Role of aldo‐keto reductase family 1 member B1 (AKR1B1) in the cancer process and its therapeutic potential
The role of aldo‐keto reductase family 1 member B1 (AKR1B1) in cancer is not totally clear but growing evidence is suggesting to have a great impact on cancer progression. AKR1B1 could participate in a complicated network of signalling pathways, proteins and miRNAs such as mir‐21 mediating mechanism...
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Published in | Journal of cellular and molecular medicine Vol. 24; no. 16; pp. 8890 - 8902 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
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England
John Wiley & Sons, Inc
01.08.2020
John Wiley and Sons Inc |
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Abstract | The role of aldo‐keto reductase family 1 member B1 (AKR1B1) in cancer is not totally clear but growing evidence is suggesting to have a great impact on cancer progression. AKR1B1 could participate in a complicated network of signalling pathways, proteins and miRNAs such as mir‐21 mediating mechanisms like inflammatory responses, cell cycle, epithelial to mesenchymal transition, cell survival and apoptosis. AKR1B1 has been shown to be mostly overexpressed in cancer. This overexpression has been associated with inflammatory mediators including nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NFκB), cell cycle mediators such as cyclins and cyclin‐dependent kinases (CDKs), survival proteins and pathways like mammalian target of rapamycin (mTOR) and protein kinase B (PKB) or AKT, and other regulatory factors in response to reactive oxygen species (ROS) and prostaglandin synthesis. In addition, inhibition of AKR1B1 has been shown to mostly have anti‐cancer effects. Several studies have also suggested that AKR1B1 inhibition as an adjuvant therapy could render tumour cells more sensitive to anti‐cancer therapy or alleviate the adverse effects of therapy. AKR1B1 could also be considered as a potential cancer diagnostic biomarker since its promoter has shown high levels of methylation. Although pre‐clinical investigations on the role of AKR1B1 in cancer and the application of its inhibitors have shown promising results, the lack of clinical studies on AKR1B1 inhibitors has hampered the use of these drugs to treat cancer. Thus, there is a need to conduct more clinical studies on the application of AKR1B1 inhibitors as adjuvant therapy on different cancers. |
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AbstractList | The role of aldo-keto reductase family 1 member B1 (AKR1B1) in cancer is not totally clear but growing evidence is suggesting to have a great impact on cancer progression. AKR1B1 could participate in a complicated network of signalling pathways, proteins and miRNAs such as mir-21 mediating mechanisms like inflammatory responses, cell cycle, epithelial to mesenchymal transition, cell survival and apoptosis. AKR1B1 has been shown to be mostly overexpressed in cancer. This overexpression has been associated with inflammatory mediators including nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), cell cycle mediators such as cyclins and cyclin-dependent kinases (CDKs), survival proteins and pathways like mammalian target of rapamycin (mTOR) and protein kinase B (PKB) or AKT, and other regulatory factors in response to reactive oxygen species (ROS) and prostaglandin synthesis. In addition, inhibition of AKR1B1 has been shown to mostly have anti-cancer effects. Several studies have also suggested that AKR1B1 inhibition as an adjuvant therapy could render tumour cells more sensitive to anti-cancer therapy or alleviate the adverse effects of therapy. AKR1B1 could also be considered as a potential cancer diagnostic biomarker since its promoter has shown high levels of methylation. Although pre-clinical investigations on the role of AKR1B1 in cancer and the application of its inhibitors have shown promising results, the lack of clinical studies on AKR1B1 inhibitors has hampered the use of these drugs to treat cancer. Thus, there is a need to conduct more clinical studies on the application of AKR1B1 inhibitors as adjuvant therapy on different cancers. The role of aldo‐keto reductase family 1 member B1 (AKR1B1) in cancer is not totally clear but growing evidence is suggesting to have a great impact on cancer progression. AKR1B1 could participate in a complicated network of signalling pathways, proteins and miRNAs such as mir‐21 mediating mechanisms like inflammatory responses, cell cycle, epithelial to mesenchymal transition, cell survival and apoptosis. AKR1B1 has been shown to be mostly overexpressed in cancer. This overexpression has been associated with inflammatory mediators including nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NFκB), cell cycle mediators such as cyclins and cyclin‐dependent kinases (CDKs), survival proteins and pathways like mammalian target of rapamycin (mTOR) and protein kinase B (PKB) or AKT, and other regulatory factors in response to reactive oxygen species (ROS) and prostaglandin synthesis. In addition, inhibition of AKR1B1 has been shown to mostly have anti‐cancer effects. Several studies have also suggested that AKR1B1 inhibition as an adjuvant therapy could render tumour cells more sensitive to anti‐cancer therapy or alleviate the adverse effects of therapy. AKR1B1 could also be considered as a potential cancer diagnostic biomarker since its promoter has shown high levels of methylation. Although pre‐clinical investigations on the role of AKR1B1 in cancer and the application of its inhibitors have shown promising results, the lack of clinical studies on AKR1B1 inhibitors has hampered the use of these drugs to treat cancer. Thus, there is a need to conduct more clinical studies on the application of AKR1B1 inhibitors as adjuvant therapy on different cancers. The role of aldo-keto reductase family 1 member B1 (AKR1B1) in cancer is not totally clear but growing evidence is suggesting to have a great impact on cancer progression. AKR1B1 could participate in a complicated network of signalling pathways, proteins and miRNAs such as mir-21 mediating mechanisms like inflammatory responses, cell cycle, epithelial to mesenchymal transition, cell survival and apoptosis. AKR1B1 has been shown to be mostly overexpressed in cancer. This overexpression has been associated with inflammatory mediators including nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), cell cycle mediators such as cyclins and cyclin-dependent kinases (CDKs), survival proteins and pathways like mammalian target of rapamycin (mTOR) and protein kinase B (PKB) or AKT, and other regulatory factors in response to reactive oxygen species (ROS) and prostaglandin synthesis. In addition, inhibition of AKR1B1 has been shown to mostly have anti-cancer effects. Several studies have also suggested that AKR1B1 inhibition as an adjuvant therapy could render tumour cells more sensitive to anti-cancer therapy or alleviate the adverse effects of therapy. AKR1B1 could also be considered as a potential cancer diagnostic biomarker since its promoter has shown high levels of methylation. Although pre-clinical investigations on the role of AKR1B1 in cancer and the application of its inhibitors have shown promising results, the lack of clinical studies on AKR1B1 inhibitors has hampered the use of these drugs to treat cancer. Thus, there is a need to conduct more clinical studies on the application of AKR1B1 inhibitors as adjuvant therapy on different cancers.The role of aldo-keto reductase family 1 member B1 (AKR1B1) in cancer is not totally clear but growing evidence is suggesting to have a great impact on cancer progression. AKR1B1 could participate in a complicated network of signalling pathways, proteins and miRNAs such as mir-21 mediating mechanisms like inflammatory responses, cell cycle, epithelial to mesenchymal transition, cell survival and apoptosis. AKR1B1 has been shown to be mostly overexpressed in cancer. This overexpression has been associated with inflammatory mediators including nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), cell cycle mediators such as cyclins and cyclin-dependent kinases (CDKs), survival proteins and pathways like mammalian target of rapamycin (mTOR) and protein kinase B (PKB) or AKT, and other regulatory factors in response to reactive oxygen species (ROS) and prostaglandin synthesis. In addition, inhibition of AKR1B1 has been shown to mostly have anti-cancer effects. Several studies have also suggested that AKR1B1 inhibition as an adjuvant therapy could render tumour cells more sensitive to anti-cancer therapy or alleviate the adverse effects of therapy. AKR1B1 could also be considered as a potential cancer diagnostic biomarker since its promoter has shown high levels of methylation. Although pre-clinical investigations on the role of AKR1B1 in cancer and the application of its inhibitors have shown promising results, the lack of clinical studies on AKR1B1 inhibitors has hampered the use of these drugs to treat cancer. Thus, there is a need to conduct more clinical studies on the application of AKR1B1 inhibitors as adjuvant therapy on different cancers. |
Author | Hashemi, Seyyed Reza Khayami, Reza Kerachian, Mohammad Amin |
AuthorAffiliation | 1 Medical Genetics Research Center Mashhad University of Medical Sciences Mashhad Iran 2 Department of Medical Genetics Faculty of Medicine Mashhad University of Medical Sciences Mashhad Iran 3 Student Research Committee Mashhad University of Medical Sciences Mashhad Iran 4 Cancer Genetics Research Unit Reza Radiotherapy and Oncology Center Mashhad Iran |
AuthorAffiliation_xml | – name: 1 Medical Genetics Research Center Mashhad University of Medical Sciences Mashhad Iran – name: 2 Department of Medical Genetics Faculty of Medicine Mashhad University of Medical Sciences Mashhad Iran – name: 4 Cancer Genetics Research Unit Reza Radiotherapy and Oncology Center Mashhad Iran – name: 3 Student Research Committee Mashhad University of Medical Sciences Mashhad Iran |
Author_xml | – sequence: 1 givenname: Reza surname: Khayami fullname: Khayami, Reza organization: Mashhad University of Medical Sciences – sequence: 2 givenname: Seyyed Reza surname: Hashemi fullname: Hashemi, Seyyed Reza organization: Mashhad University of Medical Sciences – sequence: 3 givenname: Mohammad Amin orcidid: 0000-0001-5016-2882 surname: Kerachian fullname: Kerachian, Mohammad Amin email: kerachianma@mums.ac.ir, amin.kerachian@mail.mcgill.ca organization: Reza Radiotherapy and Oncology Center |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32633024$$D View this record in MEDLINE/PubMed |
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Copyright | 2020 The Authors. published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd. 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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Snippet | The role of aldo‐keto reductase family 1 member B1 (AKR1B1) in cancer is not totally clear but growing evidence is suggesting to have a great impact on cancer... The role of aldo-keto reductase family 1 member B1 (AKR1B1) in cancer is not totally clear but growing evidence is suggesting to have a great impact on cancer... |
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SubjectTerms | AKR1B1 AKT protein Aldehyde Reductase - metabolism aldose reductase Animals Antineoplastic Agents - pharmacology Apoptosis Binding sites biomarker Biomarkers, Tumor - metabolism Cancer Cell cycle Cell survival Colorectal cancer Cyclins DNA methylation Enzyme Inhibitors - pharmacology Enzymes Glucose Growth factors Humans Inflammation Kinases Lipid peroxidation Lipids Lymphocytes B Mesenchyme Metabolism Metastasis methylation Neoplasms - drug therapy Neoplasms - metabolism Neoplasms - pathology NF-κB protein Proteins Rapamycin Reactive oxygen species Reductase Review Reviews Signal transduction TOR protein Tumor necrosis factor-TNF Tumorigenesis Tumors tumour |
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Title | Role of aldo‐keto reductase family 1 member B1 (AKR1B1) in the cancer process and its therapeutic potential |
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