Endocrine-related cancers and the role of AMPK
► AMPK has an emerging role in the regulation of endocrine-related cancer cell growth. ► In most cases, AMPK is a negative regulator of cancer cell proliferation. ► AMPK inhibits cell growth by stimulating p53 and inhibiting mTOR. ► AMPK inhibits PGE2 and estrogen biosynthesis, key mediators of cell...
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| Veröffentlicht in: | Molecular and cellular endocrinology 2013-02, Vol.366 (2), p.170-179 |
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| description | ► AMPK has an emerging role in the regulation of endocrine-related cancer cell growth. ► In most cases, AMPK is a negative regulator of cancer cell proliferation. ► AMPK inhibits cell growth by stimulating p53 and inhibiting mTOR. ► AMPK inhibits PGE2 and estrogen biosynthesis, key mediators of cell proliferation. ► AMPK-activating drugs decrease tumour cell growth and induce apoptosis.
AMP-activated protein kinase (AMPK) is a master regulator of energy homeostasis involved in the regulation of a number of physiological processes including β-oxidation of fatty acids, lipogenesis, protein and cholesterol synthesis, as well as cell cycle inhibition and apoptosis. Important changes to these processes are known to occur in cancer due to changes in AMPK activity within cancer cells and in the periphery. This review aims to present findings relating to the role and regulation of AMPK in endocrine-related cancers. Obesity is a known risk factor for many types of cancers and a number of endocrine factors, including adipokines and steroid hormones, are regulated by and regulate AMPK. A clear role for AMPK in breast cancer is evident from the already impressive body of work published to date. However, information pertaining to its role in prostate cancer is still contentious, and future work should unravel the intricacies behind its role to inhibit, in some cases, and stimulate cancer growth in others. This review also presents data relating to the role of AMPK in cancers of the endometrium, ovary and colon, and discusses the possible use of AMPK-activating drugs including metformin for the treatment of all endocrine-related cancers. |
| doi_str_mv | 10.1016/j.mce.2012.06.016 |
| format | Article |
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AMP-activated protein kinase (AMPK) is a master regulator of energy homeostasis involved in the regulation of a number of physiological processes including β-oxidation of fatty acids, lipogenesis, protein and cholesterol synthesis, as well as cell cycle inhibition and apoptosis. Important changes to these processes are known to occur in cancer due to changes in AMPK activity within cancer cells and in the periphery. This review aims to present findings relating to the role and regulation of AMPK in endocrine-related cancers. Obesity is a known risk factor for many types of cancers and a number of endocrine factors, including adipokines and steroid hormones, are regulated by and regulate AMPK. A clear role for AMPK in breast cancer is evident from the already impressive body of work published to date. However, information pertaining to its role in prostate cancer is still contentious, and future work should unravel the intricacies behind its role to inhibit, in some cases, and stimulate cancer growth in others. This review also presents data relating to the role of AMPK in cancers of the endometrium, ovary and colon, and discusses the possible use of AMPK-activating drugs including metformin for the treatment of all endocrine-related cancers.</description><identifier>ISSN: 0303-7207</identifier><identifier>EISSN: 1872-8057</identifier><identifier>DOI: 10.1016/j.mce.2012.06.016</identifier><identifier>PMID: 22801104</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>adipokines ; AMP-activated protein kinase ; AMP-Activated Protein Kinases - genetics ; AMP-Activated Protein Kinases - metabolism ; AMPK ; animal ovaries ; apoptosis ; beta oxidation ; Biological Factors - pharmacology ; Breast ; Breast cancer ; breast neoplasms ; cell cycle ; Cell Transformation, Neoplastic ; cholesterol ; colon ; Colon cancer ; Colonic Neoplasms - drug therapy ; Colonic Neoplasms - enzymology ; Colonic Neoplasms - genetics ; Endocrine System - drug effects ; Endocrine System - enzymology ; Endocrine System - pathology ; Endometrial cancer ; Endometrial Neoplasms - drug therapy ; Endometrial Neoplasms - enzymology ; Endometrial Neoplasms - genetics ; endometrium ; energy ; fatty acids ; Female ; Gene Expression Regulation, Neoplastic ; homeostasis ; Humans ; Hypoglycemic Agents - pharmacology ; Hypoglycemic Agents - therapeutic use ; lipogenesis ; Male ; metformin ; Metformin - pharmacology ; Metformin - therapeutic use ; neoplasm cells ; obesity ; Obesity - enzymology ; Obesity - genetics ; Ovarian cancer ; Ovarian Neoplasms - drug therapy ; Ovarian Neoplasms - enzymology ; Ovarian Neoplasms - genetics ; Prostate cancer ; prostatic neoplasms ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - enzymology ; Prostatic Neoplasms - genetics ; risk factors ; steroid hormones</subject><ispartof>Molecular and cellular endocrinology, 2013-02, Vol.366 (2), p.170-179</ispartof><rights>2012 Elsevier Ireland Ltd</rights><rights>Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c410t-b5d8e7d04fa0bd3b9176077316f2bfce10e15520be7622cd7e4ae243a76f36413</citedby><cites>FETCH-LOGICAL-c410t-b5d8e7d04fa0bd3b9176077316f2bfce10e15520be7622cd7e4ae243a76f36413</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0303720712003309$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22801104$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Brown, Kristy A.</creatorcontrib><creatorcontrib>Samarajeewa, Nirukshi U.</creatorcontrib><creatorcontrib>Simpson, Evan R.</creatorcontrib><title>Endocrine-related cancers and the role of AMPK</title><title>Molecular and cellular endocrinology</title><addtitle>Mol Cell Endocrinol</addtitle><description>► AMPK has an emerging role in the regulation of endocrine-related cancer cell growth. ► In most cases, AMPK is a negative regulator of cancer cell proliferation. ► AMPK inhibits cell growth by stimulating p53 and inhibiting mTOR. ► AMPK inhibits PGE2 and estrogen biosynthesis, key mediators of cell proliferation. ► AMPK-activating drugs decrease tumour cell growth and induce apoptosis.
AMP-activated protein kinase (AMPK) is a master regulator of energy homeostasis involved in the regulation of a number of physiological processes including β-oxidation of fatty acids, lipogenesis, protein and cholesterol synthesis, as well as cell cycle inhibition and apoptosis. Important changes to these processes are known to occur in cancer due to changes in AMPK activity within cancer cells and in the periphery. This review aims to present findings relating to the role and regulation of AMPK in endocrine-related cancers. Obesity is a known risk factor for many types of cancers and a number of endocrine factors, including adipokines and steroid hormones, are regulated by and regulate AMPK. A clear role for AMPK in breast cancer is evident from the already impressive body of work published to date. However, information pertaining to its role in prostate cancer is still contentious, and future work should unravel the intricacies behind its role to inhibit, in some cases, and stimulate cancer growth in others. This review also presents data relating to the role of AMPK in cancers of the endometrium, ovary and colon, and discusses the possible use of AMPK-activating drugs including metformin for the treatment of all endocrine-related cancers.</description><subject>adipokines</subject><subject>AMP-activated protein kinase</subject><subject>AMP-Activated Protein Kinases - genetics</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>AMPK</subject><subject>animal ovaries</subject><subject>apoptosis</subject><subject>beta oxidation</subject><subject>Biological Factors - pharmacology</subject><subject>Breast</subject><subject>Breast cancer</subject><subject>breast neoplasms</subject><subject>cell cycle</subject><subject>Cell Transformation, Neoplastic</subject><subject>cholesterol</subject><subject>colon</subject><subject>Colon cancer</subject><subject>Colonic Neoplasms - drug therapy</subject><subject>Colonic Neoplasms - enzymology</subject><subject>Colonic Neoplasms - genetics</subject><subject>Endocrine System - drug effects</subject><subject>Endocrine System - enzymology</subject><subject>Endocrine System - pathology</subject><subject>Endometrial cancer</subject><subject>Endometrial Neoplasms - drug therapy</subject><subject>Endometrial Neoplasms - enzymology</subject><subject>Endometrial Neoplasms - genetics</subject><subject>endometrium</subject><subject>energy</subject><subject>fatty acids</subject><subject>Female</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>homeostasis</subject><subject>Humans</subject><subject>Hypoglycemic Agents - pharmacology</subject><subject>Hypoglycemic Agents - therapeutic use</subject><subject>lipogenesis</subject><subject>Male</subject><subject>metformin</subject><subject>Metformin - pharmacology</subject><subject>Metformin - therapeutic use</subject><subject>neoplasm cells</subject><subject>obesity</subject><subject>Obesity - enzymology</subject><subject>Obesity - genetics</subject><subject>Ovarian cancer</subject><subject>Ovarian Neoplasms - drug therapy</subject><subject>Ovarian Neoplasms - enzymology</subject><subject>Ovarian Neoplasms - genetics</subject><subject>Prostate cancer</subject><subject>prostatic neoplasms</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - enzymology</subject><subject>Prostatic Neoplasms - genetics</subject><subject>risk factors</subject><subject>steroid hormones</subject><issn>0303-7207</issn><issn>1872-8057</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtOwzAQRS0EgvL4ADaQJZuEGSe2U7GqKl6iCCRgbTn2BFKlSbFTJP4eVwWWsBrp6tyr0WHsGCFDQHk-zxaWMg7IM5BZTLbYCEvF0xKE2mYjyCFPFQe1x_ZDmAOAErzcZXucl4AIxYhll53rrW86Sj21ZiCXWNNZ8iExnUuGN0p831LS18nk_vHukO3Upg109H0P2MvV5fP0Jp09XN9OJ7PUFghDWglXknJQ1AYql1djVBKUylHWvKotIRAKwaEiJTm3TlFhiBe5UbLOZYH5ATvb7C59_76iMOhFEyy1remoXwWNOQqplBiX_6O85AKLMRQRxQ1qfR-Cp1ovfbMw_lMj6LVRPdfRqF4b1SB1TGLn5Ht-VS3I_TZ-FEbgdAPUptfm1TdBvzzFBQGAJXIYR-JiQ1A09tGQ18E2FCW7xpMdtOubPx74AmD_jB0</recordid><startdate>20130225</startdate><enddate>20130225</enddate><creator>Brown, Kristy A.</creator><creator>Samarajeewa, Nirukshi U.</creator><creator>Simpson, Evan R.</creator><general>Elsevier Ireland Ltd</general><scope>FBQ</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7U5</scope><scope>8FD</scope><scope>L7M</scope></search><sort><creationdate>20130225</creationdate><title>Endocrine-related cancers and the role of AMPK</title><author>Brown, Kristy A. ; Samarajeewa, Nirukshi U. ; Simpson, Evan R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c410t-b5d8e7d04fa0bd3b9176077316f2bfce10e15520be7622cd7e4ae243a76f36413</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>adipokines</topic><topic>AMP-activated protein kinase</topic><topic>AMP-Activated Protein Kinases - genetics</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>AMPK</topic><topic>animal ovaries</topic><topic>apoptosis</topic><topic>beta oxidation</topic><topic>Biological Factors - pharmacology</topic><topic>Breast</topic><topic>Breast cancer</topic><topic>breast neoplasms</topic><topic>cell cycle</topic><topic>Cell Transformation, Neoplastic</topic><topic>cholesterol</topic><topic>colon</topic><topic>Colon cancer</topic><topic>Colonic Neoplasms - drug therapy</topic><topic>Colonic Neoplasms - enzymology</topic><topic>Colonic Neoplasms - genetics</topic><topic>Endocrine System - drug effects</topic><topic>Endocrine System - enzymology</topic><topic>Endocrine System - pathology</topic><topic>Endometrial cancer</topic><topic>Endometrial Neoplasms - drug therapy</topic><topic>Endometrial Neoplasms - enzymology</topic><topic>Endometrial Neoplasms - genetics</topic><topic>endometrium</topic><topic>energy</topic><topic>fatty acids</topic><topic>Female</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>homeostasis</topic><topic>Humans</topic><topic>Hypoglycemic Agents - pharmacology</topic><topic>Hypoglycemic Agents - therapeutic use</topic><topic>lipogenesis</topic><topic>Male</topic><topic>metformin</topic><topic>Metformin - pharmacology</topic><topic>Metformin - therapeutic use</topic><topic>neoplasm cells</topic><topic>obesity</topic><topic>Obesity - enzymology</topic><topic>Obesity - genetics</topic><topic>Ovarian cancer</topic><topic>Ovarian Neoplasms - drug therapy</topic><topic>Ovarian Neoplasms - enzymology</topic><topic>Ovarian Neoplasms - genetics</topic><topic>Prostate cancer</topic><topic>prostatic neoplasms</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - enzymology</topic><topic>Prostatic Neoplasms - genetics</topic><topic>risk factors</topic><topic>steroid hormones</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brown, Kristy A.</creatorcontrib><creatorcontrib>Samarajeewa, Nirukshi U.</creatorcontrib><creatorcontrib>Simpson, Evan R.</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Solid State and Superconductivity Abstracts</collection><collection>Technology Research Database</collection><collection>Advanced Technologies Database with Aerospace</collection><jtitle>Molecular and cellular endocrinology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Brown, Kristy A.</au><au>Samarajeewa, Nirukshi U.</au><au>Simpson, Evan R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Endocrine-related cancers and the role of AMPK</atitle><jtitle>Molecular and cellular endocrinology</jtitle><addtitle>Mol Cell Endocrinol</addtitle><date>2013-02-25</date><risdate>2013</risdate><volume>366</volume><issue>2</issue><spage>170</spage><epage>179</epage><pages>170-179</pages><issn>0303-7207</issn><eissn>1872-8057</eissn><abstract>► AMPK has an emerging role in the regulation of endocrine-related cancer cell growth. ► In most cases, AMPK is a negative regulator of cancer cell proliferation. ► AMPK inhibits cell growth by stimulating p53 and inhibiting mTOR. ► AMPK inhibits PGE2 and estrogen biosynthesis, key mediators of cell proliferation. ► AMPK-activating drugs decrease tumour cell growth and induce apoptosis.
AMP-activated protein kinase (AMPK) is a master regulator of energy homeostasis involved in the regulation of a number of physiological processes including β-oxidation of fatty acids, lipogenesis, protein and cholesterol synthesis, as well as cell cycle inhibition and apoptosis. Important changes to these processes are known to occur in cancer due to changes in AMPK activity within cancer cells and in the periphery. This review aims to present findings relating to the role and regulation of AMPK in endocrine-related cancers. Obesity is a known risk factor for many types of cancers and a number of endocrine factors, including adipokines and steroid hormones, are regulated by and regulate AMPK. A clear role for AMPK in breast cancer is evident from the already impressive body of work published to date. However, information pertaining to its role in prostate cancer is still contentious, and future work should unravel the intricacies behind its role to inhibit, in some cases, and stimulate cancer growth in others. This review also presents data relating to the role of AMPK in cancers of the endometrium, ovary and colon, and discusses the possible use of AMPK-activating drugs including metformin for the treatment of all endocrine-related cancers.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>22801104</pmid><doi>10.1016/j.mce.2012.06.016</doi><tpages>10</tpages></addata></record> |
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| subjects | adipokines AMP-activated protein kinase AMP-Activated Protein Kinases - genetics AMP-Activated Protein Kinases - metabolism AMPK animal ovaries apoptosis beta oxidation Biological Factors - pharmacology Breast Breast cancer breast neoplasms cell cycle Cell Transformation, Neoplastic cholesterol colon Colon cancer Colonic Neoplasms - drug therapy Colonic Neoplasms - enzymology Colonic Neoplasms - genetics Endocrine System - drug effects Endocrine System - enzymology Endocrine System - pathology Endometrial cancer Endometrial Neoplasms - drug therapy Endometrial Neoplasms - enzymology Endometrial Neoplasms - genetics endometrium energy fatty acids Female Gene Expression Regulation, Neoplastic homeostasis Humans Hypoglycemic Agents - pharmacology Hypoglycemic Agents - therapeutic use lipogenesis Male metformin Metformin - pharmacology Metformin - therapeutic use neoplasm cells obesity Obesity - enzymology Obesity - genetics Ovarian cancer Ovarian Neoplasms - drug therapy Ovarian Neoplasms - enzymology Ovarian Neoplasms - genetics Prostate cancer prostatic neoplasms Prostatic Neoplasms - drug therapy Prostatic Neoplasms - enzymology Prostatic Neoplasms - genetics risk factors steroid hormones |
| title | Endocrine-related cancers and the role of AMPK |
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