Metformin Activity against Breast Cancer: Mechanistic Differences by Molecular Subtype and Metabolic Conditions
Obesity and type 2 diabetes increase the risk of and reduce survival in breast cancer (BC) patients. Metformin is the only anti-diabetic drug that alters this risk, with a reduction in BC incidence and improved outcomes. Metformin has AMP-kinase (AMPK) dependent and independent mechanisms of action,...
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| Formato: | Capítulo de libro |
| Lenguaje: | inglés |
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IntechOpen
2020
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| Acceso en línea: | https://www.intechopen.com/chapters/71075 |
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| _version_ | 1879164698143752192 |
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| author | Wahdan-Alaswad, Reema S. Thor, Ann D. |
| author_browse | Thor, Ann D. Wahdan-Alaswad, Reema S. |
| author_facet | Wahdan-Alaswad, Reema S. Thor, Ann D. |
| author_sort | Wahdan-Alaswad, Reema S. |
| building | IntechOpen |
| collection | Acceso abierto |
| description | Obesity and type 2 diabetes increase the risk of and reduce survival in breast cancer (BC) patients. Metformin is the only anti-diabetic drug that alters this risk, with a reduction in BC incidence and improved outcomes. Metformin has AMP-kinase (AMPK) dependent and independent mechanisms of action, most notably affecting the liver and skeletal muscle. We and others have shown that metformin also downregulates protein and lipid synthesis; deactivates various receptor tyrosine kinases; alters cell cycle transcription/translation; modulates mitochondrial respiration and miRNA activation; targets key metabolic molecules; induces stem cell death and may induce apoptosis or autophagy in BC cells. Many of these anti-cancer effects are molecular subtype-specific. Metformin is most potent against triple negative (basal), followed by luminal BCs. The efficacy of metformin, as well as dose needed for the activity, is also modulated by the extracellular glucose concentration, cellular expression of the glucose transporter protein 1 (GLUT1), and the organic cation transporter protein 1 (OCT1, which transports metformin into cells). This chapter summarizes the diverse clinical and preclinical data related to the anti-cancer effects of metformin, focused against breast cancer. |
| doi_str_mv | 10.5772/intechopen.91183 |
| first_indexed | 2026-10-15T21:38:28Z |
| format | Book Chapter |
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<dc:title>Metformin Activity against Breast Cancer: Mechanistic Differences by Molecular Subtype and Metabolic Conditions</dc:title>
<dc:creator>Reema S. Wahdan-Alaswad</dc:creator>
<dc:creator>Ann D. Thor</dc:creator>
<dc:subject>Health Sciences</dc:subject>
<dc:description>Obesity and type 2 diabetes increase the risk of and reduce survival in breast cancer (BC) patients. Metformin is the only anti-diabetic drug that alters this risk, with a reduction in BC incidence and improved outcomes. Metformin has AMP-kinase (AMPK) dependent and independent mechanisms of action, most notably affecting the liver and skeletal muscle. We and others have shown that metformin also downregulates protein and lipid synthesis; deactivates various receptor tyrosine kinases; alters cell cycle transcription/translation; modulates mitochondrial respiration and miRNA activation; targets key metabolic molecules; induces stem cell death and may induce apoptosis or autophagy in BC cells. Many of these anti-cancer effects are molecular subtype-specific. Metformin is most potent against triple negative (basal), followed by luminal BCs. The efficacy of metformin, as well as dose needed for the activity, is also modulated by the extracellular glucose concentration, cellular expression of the glucose transporter protein 1 (GLUT1), and the organic cation transporter protein 1 (OCT1, which transports metformin into cells). This chapter summarizes the diverse clinical and preclinical data related to the anti-cancer effects of metformin, focused against breast cancer.</dc:description>
<dc:publisher>IntechOpen</dc:publisher>
<dc:date>2020-02-12</dc:date>
<dc:type>Chapter, Part Of Book</dc:type>
<dc:identifier>https://www.intechopen.com/chapters/71075</dc:identifier>
<dc:identifier>doi:10.5772/intechopen.91183</dc:identifier>
<dc:language>en</dc:language>
<dc:relation>ISBN:978-1-83880-427-5</dc:relation>
<dc:rights>https://creativecommons.org/licenses/by/3.0/</dc:rights>
<dc:source>https://www.intechopen.com/books/7994 ; Metformin</dc:source>
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| id | intech-71075 |
| institution | IntechOpen |
| isbn | 978-1-83880-427-5 |
| language | English |
| last_indexed | 2026-10-15T21:38:28Z |
| publishDate | 2020 |
| publishDateRange | 2020 |
| publishDateSort | 2020 |
| publisher | IntechOpen |
| publisherStr | IntechOpen |
| record_format | oai_dc |
| spelling | intech-710752020-02-12 Metformin Activity against Breast Cancer: Mechanistic Differences by Molecular Subtype and Metabolic Conditions Reema S. Wahdan-Alaswad Ann D. Thor Health Sciences Obesity and type 2 diabetes increase the risk of and reduce survival in breast cancer (BC) patients. Metformin is the only anti-diabetic drug that alters this risk, with a reduction in BC incidence and improved outcomes. Metformin has AMP-kinase (AMPK) dependent and independent mechanisms of action, most notably affecting the liver and skeletal muscle. We and others have shown that metformin also downregulates protein and lipid synthesis; deactivates various receptor tyrosine kinases; alters cell cycle transcription/translation; modulates mitochondrial respiration and miRNA activation; targets key metabolic molecules; induces stem cell death and may induce apoptosis or autophagy in BC cells. Many of these anti-cancer effects are molecular subtype-specific. Metformin is most potent against triple negative (basal), followed by luminal BCs. The efficacy of metformin, as well as dose needed for the activity, is also modulated by the extracellular glucose concentration, cellular expression of the glucose transporter protein 1 (GLUT1), and the organic cation transporter protein 1 (OCT1, which transports metformin into cells). This chapter summarizes the diverse clinical and preclinical data related to the anti-cancer effects of metformin, focused against breast cancer. IntechOpen 2020-02-12 Chapter, Part Of Book https://www.intechopen.com/chapters/71075 doi:10.5772/intechopen.91183 en ISBN:978-1-83880-427-5 https://creativecommons.org/licenses/by/3.0/ https://www.intechopen.com/books/7994 ; Metformin |
| spellingShingle | Health Sciences Wahdan-Alaswad, Reema S. Thor, Ann D. Metformin Activity against Breast Cancer: Mechanistic Differences by Molecular Subtype and Metabolic Conditions |
| title | Metformin Activity against Breast Cancer: Mechanistic Differences by Molecular Subtype and Metabolic Conditions |
| title_full | Metformin Activity against Breast Cancer: Mechanistic Differences by Molecular Subtype and Metabolic Conditions |
| title_fullStr | Metformin Activity against Breast Cancer: Mechanistic Differences by Molecular Subtype and Metabolic Conditions |
| title_full_unstemmed | Metformin Activity against Breast Cancer: Mechanistic Differences by Molecular Subtype and Metabolic Conditions |
| title_short | Metformin Activity against Breast Cancer: Mechanistic Differences by Molecular Subtype and Metabolic Conditions |
| title_sort | metformin activity against breast cancer mechanistic differences by molecular subtype and metabolic conditions |
| topic | Health Sciences |
| url | https://www.intechopen.com/chapters/71075 |
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