metabolic reprogramming events required for breast cancer cell transformation. Metabolic reprogramming is the basis for the development, swift proliferation, and survival of cancer cells. Metabolism must also be reprogrammed to support the energy requirements of the biosynthetic processes in cancer cells. In addition, metabolic reprogramming is essential to enable cancer cells to overcome apoptosis signals and promote invasion and metastasis. This review aims to describe the major metabolic changes in diabetes and outline how cancer cells can use cellular metabolic changes to drive abnormal growth and proliferation. We will specifically examine the mechanism of metabolic reprogramming by which diabetes may promote the development of breast cancer, focusing on the role of glucose metabolism, amino acid metabolism, and lipid metabolism in this process and potential therapeutic targets. Although diabetes-associated breast cancer has always been a common health problem, research focused on finding treatments suitable for the specific needs of patients with concurrent conditions is still limited. Most studies are still currently in the pre-clinical stage and mainly focus on reprogramming the glucose metabolism. More research targeting the amino acid and lipid metabolism is needed.
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spelling pubmed-98614702023-01-22 Potential Therapies Targeting the Metabolic Reprogramming of Diabetes-Associated Breast Cancer Shum, Hang Chee Erin Wu, Ke Vadgama, Jaydutt Wu, Yong J Pers Med Review In recent years, diabetes-associated breast cancer has become a significant clinical challenge. Diabetes is not only a risk factor for breast cancer but also worsens its prognosis. Patients with diabetes usually show hyperglycemia and hyperinsulinemia, which are accompanied by different glucose, protein, and lipid metabolism disorders. Metabolic abnormalities observed in diabetes can induce the occurrence and development of breast cancer. The changes in substrate availability and hormone environment not only create a favorable metabolic environment for tumorigenesis but also induce metabolic reprogramming events required for breast cancer cell transformation. Metabolic reprogramming is the basis for the development, swift proliferation, and survival of cancer cells. Metabolism must also be reprogrammed to support the energy requirements of the biosynthetic processes in cancer cells. In addition, metabolic reprogramming is essential to enable cancer cells to overcome apoptosis signals and promote invasion and metastasis. This review aims to describe the major metabolic changes in diabetes and outline how cancer cells can use cellular metabolic changes to drive abnormal growth and proliferation. We will specifically examine the mechanism of metabolic reprogramming by which diabetes may promote the development of breast cancer, focusing on the role of glucose metabolism, amino acid metabolism, and lipid metabolism in this process and potential therapeutic targets. Although diabetes-associated breast cancer has always been a common health problem, research focused on finding treatments suitable for the specific needs of patients with concurrent conditions is still limited. Most studies are still currently in the pre-clinical stage and mainly focus on reprogramming the glucose metabolism. More research targeting the amino acid and lipid metabolism is needed. MDPI 2023-01-14 /pmc/articles/PMC9861470/ /pubmed/36675817 http://dx.doi.org/10.3390/jpm13010157 Text en © 2023 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
Shum, Hang Chee Erin
Wu, Ke
Vadgama, Jaydutt
Wu, Yong
Potential Therapies Targeting the Metabolic Reprogramming of Diabetes-Associated Breast Cancer
title Potential Therapies Targeting the Metabolic Reprogramming of Diabetes-Associated Breast Cancer
title_full Potential Therapies Targeting the Metabolic Reprogramming of Diabetes-Associated Breast Cancer
title_fullStr Potential Therapies Targeting the Metabolic Reprogramming of Diabetes-Associated Breast Cancer
title_full_unstemmed Potential Therapies Targeting the Metabolic Reprogramming of Diabetes-Associated Breast Cancer
title_short Potential Therapies Targeting the Metabolic Reprogramming of Diabetes-Associated Breast Cancer
title_sort potential therapies targeting the metabolic reprogramming of diabetes-associated breast cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9861470/
https://www.ncbi.nlm.nih.gov/pubmed/36675817
http://dx.doi.org/10.3390/jpm13010157
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