Tumor Metabolic Reprogramming by Adipokines as a Critical Driver of Obesity-Associated Cancer Progression
Adiposity is associated with an increased risk of various types of carcinoma. One of the plausible mechanisms underlying the tumor-promoting role of obesity is an aberrant secretion of adipokines, a group of hormones secreted from adipose tissue, which have exhibited both oncogenic and tumor-suppres...
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description | Adiposity is associated with an increased risk of various types of carcinoma. One of the plausible mechanisms underlying the tumor-promoting role of obesity is an aberrant secretion of adipokines, a group of hormones secreted from adipose tissue, which have exhibited both oncogenic and tumor-suppressing properties in an adipokine type- and context-dependent manner. Increasing evidence has indicated that these adipose tissue-derived hormones differentially modulate cancer cell-specific metabolism. Some adipokines, such as leptin, resistin, and visfatin, which are overproduced in obesity and widely implicated in different stages of cancer, promote cellular glucose and lipid metabolism. Conversely, adiponectin, an adipokine possessing potent anti-tumor activities, is linked to a more favorable metabolic phenotype. Adipokines may also play a pivotal role under the reciprocal regulation of metabolic rewiring of cancer cells in tumor microenvironment. Given the fact that metabolic reprogramming is one of the major hallmarks of cancer, understanding the modulatory effects of adipokines on alterations in cancer cell metabolism would provide insight into the crosstalk between obesity, adipokines, and tumorigenesis. In this review, we summarize recent insights into putative roles of adipokines as mediators of cellular metabolic rewiring in obesity-associated tumors, which plays a crucial role in determining the fate of tumor cells. |
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One of the plausible mechanisms underlying the tumor-promoting role of obesity is an aberrant secretion of adipokines, a group of hormones secreted from adipose tissue, which have exhibited both oncogenic and tumor-suppressing properties in an adipokine type- and context-dependent manner. Increasing evidence has indicated that these adipose tissue-derived hormones differentially modulate cancer cell-specific metabolism. Some adipokines, such as leptin, resistin, and visfatin, which are overproduced in obesity and widely implicated in different stages of cancer, promote cellular glucose and lipid metabolism. Conversely, adiponectin, an adipokine possessing potent anti-tumor activities, is linked to a more favorable metabolic phenotype. Adipokines may also play a pivotal role under the reciprocal regulation of metabolic rewiring of cancer cells in tumor microenvironment. Given the fact that metabolic reprogramming is one of the major hallmarks of cancer, understanding the modulatory effects of adipokines on alterations in cancer cell metabolism would provide insight into the crosstalk between obesity, adipokines, and tumorigenesis. In this review, we summarize recent insights into putative roles of adipokines as mediators of cellular metabolic rewiring in obesity-associated tumors, which plays a crucial role in determining the fate of tumor cells.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms22031444</identifier><identifier>PMID: 33535537</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Acidification ; Adipocytes ; Adiponectin ; Adipose tissue ; Angiogenesis ; Autophagy ; Biosynthesis ; Breast cancer ; Cell adhesion & migration ; Cell cycle ; Crosstalk ; Cytokines ; Glucose metabolism ; Hypoxia ; Kinases ; Leptin ; Lipid metabolism ; Lipids ; Liver cancer ; Medical prognosis ; Metabolism ; Metabolites ; Metastasis ; Obesity ; Phenotypes ; Phosphorylation ; Proteins ; Review ; Rewiring ; Roles ; Tumor cells ; Tumor microenvironment ; Tumorigenesis ; Tumors</subject><ispartof>International journal of molecular sciences, 2021-02, Vol.22 (3), p.1444</ispartof><rights>2021. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). 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One of the plausible mechanisms underlying the tumor-promoting role of obesity is an aberrant secretion of adipokines, a group of hormones secreted from adipose tissue, which have exhibited both oncogenic and tumor-suppressing properties in an adipokine type- and context-dependent manner. Increasing evidence has indicated that these adipose tissue-derived hormones differentially modulate cancer cell-specific metabolism. Some adipokines, such as leptin, resistin, and visfatin, which are overproduced in obesity and widely implicated in different stages of cancer, promote cellular glucose and lipid metabolism. Conversely, adiponectin, an adipokine possessing potent anti-tumor activities, is linked to a more favorable metabolic phenotype. Adipokines may also play a pivotal role under the reciprocal regulation of metabolic rewiring of cancer cells in tumor microenvironment. Given the fact that metabolic reprogramming is one of the major hallmarks of cancer, understanding the modulatory effects of adipokines on alterations in cancer cell metabolism would provide insight into the crosstalk between obesity, adipokines, and tumorigenesis. In this review, we summarize recent insights into putative roles of adipokines as mediators of cellular metabolic rewiring in obesity-associated tumors, which plays a crucial role in determining the fate of tumor cells.</description><subject>Acidification</subject><subject>Adipocytes</subject><subject>Adiponectin</subject><subject>Adipose tissue</subject><subject>Angiogenesis</subject><subject>Autophagy</subject><subject>Biosynthesis</subject><subject>Breast cancer</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Crosstalk</subject><subject>Cytokines</subject><subject>Glucose metabolism</subject><subject>Hypoxia</subject><subject>Kinases</subject><subject>Leptin</subject><subject>Lipid metabolism</subject><subject>Lipids</subject><subject>Liver cancer</subject><subject>Medical prognosis</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Metastasis</subject><subject>Obesity</subject><subject>Phenotypes</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Review</subject><subject>Rewiring</subject><subject>Roles</subject><subject>Tumor cells</subject><subject>Tumor microenvironment</subject><subject>Tumorigenesis</subject><subject>Tumors</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdkd1L3EAUxYeiqFXf-iwDvvShqZP5SDIvhWX7oaCsiD4PNzM321mTzDqTCPvfN3atbIUL98L5cbiHQ8innH0VQrMLv-oS50zkUsoP5CiXnGeMFeXezn1IPqa0YowLrvQBORRCCaVEeUT8_diFSG9wgDq03tI7XMewjNB1vl_SekNnzq_Do-8xUZiGzqMfvIWWfo_-GSMNDV3UmPywyWYpBethQEfn0NtJvH3xwpR86E_IfgNtwtPXfUwefv64n19m14tfV_PZdWalUkMmbWm1LhtRc8EKUZUVIsttVYNTOucNVw6kywGYdco2XLtaOQ1aSM1qZCCOybet73qsO3QW-yFCa9bRdxA3JoA3_yu9_22W4dmUVVEyzSeDz68GMTyNmAbT-WSxbaHHMCbDZVXIgleVmNDzd-gqjLGf4v2lJiTXbKK-bCkbQ0oRm7dncmZeOjS7HU742W6AN_hfaeIPTImZrA</recordid><startdate>20210201</startdate><enddate>20210201</enddate><creator>Pham, Duc-Vinh</creator><creator>Park, Pil-Hoon</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4057-1313</orcidid></search><sort><creationdate>20210201</creationdate><title>Tumor Metabolic Reprogramming by Adipokines as a Critical Driver of Obesity-Associated Cancer Progression</title><author>Pham, Duc-Vinh ; Park, Pil-Hoon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-4c7c997f3b23063878ee01c8bad5912f25da4d1aa0cd5cf29db5d9a93490be0a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acidification</topic><topic>Adipocytes</topic><topic>Adiponectin</topic><topic>Adipose tissue</topic><topic>Angiogenesis</topic><topic>Autophagy</topic><topic>Biosynthesis</topic><topic>Breast cancer</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Crosstalk</topic><topic>Cytokines</topic><topic>Glucose metabolism</topic><topic>Hypoxia</topic><topic>Kinases</topic><topic>Leptin</topic><topic>Lipid metabolism</topic><topic>Lipids</topic><topic>Liver cancer</topic><topic>Medical prognosis</topic><topic>Metabolism</topic><topic>Metabolites</topic><topic>Metastasis</topic><topic>Obesity</topic><topic>Phenotypes</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Review</topic><topic>Rewiring</topic><topic>Roles</topic><topic>Tumor cells</topic><topic>Tumor microenvironment</topic><topic>Tumorigenesis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pham, Duc-Vinh</creatorcontrib><creatorcontrib>Park, Pil-Hoon</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pham, Duc-Vinh</au><au>Park, Pil-Hoon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Tumor Metabolic Reprogramming by Adipokines as a Critical Driver of Obesity-Associated Cancer Progression</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2021-02-01</date><risdate>2021</risdate><volume>22</volume><issue>3</issue><spage>1444</spage><pages>1444-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Adiposity is associated with an increased risk of various types of carcinoma. One of the plausible mechanisms underlying the tumor-promoting role of obesity is an aberrant secretion of adipokines, a group of hormones secreted from adipose tissue, which have exhibited both oncogenic and tumor-suppressing properties in an adipokine type- and context-dependent manner. Increasing evidence has indicated that these adipose tissue-derived hormones differentially modulate cancer cell-specific metabolism. Some adipokines, such as leptin, resistin, and visfatin, which are overproduced in obesity and widely implicated in different stages of cancer, promote cellular glucose and lipid metabolism. Conversely, adiponectin, an adipokine possessing potent anti-tumor activities, is linked to a more favorable metabolic phenotype. Adipokines may also play a pivotal role under the reciprocal regulation of metabolic rewiring of cancer cells in tumor microenvironment. Given the fact that metabolic reprogramming is one of the major hallmarks of cancer, understanding the modulatory effects of adipokines on alterations in cancer cell metabolism would provide insight into the crosstalk between obesity, adipokines, and tumorigenesis. In this review, we summarize recent insights into putative roles of adipokines as mediators of cellular metabolic rewiring in obesity-associated tumors, which plays a crucial role in determining the fate of tumor cells.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>33535537</pmid><doi>10.3390/ijms22031444</doi><orcidid>https://orcid.org/0000-0002-4057-1313</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Acidification Adipocytes Adiponectin Adipose tissue Angiogenesis Autophagy Biosynthesis Breast cancer Cell adhesion & migration Cell cycle Crosstalk Cytokines Glucose metabolism Hypoxia Kinases Leptin Lipid metabolism Lipids Liver cancer Medical prognosis Metabolism Metabolites Metastasis Obesity Phenotypes Phosphorylation Proteins Review Rewiring Roles Tumor cells Tumor microenvironment Tumorigenesis Tumors |
title | Tumor Metabolic Reprogramming by Adipokines as a Critical Driver of Obesity-Associated Cancer Progression |
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