VLDL and LDL, but not HDL, promote breast cancer cell proliferation, metastasis and angiogenesis
Abstract Abnormal lipoprotein profiles are associated with breast cancer progression. However, the mechanisms linking abnormal lipoprotein levels to breast cancer progression, especially metastasis, remain unclear. Herein, we found that L1 and L5 subfractions of LDL and VLDL, but not HDL, enhanced b...
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| Veröffentlicht in: | Cancer letters 2017-03, Vol.388, p.130-138 |
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| creator | Lu, Chun-Wun Lo, Yi-Hsuan Chen, Chu-Huang Lin, Ching-Yi Tsai, Chun-Hao Chen, Po-Jung Yang, Yi-Fang Wang, Chie-Hong Tan, Chun-Hsiang Hou, Ming-Feng Yuan, Shyng-Shiou F |
| description | Abstract Abnormal lipoprotein profiles are associated with breast cancer progression. However, the mechanisms linking abnormal lipoprotein levels to breast cancer progression, especially metastasis, remain unclear. Herein, we found that L1 and L5 subfractions of LDL and VLDL, but not HDL, enhanced breast cancer cell viability. L1, L5, and VLDL also increased the in vitro tumorigenesis of breast cancer cells in anchorage-independent soft agar assay. In addition, L1, L5, and VLDL, but not HDL, increased the levels of mesenchymal markers Slug, Vimentin, and β-Catenin, and promoted breast cancer cell migration and invasion. L1, L5, and VLDL increased Akt Ser473 phosphorylation and promoted cell migration, which were reversed by the PI3K/Akt inhibitor wortmannin. Further in vitro angiogenesis assay and cytokine array analysis demonstrated that L1, L5, and VLDL enhanced secretion of angiogenic factors in breast cancer cells and promoted angiogenic activity. However, only VLDL reduced anchorage-dependent cell death and promoted lung metastasis in nude mice. In summary, our data suggest that L1, L5, and especially VLDL promote breast cancer progression and metastasis through Akt-induced EMT and angiogenesis, and provide a novel mechanism of how dyslipoproteinemia promotes breast cancer progression. |
| doi_str_mv | 10.1016/j.canlet.2016.11.033 |
| format | Article |
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However, the mechanisms linking abnormal lipoprotein levels to breast cancer progression, especially metastasis, remain unclear. Herein, we found that L1 and L5 subfractions of LDL and VLDL, but not HDL, enhanced breast cancer cell viability. L1, L5, and VLDL also increased the in vitro tumorigenesis of breast cancer cells in anchorage-independent soft agar assay. In addition, L1, L5, and VLDL, but not HDL, increased the levels of mesenchymal markers Slug, Vimentin, and β-Catenin, and promoted breast cancer cell migration and invasion. L1, L5, and VLDL increased Akt Ser473 phosphorylation and promoted cell migration, which were reversed by the PI3K/Akt inhibitor wortmannin. Further in vitro angiogenesis assay and cytokine array analysis demonstrated that L1, L5, and VLDL enhanced secretion of angiogenic factors in breast cancer cells and promoted angiogenic activity. However, only VLDL reduced anchorage-dependent cell death and promoted lung metastasis in nude mice. In summary, our data suggest that L1, L5, and especially VLDL promote breast cancer progression and metastasis through Akt-induced EMT and angiogenesis, and provide a novel mechanism of how dyslipoproteinemia promotes breast cancer progression.</description><identifier>ISSN: 0304-3835</identifier><identifier>EISSN: 1872-7980</identifier><identifier>DOI: 10.1016/j.canlet.2016.11.033</identifier><identifier>PMID: 27940127</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Angiogenesis ; Animals ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - pathology ; Cancer therapies ; Cell growth ; Cell Line, Tumor ; Cell Proliferation ; Cholesterol ; Chromatography ; Female ; Hematology, Oncology and Palliative Medicine ; Humans ; Industrialized nations ; LDL ; Lipids ; Lipoprotein ; Lipoproteins, HDL - metabolism ; Lipoproteins, LDL - metabolism ; Lipoproteins, VLDL - metabolism ; Low density lipoprotein ; Metastasis ; Mice ; Mice, Inbred BALB C ; Neoplasm Metastasis ; Neovascularization, Pathologic ; Obesity ; Software ; Studies ; VLDL</subject><ispartof>Cancer letters, 2017-03, Vol.388, p.130-138</ispartof><rights>Elsevier Ireland Ltd</rights><rights>2016 Elsevier Ireland Ltd</rights><rights>Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.</rights><rights>Copyright Elsevier Limited Mar 1, 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-76f556cfda4ed7180d994e7e60f12da7d7b60e54485dc3cb8ac5b206dc2c7d953</citedby><cites>FETCH-LOGICAL-c478t-76f556cfda4ed7180d994e7e60f12da7d7b60e54485dc3cb8ac5b206dc2c7d953</cites><orcidid>0000-0003-2564-1341 ; 0000-0003-0774-5323</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.canlet.2016.11.033$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27911,27912,45982</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27940127$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Chun-Wun</creatorcontrib><creatorcontrib>Lo, Yi-Hsuan</creatorcontrib><creatorcontrib>Chen, Chu-Huang</creatorcontrib><creatorcontrib>Lin, Ching-Yi</creatorcontrib><creatorcontrib>Tsai, Chun-Hao</creatorcontrib><creatorcontrib>Chen, Po-Jung</creatorcontrib><creatorcontrib>Yang, Yi-Fang</creatorcontrib><creatorcontrib>Wang, Chie-Hong</creatorcontrib><creatorcontrib>Tan, Chun-Hsiang</creatorcontrib><creatorcontrib>Hou, Ming-Feng</creatorcontrib><creatorcontrib>Yuan, Shyng-Shiou F</creatorcontrib><title>VLDL and LDL, but not HDL, promote breast cancer cell proliferation, metastasis and angiogenesis</title><title>Cancer letters</title><addtitle>Cancer Lett</addtitle><description>Abstract Abnormal lipoprotein profiles are associated with breast cancer progression. However, the mechanisms linking abnormal lipoprotein levels to breast cancer progression, especially metastasis, remain unclear. Herein, we found that L1 and L5 subfractions of LDL and VLDL, but not HDL, enhanced breast cancer cell viability. L1, L5, and VLDL also increased the in vitro tumorigenesis of breast cancer cells in anchorage-independent soft agar assay. In addition, L1, L5, and VLDL, but not HDL, increased the levels of mesenchymal markers Slug, Vimentin, and β-Catenin, and promoted breast cancer cell migration and invasion. L1, L5, and VLDL increased Akt Ser473 phosphorylation and promoted cell migration, which were reversed by the PI3K/Akt inhibitor wortmannin. Further in vitro angiogenesis assay and cytokine array analysis demonstrated that L1, L5, and VLDL enhanced secretion of angiogenic factors in breast cancer cells and promoted angiogenic activity. However, only VLDL reduced anchorage-dependent cell death and promoted lung metastasis in nude mice. In summary, our data suggest that L1, L5, and especially VLDL promote breast cancer progression and metastasis through Akt-induced EMT and angiogenesis, and provide a novel mechanism of how dyslipoproteinemia promotes breast cancer progression.</description><subject>Angiogenesis</subject><subject>Animals</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - pathology</subject><subject>Cancer therapies</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cholesterol</subject><subject>Chromatography</subject><subject>Female</subject><subject>Hematology, Oncology and Palliative Medicine</subject><subject>Humans</subject><subject>Industrialized nations</subject><subject>LDL</subject><subject>Lipids</subject><subject>Lipoprotein</subject><subject>Lipoproteins, HDL - metabolism</subject><subject>Lipoproteins, LDL - metabolism</subject><subject>Lipoproteins, VLDL - metabolism</subject><subject>Low density lipoprotein</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Neoplasm Metastasis</subject><subject>Neovascularization, Pathologic</subject><subject>Obesity</subject><subject>Software</subject><subject>Studies</subject><subject>VLDL</subject><issn>0304-3835</issn><issn>1872-7980</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkklv1TAQxy0Eoo_CN0AoEhcOTRhvsXNBqspSpCdxYLkax55UfmQptoPUb4_DKyD1AqfR2L9Z_0PIUwoNBdq-PDTOziPmhhWvobQBzu-RHdWK1arTcJ_sgIOouebyhDxK6QAAUij5kJww1QmgTO3I1y_71_vKzr4q9qzq11zNS64uN-c6LtOSseoj2pSrUs5hrByO4_Y1hgGjzWGZz6oJcyFsCulXKjtfheUKZywPj8mDwY4Jn9zaU_L57ZtPF5f1_sO79xfn-9oJpXOt2kHK1g3eCvSKavBdJ1BhCwNl3iqv-hZQCqGld9z12jrZM2i9Y075TvJT8uKYt7T2fcWUzRTS1qudcVmT2faiRcd09x-opEwz0bUFfX4HPSxrnMsghWpLi0rDVlscKReXlCIO5jqGycYbQ8FsYpmDOYplNrEMpaaIVcKe3SZf-wn9n6Df6hTg1RHAsrgfAaNJLmBRwYeILhu_hH9VuJvAjWEOzo7f8AbT31lMYgbMx-1gtnuhLQfFBfCf0be6YA</recordid><startdate>20170301</startdate><enddate>20170301</enddate><creator>Lu, Chun-Wun</creator><creator>Lo, Yi-Hsuan</creator><creator>Chen, Chu-Huang</creator><creator>Lin, Ching-Yi</creator><creator>Tsai, Chun-Hao</creator><creator>Chen, Po-Jung</creator><creator>Yang, Yi-Fang</creator><creator>Wang, Chie-Hong</creator><creator>Tan, Chun-Hsiang</creator><creator>Hou, Ming-Feng</creator><creator>Yuan, Shyng-Shiou F</creator><general>Elsevier B.V</general><general>Elsevier Limited</general><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>7TO</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-2564-1341</orcidid><orcidid>https://orcid.org/0000-0003-0774-5323</orcidid></search><sort><creationdate>20170301</creationdate><title>VLDL and LDL, but not HDL, promote breast cancer cell proliferation, metastasis and angiogenesis</title><author>Lu, Chun-Wun ; Lo, Yi-Hsuan ; Chen, Chu-Huang ; Lin, Ching-Yi ; Tsai, Chun-Hao ; Chen, Po-Jung ; Yang, Yi-Fang ; Wang, Chie-Hong ; Tan, Chun-Hsiang ; Hou, Ming-Feng ; Yuan, Shyng-Shiou F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c478t-76f556cfda4ed7180d994e7e60f12da7d7b60e54485dc3cb8ac5b206dc2c7d953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Angiogenesis</topic><topic>Animals</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - pathology</topic><topic>Cancer therapies</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cholesterol</topic><topic>Chromatography</topic><topic>Female</topic><topic>Hematology, Oncology and Palliative Medicine</topic><topic>Humans</topic><topic>Industrialized nations</topic><topic>LDL</topic><topic>Lipids</topic><topic>Lipoprotein</topic><topic>Lipoproteins, HDL - metabolism</topic><topic>Lipoproteins, LDL - metabolism</topic><topic>Lipoproteins, VLDL - metabolism</topic><topic>Low density lipoprotein</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Neoplasm Metastasis</topic><topic>Neovascularization, Pathologic</topic><topic>Obesity</topic><topic>Software</topic><topic>Studies</topic><topic>VLDL</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lu, Chun-Wun</creatorcontrib><creatorcontrib>Lo, Yi-Hsuan</creatorcontrib><creatorcontrib>Chen, Chu-Huang</creatorcontrib><creatorcontrib>Lin, Ching-Yi</creatorcontrib><creatorcontrib>Tsai, Chun-Hao</creatorcontrib><creatorcontrib>Chen, Po-Jung</creatorcontrib><creatorcontrib>Yang, Yi-Fang</creatorcontrib><creatorcontrib>Wang, Chie-Hong</creatorcontrib><creatorcontrib>Tan, Chun-Hsiang</creatorcontrib><creatorcontrib>Hou, Ming-Feng</creatorcontrib><creatorcontrib>Yuan, Shyng-Shiou F</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Chun-Wun</au><au>Lo, Yi-Hsuan</au><au>Chen, Chu-Huang</au><au>Lin, Ching-Yi</au><au>Tsai, Chun-Hao</au><au>Chen, Po-Jung</au><au>Yang, Yi-Fang</au><au>Wang, Chie-Hong</au><au>Tan, Chun-Hsiang</au><au>Hou, Ming-Feng</au><au>Yuan, Shyng-Shiou F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>VLDL and LDL, but not HDL, promote breast cancer cell proliferation, metastasis and angiogenesis</atitle><jtitle>Cancer letters</jtitle><addtitle>Cancer Lett</addtitle><date>2017-03-01</date><risdate>2017</risdate><volume>388</volume><spage>130</spage><epage>138</epage><pages>130-138</pages><issn>0304-3835</issn><eissn>1872-7980</eissn><abstract>Abstract Abnormal lipoprotein profiles are associated with breast cancer progression. However, the mechanisms linking abnormal lipoprotein levels to breast cancer progression, especially metastasis, remain unclear. Herein, we found that L1 and L5 subfractions of LDL and VLDL, but not HDL, enhanced breast cancer cell viability. L1, L5, and VLDL also increased the in vitro tumorigenesis of breast cancer cells in anchorage-independent soft agar assay. In addition, L1, L5, and VLDL, but not HDL, increased the levels of mesenchymal markers Slug, Vimentin, and β-Catenin, and promoted breast cancer cell migration and invasion. L1, L5, and VLDL increased Akt Ser473 phosphorylation and promoted cell migration, which were reversed by the PI3K/Akt inhibitor wortmannin. Further in vitro angiogenesis assay and cytokine array analysis demonstrated that L1, L5, and VLDL enhanced secretion of angiogenic factors in breast cancer cells and promoted angiogenic activity. However, only VLDL reduced anchorage-dependent cell death and promoted lung metastasis in nude mice. In summary, our data suggest that L1, L5, and especially VLDL promote breast cancer progression and metastasis through Akt-induced EMT and angiogenesis, and provide a novel mechanism of how dyslipoproteinemia promotes breast cancer progression.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>27940127</pmid><doi>10.1016/j.canlet.2016.11.033</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-2564-1341</orcidid><orcidid>https://orcid.org/0000-0003-0774-5323</orcidid></addata></record> |
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| subjects | Angiogenesis Animals Breast cancer Breast Neoplasms - genetics Breast Neoplasms - pathology Cancer therapies Cell growth Cell Line, Tumor Cell Proliferation Cholesterol Chromatography Female Hematology, Oncology and Palliative Medicine Humans Industrialized nations LDL Lipids Lipoprotein Lipoproteins, HDL - metabolism Lipoproteins, LDL - metabolism Lipoproteins, VLDL - metabolism Low density lipoprotein Metastasis Mice Mice, Inbred BALB C Neoplasm Metastasis Neovascularization, Pathologic Obesity Software Studies VLDL |
| title | VLDL and LDL, but not HDL, promote breast cancer cell proliferation, metastasis and angiogenesis |
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