Autotaxin protects MCF-7 breast cancer and MDA-MB-435 melanoma cells against Taxol-induced apoptosis
Autotaxin (ATX) promotes cancer cell survival, growth, migration, invasion and metastasis. ATX converts extracellular lysophosphatidylcholine (LPC) into lysophosphatidate (LPA). As these lipids have been reported to affect cell signaling through their own G-protein-coupled receptors, ATX could modif...
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| Veröffentlicht in: | Oncogene 2009-02, Vol.28 (7), p.1028-1039 |
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| creator | Samadi, N Gaetano, C Goping, I S Brindley, D N |
| description | Autotaxin (ATX) promotes cancer cell survival, growth, migration, invasion and metastasis. ATX converts extracellular lysophosphatidylcholine (LPC) into lysophosphatidate (LPA). As these lipids have been reported to affect cell signaling through their own G-protein-coupled receptors, ATX could modify the balance of this signaling. Also, ATX affects cell adhesion independently of its catalytic activity. We investigated the interactions of ATX, LPC and LPA on the apoptotic effects of Taxol, which is commonly used in breast cancer treatment. LPC had no significant effect on Taxol-induced apoptosis in MCF-7 breast cancer cells, which do not secrete significant ATX. Addition of incubation medium from MDA-MB-435 melanoma cells, which secrete ATX, or recombinat ATX enabled LPC to inhibit Taxol-induced apoptosis of MCF-7 cells. Inhibiting ATX activity blocked this protection against apoptosis. We conclude that LPC has no significant effect in protecting MCF-7 cells against Taxol treatment unless it is converted to LPA by ATX. LPA strongly antagonized Taxol-induced apoptosis through stimulating phosphatidylinositol 3-kinase and inhibiting ceramide formation. LPA also partially reversed the Taxol-induced arrest in the G2/M phase of the cell cycle. Our results support the hypothesis that therapeutic inhibition of ATX activity could improve the efficacy of Taxol as a chemotherapeutic agent for cancer treatment. |
| doi_str_mv | 10.1038/onc.2008.442 |
| format | Article |
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ATX converts extracellular lysophosphatidylcholine (LPC) into lysophosphatidate (LPA). As these lipids have been reported to affect cell signaling through their own G-protein-coupled receptors, ATX could modify the balance of this signaling. Also, ATX affects cell adhesion independently of its catalytic activity. We investigated the interactions of ATX, LPC and LPA on the apoptotic effects of Taxol, which is commonly used in breast cancer treatment. LPC had no significant effect on Taxol-induced apoptosis in MCF-7 breast cancer cells, which do not secrete significant ATX. Addition of incubation medium from MDA-MB-435 melanoma cells, which secrete ATX, or recombinat ATX enabled LPC to inhibit Taxol-induced apoptosis of MCF-7 cells. Inhibiting ATX activity blocked this protection against apoptosis. We conclude that LPC has no significant effect in protecting MCF-7 cells against Taxol treatment unless it is converted to LPA by ATX. LPA strongly antagonized Taxol-induced apoptosis through stimulating phosphatidylinositol 3-kinase and inhibiting ceramide formation. LPA also partially reversed the Taxol-induced arrest in the G2/M phase of the cell cycle. Our results support the hypothesis that therapeutic inhibition of ATX activity could improve the efficacy of Taxol as a chemotherapeutic agent for cancer treatment.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/onc.2008.442</identifier><identifier>PMID: 19079345</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>1-Phosphatidylinositol 3-kinase ; Apoptosis ; Apoptosis - drug effects ; Biological and medical sciences ; Blotting, Western ; Breast cancer ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Breast Neoplasms - prevention & control ; Cancer therapies ; Cell adhesion ; Cell adhesion & migration ; Cell Biology ; Cell cycle ; Cell Cycle - drug effects ; Cell Line, Tumor ; Cell migration ; Cell physiology ; Cell signaling ; Cell survival ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Ceramide ; Ceramides - metabolism ; Dermatology ; Dosage and administration ; Drug therapy ; Enzyme inhibitors ; Fundamental and applied biological sciences. Psychology ; G protein-coupled receptors ; Genetics ; Gynecology. Andrology. Obstetrics ; Health aspects ; Human Genetics ; Humans ; Internal Medicine ; Kinases ; Lipids ; Lysophosphatidylcholine ; Lysophosphatidylcholines - metabolism ; Lysophospholipids - physiology ; Mammary gland diseases ; Medical sciences ; Medicine ; Medicine & Public Health ; Melanoma ; Melanoma - metabolism ; Melanoma - pathology ; Melanoma - prevention & control ; Membrane Potential, Mitochondrial - drug effects ; Metastases ; Molecular and cellular biology ; Multienzyme Complexes - physiology ; Oncology ; original-article ; Paclitaxel ; Paclitaxel - pharmacology ; Phosphodiesterase I - physiology ; Phosphodiesterases ; Phosphoric Diester Hydrolases ; Physiological aspects ; Pyrophosphatases - physiology ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Tumors ; Tumors of the skin and soft tissue. Premalignant lesions</subject><ispartof>Oncogene, 2009-02, Vol.28 (7), p.1028-1039</ispartof><rights>Macmillan Publishers Limited 2009</rights><rights>2009 INIST-CNRS</rights><rights>COPYRIGHT 2009 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Feb 19, 2009</rights><rights>Macmillan Publishers Limited 2009.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c576t-dedf4e2ae2189e9a2be7451b01fae6d17808605dde65177ea337825b8a5cb9b43</citedby><cites>FETCH-LOGICAL-c576t-dedf4e2ae2189e9a2be7451b01fae6d17808605dde65177ea337825b8a5cb9b43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/onc.2008.442$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/onc.2008.442$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21262088$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19079345$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Samadi, N</creatorcontrib><creatorcontrib>Gaetano, C</creatorcontrib><creatorcontrib>Goping, I S</creatorcontrib><creatorcontrib>Brindley, D N</creatorcontrib><title>Autotaxin protects MCF-7 breast cancer and MDA-MB-435 melanoma cells against Taxol-induced apoptosis</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Autotaxin (ATX) promotes cancer cell survival, growth, migration, invasion and metastasis. ATX converts extracellular lysophosphatidylcholine (LPC) into lysophosphatidate (LPA). As these lipids have been reported to affect cell signaling through their own G-protein-coupled receptors, ATX could modify the balance of this signaling. Also, ATX affects cell adhesion independently of its catalytic activity. We investigated the interactions of ATX, LPC and LPA on the apoptotic effects of Taxol, which is commonly used in breast cancer treatment. LPC had no significant effect on Taxol-induced apoptosis in MCF-7 breast cancer cells, which do not secrete significant ATX. Addition of incubation medium from MDA-MB-435 melanoma cells, which secrete ATX, or recombinat ATX enabled LPC to inhibit Taxol-induced apoptosis of MCF-7 cells. Inhibiting ATX activity blocked this protection against apoptosis. We conclude that LPC has no significant effect in protecting MCF-7 cells against Taxol treatment unless it is converted to LPA by ATX. LPA strongly antagonized Taxol-induced apoptosis through stimulating phosphatidylinositol 3-kinase and inhibiting ceramide formation. LPA also partially reversed the Taxol-induced arrest in the G2/M phase of the cell cycle. Our results support the hypothesis that therapeutic inhibition of ATX activity could improve the efficacy of Taxol as a chemotherapeutic agent for cancer treatment.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Breast Neoplasms - prevention & control</subject><subject>Cancer therapies</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell Biology</subject><subject>Cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell physiology</subject><subject>Cell signaling</subject><subject>Cell survival</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Ceramide</subject><subject>Ceramides - metabolism</subject><subject>Dermatology</subject><subject>Dosage and administration</subject><subject>Drug therapy</subject><subject>Enzyme inhibitors</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>G protein-coupled receptors</subject><subject>Genetics</subject><subject>Gynecology. Andrology. Obstetrics</subject><subject>Health aspects</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Kinases</subject><subject>Lipids</subject><subject>Lysophosphatidylcholine</subject><subject>Lysophosphatidylcholines - metabolism</subject><subject>Lysophospholipids - physiology</subject><subject>Mammary gland diseases</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Melanoma</subject><subject>Melanoma - metabolism</subject><subject>Melanoma - pathology</subject><subject>Melanoma - prevention & control</subject><subject>Membrane Potential, Mitochondrial - drug effects</subject><subject>Metastases</subject><subject>Molecular and cellular biology</subject><subject>Multienzyme Complexes - physiology</subject><subject>Oncology</subject><subject>original-article</subject><subject>Paclitaxel</subject><subject>Paclitaxel - pharmacology</subject><subject>Phosphodiesterase I - physiology</subject><subject>Phosphodiesterases</subject><subject>Phosphoric Diester Hydrolases</subject><subject>Physiological aspects</subject><subject>Pyrophosphatases - physiology</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Tumors</subject><subject>Tumors of the skin and soft tissue. Premalignant lesions</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFktGP1CAQxhuj8c7VN59N40Wf7AoUCjyuq6cmt_HlfCZTmG56aWGFNjn_e2l240ZzxvAAgd98M8N8RfGSkjUltXofvF0zQtSac_aouKRcNpUQmj8uLokWpNKsZhfFs5TuCCFSE_a0uKA6n2ouLgu3macwwX3vy0MME9oplbvtdSXLNiKkqbTgLcYSvCt3HzfV7kPFa1GOOIAPI5QWhyGVsIfeZ_gW7sNQ9d7NFl0Jh3CYQurT8-JJB0PCF6d9VXy__nS7_VLdfPv8dbu5qayQzVQ5dB1HBsio0qiBtSi5oC2hHWDjqFRENUQ4h42gUiLUtVRMtAqEbXXL61Xx9qibW_kxY5rM2KelQvAY5mSaRnMm84f8D2SEE0rponj1F3gX5uhzE4Y1nNZKqjyEVfH6nxSTNc9VsrPUHgY0ve_CFMEuec2Gasl1TrdIrR-g8nI49jZ47Pp8_0fAu2OAjSGliJ05xH6E-NNQYhaDmGwQsxjEZINk_NWp1Lkd0Z3hkyMy8OYEQLIwdDHPv0-_OUZZw4hSmauOXMpPfo_x3PODiX8B2lDNtQ</recordid><startdate>20090219</startdate><enddate>20090219</enddate><creator>Samadi, N</creator><creator>Gaetano, C</creator><creator>Goping, I S</creator><creator>Brindley, D N</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>IQODW</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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20090219</creationdate><title>Autotaxin protects MCF-7 breast cancer and MDA-MB-435 melanoma cells against Taxol-induced apoptosis</title><author>Samadi, N ; Gaetano, C ; Goping, I S ; Brindley, D N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c576t-dedf4e2ae2189e9a2be7451b01fae6d17808605dde65177ea337825b8a5cb9b43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - metabolism</topic><topic>Breast Neoplasms - pathology</topic><topic>Breast Neoplasms - prevention & control</topic><topic>Cancer therapies</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell Biology</topic><topic>Cell cycle</topic><topic>Cell Cycle - drug effects</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell physiology</topic><topic>Cell signaling</topic><topic>Cell survival</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Ceramide</topic><topic>Ceramides - metabolism</topic><topic>Dermatology</topic><topic>Dosage and administration</topic><topic>Drug therapy</topic><topic>Enzyme inhibitors</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>G protein-coupled receptors</topic><topic>Genetics</topic><topic>Gynecology. Andrology. Obstetrics</topic><topic>Health aspects</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Kinases</topic><topic>Lipids</topic><topic>Lysophosphatidylcholine</topic><topic>Lysophosphatidylcholines - metabolism</topic><topic>Lysophospholipids - physiology</topic><topic>Mammary gland diseases</topic><topic>Medical sciences</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Melanoma</topic><topic>Melanoma - metabolism</topic><topic>Melanoma - pathology</topic><topic>Melanoma - prevention & control</topic><topic>Membrane Potential, Mitochondrial - drug effects</topic><topic>Metastases</topic><topic>Molecular and cellular biology</topic><topic>Multienzyme Complexes - physiology</topic><topic>Oncology</topic><topic>original-article</topic><topic>Paclitaxel</topic><topic>Paclitaxel - pharmacology</topic><topic>Phosphodiesterase I - physiology</topic><topic>Phosphodiesterases</topic><topic>Phosphoric Diester Hydrolases</topic><topic>Physiological aspects</topic><topic>Pyrophosphatases - physiology</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Tumors</topic><topic>Tumors of the skin and soft tissue. Premalignant lesions</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Samadi, N</creatorcontrib><creatorcontrib>Gaetano, C</creatorcontrib><creatorcontrib>Goping, I S</creatorcontrib><creatorcontrib>Brindley, D N</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Research Library</collection><collection>ProQuest Biological Science Journals</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Samadi, N</au><au>Gaetano, C</au><au>Goping, I S</au><au>Brindley, D N</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autotaxin protects MCF-7 breast cancer and MDA-MB-435 melanoma cells against Taxol-induced apoptosis</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2009-02-19</date><risdate>2009</risdate><volume>28</volume><issue>7</issue><spage>1028</spage><epage>1039</epage><pages>1028-1039</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Autotaxin (ATX) promotes cancer cell survival, growth, migration, invasion and metastasis. ATX converts extracellular lysophosphatidylcholine (LPC) into lysophosphatidate (LPA). As these lipids have been reported to affect cell signaling through their own G-protein-coupled receptors, ATX could modify the balance of this signaling. Also, ATX affects cell adhesion independently of its catalytic activity. We investigated the interactions of ATX, LPC and LPA on the apoptotic effects of Taxol, which is commonly used in breast cancer treatment. LPC had no significant effect on Taxol-induced apoptosis in MCF-7 breast cancer cells, which do not secrete significant ATX. Addition of incubation medium from MDA-MB-435 melanoma cells, which secrete ATX, or recombinat ATX enabled LPC to inhibit Taxol-induced apoptosis of MCF-7 cells. Inhibiting ATX activity blocked this protection against apoptosis. We conclude that LPC has no significant effect in protecting MCF-7 cells against Taxol treatment unless it is converted to LPA by ATX. LPA strongly antagonized Taxol-induced apoptosis through stimulating phosphatidylinositol 3-kinase and inhibiting ceramide formation. LPA also partially reversed the Taxol-induced arrest in the G2/M phase of the cell cycle. Our results support the hypothesis that therapeutic inhibition of ATX activity could improve the efficacy of Taxol as a chemotherapeutic agent for cancer treatment.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>19079345</pmid><doi>10.1038/onc.2008.442</doi><tpages>12</tpages></addata></record> |
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| issn | 0950-9232 1476-5594 |
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| source | MEDLINE; Springer Online Journals; Nature; EZB-FREE-00999 freely available EZB journals |
| subjects | 1-Phosphatidylinositol 3-kinase Apoptosis Apoptosis - drug effects Biological and medical sciences Blotting, Western Breast cancer Breast Neoplasms - metabolism Breast Neoplasms - pathology Breast Neoplasms - prevention & control Cancer therapies Cell adhesion Cell adhesion & migration Cell Biology Cell cycle Cell Cycle - drug effects Cell Line, Tumor Cell migration Cell physiology Cell signaling Cell survival Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Ceramide Ceramides - metabolism Dermatology Dosage and administration Drug therapy Enzyme inhibitors Fundamental and applied biological sciences. Psychology G protein-coupled receptors Genetics Gynecology. Andrology. Obstetrics Health aspects Human Genetics Humans Internal Medicine Kinases Lipids Lysophosphatidylcholine Lysophosphatidylcholines - metabolism Lysophospholipids - physiology Mammary gland diseases Medical sciences Medicine Medicine & Public Health Melanoma Melanoma - metabolism Melanoma - pathology Melanoma - prevention & control Membrane Potential, Mitochondrial - drug effects Metastases Molecular and cellular biology Multienzyme Complexes - physiology Oncology original-article Paclitaxel Paclitaxel - pharmacology Phosphodiesterase I - physiology Phosphodiesterases Phosphoric Diester Hydrolases Physiological aspects Pyrophosphatases - physiology Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics RNA, Messenger - metabolism Tumors Tumors of the skin and soft tissue. Premalignant lesions |
| title | Autotaxin protects MCF-7 breast cancer and MDA-MB-435 melanoma cells against Taxol-induced apoptosis |
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