Targeting cytochrome P450-dependent cancer cell mitochondria: cancer associated CYPs and where to find them
While cytochrome P450 (CYP)-mediated biosynthesis of arachidonic acid (AA) epoxides promotes tumor growth by driving angiogenesis, cancer cell intrinsic functions of CYPs are less understood. CYP-derived AA epoxides, called epoxyeicosatrienoic acids (EETs), also promote the growth of tumor epithelia...
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| Veröffentlicht in: | Cancer and metastasis reviews 2018-09, Vol.37 (2-3), p.409-423 |
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| creator | Guo, Zhijun Johnson, Veronica Barrera, Jaime Porras, Mariel Hinojosa, Diego Hernández, Irwin McGarrah, Patrick Potter, David A. |
| description | While cytochrome P450 (CYP)-mediated biosynthesis of arachidonic acid (AA) epoxides promotes tumor growth by driving angiogenesis, cancer cell intrinsic functions of CYPs are less understood. CYP-derived AA epoxides, called epoxyeicosatrienoic acids (EETs), also promote the growth of tumor epithelia. In cancer cells, CYP AA epoxygenase enzymes are associated with STAT3 and mTOR signaling, but also localize in mitochondria, where they promote the electron transport chain (ETC). Recently, the diabetes drug metformin was found to inhibit CYP AA epoxygenase activity, allowing the design of more potent biguanides to target tumor growth. Biguanide inhibition of EET synthesis suppresses STAT3 and mTOR pathways, as well as the ETC
.
Convergence of biguanide activity and eicosanoid biology in cancer has shown a new pathway to attack cancer metabolism and provides hope for improved treatments that target this vulnerability. Inhibition of EET-mediated cancer metabolism and angiogenesis therefore provides a dual approach for targeted cancer therapeutics. |
| doi_str_mv | 10.1007/s10555-018-9749-6 |
| format | Article |
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.
Convergence of biguanide activity and eicosanoid biology in cancer has shown a new pathway to attack cancer metabolism and provides hope for improved treatments that target this vulnerability. Inhibition of EET-mediated cancer metabolism and angiogenesis therefore provides a dual approach for targeted cancer therapeutics.</description><identifier>ISSN: 0167-7659</identifier><identifier>EISSN: 1573-7233</identifier><identifier>DOI: 10.1007/s10555-018-9749-6</identifier><identifier>PMID: 30066055</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Angiogenesis ; Animals ; Antidiabetics ; Antineoplastic Agents - pharmacology ; Antineoplastic Agents - therapeutic use ; Arachidonic acid ; Autophagy - drug effects ; Autophagy - genetics ; Biomedical and Life Sciences ; Biomedicine ; Biosynthesis ; Breast cancer ; Cancer ; Cancer Research ; Clinical Trials as Topic ; Cytochrome ; Cytochrome P-450 ; Cytochrome P-450 Enzyme Inhibitors - pharmacology ; Cytochrome P-450 Enzyme Inhibitors - therapeutic use ; Cytochrome P-450 Enzyme System - genetics ; Cytochrome P-450 Enzyme System - metabolism ; Cytochrome P450 ; Diabetes mellitus ; Diabetes therapy ; Drug Discovery ; Drug Interactions ; Drug Repositioning ; Electron transport ; Electron transport chain ; Electron Transport Chain Complex Proteins - genetics ; Electron Transport Chain Complex Proteins - metabolism ; Epoxides ; Humans ; Inhibition ; Metabolism ; Metformin ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - genetics ; Mitochondria - metabolism ; Molecular Targeted Therapy ; Neoplasms - drug therapy ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - pathology ; Oncology ; Physiological aspects ; Signal Transduction - drug effects ; Stat3 protein ; TOR protein ; Treatment Outcome ; Tumor Microenvironment ; Unsaturated fatty acids</subject><ispartof>Cancer and metastasis reviews, 2018-09, Vol.37 (2-3), p.409-423</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2018</rights><rights>COPYRIGHT 2018 Springer</rights><rights>Cancer and Metastasis Reviews is a copyright of Springer, (2018). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-53d9a6dcbd2e183596dc82b4b2168d2f89f75a4191a4a4d17a734fdd153704b63</citedby><cites>FETCH-LOGICAL-c499t-53d9a6dcbd2e183596dc82b4b2168d2f89f75a4191a4a4d17a734fdd153704b63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10555-018-9749-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10555-018-9749-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30066055$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Zhijun</creatorcontrib><creatorcontrib>Johnson, Veronica</creatorcontrib><creatorcontrib>Barrera, Jaime</creatorcontrib><creatorcontrib>Porras, Mariel</creatorcontrib><creatorcontrib>Hinojosa, Diego</creatorcontrib><creatorcontrib>Hernández, Irwin</creatorcontrib><creatorcontrib>McGarrah, Patrick</creatorcontrib><creatorcontrib>Potter, David A.</creatorcontrib><title>Targeting cytochrome P450-dependent cancer cell mitochondria: cancer associated CYPs and where to find them</title><title>Cancer and metastasis reviews</title><addtitle>Cancer Metastasis Rev</addtitle><addtitle>Cancer Metastasis Rev</addtitle><description>While cytochrome P450 (CYP)-mediated biosynthesis of arachidonic acid (AA) epoxides promotes tumor growth by driving angiogenesis, cancer cell intrinsic functions of CYPs are less understood. CYP-derived AA epoxides, called epoxyeicosatrienoic acids (EETs), also promote the growth of tumor epithelia. In cancer cells, CYP AA epoxygenase enzymes are associated with STAT3 and mTOR signaling, but also localize in mitochondria, where they promote the electron transport chain (ETC). Recently, the diabetes drug metformin was found to inhibit CYP AA epoxygenase activity, allowing the design of more potent biguanides to target tumor growth. Biguanide inhibition of EET synthesis suppresses STAT3 and mTOR pathways, as well as the ETC
.
Convergence of biguanide activity and eicosanoid biology in cancer has shown a new pathway to attack cancer metabolism and provides hope for improved treatments that target this vulnerability. Inhibition of EET-mediated cancer metabolism and angiogenesis therefore provides a dual approach for targeted cancer therapeutics.</description><subject>Angiogenesis</subject><subject>Animals</subject><subject>Antidiabetics</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Antineoplastic Agents - therapeutic use</subject><subject>Arachidonic acid</subject><subject>Autophagy - drug effects</subject><subject>Autophagy - genetics</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Biosynthesis</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>Clinical Trials as Topic</subject><subject>Cytochrome</subject><subject>Cytochrome P-450</subject><subject>Cytochrome P-450 Enzyme Inhibitors - pharmacology</subject><subject>Cytochrome P-450 Enzyme Inhibitors - therapeutic use</subject><subject>Cytochrome P-450 Enzyme System - genetics</subject><subject>Cytochrome P-450 Enzyme System - 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CYP-derived AA epoxides, called epoxyeicosatrienoic acids (EETs), also promote the growth of tumor epithelia. In cancer cells, CYP AA epoxygenase enzymes are associated with STAT3 and mTOR signaling, but also localize in mitochondria, where they promote the electron transport chain (ETC). Recently, the diabetes drug metformin was found to inhibit CYP AA epoxygenase activity, allowing the design of more potent biguanides to target tumor growth. Biguanide inhibition of EET synthesis suppresses STAT3 and mTOR pathways, as well as the ETC
.
Convergence of biguanide activity and eicosanoid biology in cancer has shown a new pathway to attack cancer metabolism and provides hope for improved treatments that target this vulnerability. Inhibition of EET-mediated cancer metabolism and angiogenesis therefore provides a dual approach for targeted cancer therapeutics.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>30066055</pmid><doi>10.1007/s10555-018-9749-6</doi><tpages>15</tpages></addata></record> |
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| subjects | Angiogenesis Animals Antidiabetics Antineoplastic Agents - pharmacology Antineoplastic Agents - therapeutic use Arachidonic acid Autophagy - drug effects Autophagy - genetics Biomedical and Life Sciences Biomedicine Biosynthesis Breast cancer Cancer Cancer Research Clinical Trials as Topic Cytochrome Cytochrome P-450 Cytochrome P-450 Enzyme Inhibitors - pharmacology Cytochrome P-450 Enzyme Inhibitors - therapeutic use Cytochrome P-450 Enzyme System - genetics Cytochrome P-450 Enzyme System - metabolism Cytochrome P450 Diabetes mellitus Diabetes therapy Drug Discovery Drug Interactions Drug Repositioning Electron transport Electron transport chain Electron Transport Chain Complex Proteins - genetics Electron Transport Chain Complex Proteins - metabolism Epoxides Humans Inhibition Metabolism Metformin Mitochondria Mitochondria - drug effects Mitochondria - genetics Mitochondria - metabolism Molecular Targeted Therapy Neoplasms - drug therapy Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Oncology Physiological aspects Signal Transduction - drug effects Stat3 protein TOR protein Treatment Outcome Tumor Microenvironment Unsaturated fatty acids |
| title | Targeting cytochrome P450-dependent cancer cell mitochondria: cancer associated CYPs and where to find them |
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