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 inJournal of cellular and molecular medicine Vol. 24; no. 16; pp. 8890 - 8902
Main Authors Khayami, Reza, Hashemi, Seyyed Reza, Kerachian, Mohammad Amin
Format Journal Article
LanguageEnglish
Published 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.
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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ContentType Journal Article
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Issue 16
Keywords aldose reductase
AKR1B1
cancer
biomarker
methylation
tumour
Language English
License Attribution
2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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ORCID 0000-0001-5016-2882
OpenAccessLink http://journals.scholarsportal.info/openUrl.xqy?doi=10.1111/jcmm.15581
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SecondaryResourceType review_article
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...
SourceID pubmedcentral
proquest
pubmed
crossref
wiley
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 8890
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
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjcmm.15581
https://www.ncbi.nlm.nih.gov/pubmed/32633024
https://www.proquest.com/docview/2432290538
https://www.proquest.com/docview/2467811763
https://www.proquest.com/docview/2421107924
https://pubmed.ncbi.nlm.nih.gov/PMC7417692
Volume 24
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