Triple Negative Breast Cancer Depends on Sphingosine Kinase 1 (SphK1)/Sphingosine-1-Phosphate (S1P)/Sphingosine 1-Phosphate Receptor 3 (S1PR3)/Notch Signaling for Metastasis
BACKGROUND Triple negative breast cancer (TNBC) has a more aggressive recurrence. Previous reports have demonstrated that sphingosine kinase 1 (SphK1) is a crucial regulator of breast cancer progression. However, the correlation of SphK1 with clinical prognosis has been poorly investigated. Thus, we...
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| description | BACKGROUND Triple negative breast cancer (TNBC) has a more aggressive recurrence. Previous reports have demonstrated that sphingosine kinase 1 (SphK1) is a crucial regulator of breast cancer progression. However, the correlation of SphK1 with clinical prognosis has been poorly investigated. Thus, we aimed to elaborate the role of SphK1 in TNBC metastasis. MATERIAL AND METHODS We first determined the level of SphK1 in breast cancer tissue samples and breast cancer cells. Furthermore, the expression of HER2 and phosphor-SphK1 (pSphK1) in human breast cancer tissue samples was determined by immunohistochemical analysis. Associations between SphK1 and clinical parameters of tumors were analyzed. The activity of SphK1 was measured by fluorescence analysis. Extracellular sphingosine-1-phosphate (S1P) was detected using an ELISA kit. Associations between SphK1 and metastasis potential were analyzed by Transwell assay. RESULTS Levels of SphK1 in TNBC patients were significantly higher than levels in other patients with other breast tumors. The expression of SphK1 was positively correlated with poor overall survival (OS) and progression-free survival (PFS), as well as poor response to 5-FU and doxorubicin. The depression of SphK1 thus could repress the Notch signaling pathway, reduce migration, and invasion of TNBC cells in vivo and in vitro. Furthermore, silencing of SphK1 by Ad-SPHK1-siRNA or SphK1 inhibitor PF543 sensitized TNBCs to 5-FU and doxorubicin. Our results also indicated that SphK1 inhibition could effectively counteracts tumors metastasis via Notch signaling pathways, indicating a potentially anti-tumor strategy in TNBC. CONCLUSIONS We found that elevated levels of pSphK1 were positive correlation with high expression of S1P, which in turn promoted metastasis of TNBC through S1P/S1PR3/Notch signaling pathway. |
| doi_str_mv | 10.12659/msm.905833 |
| format | Article |
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Previous reports have demonstrated that sphingosine kinase 1 (SphK1) is a crucial regulator of breast cancer progression. However, the correlation of SphK1 with clinical prognosis has been poorly investigated. Thus, we aimed to elaborate the role of SphK1 in TNBC metastasis. MATERIAL AND METHODS We first determined the level of SphK1 in breast cancer tissue samples and breast cancer cells. Furthermore, the expression of HER2 and phosphor-SphK1 (pSphK1) in human breast cancer tissue samples was determined by immunohistochemical analysis. Associations between SphK1 and clinical parameters of tumors were analyzed. The activity of SphK1 was measured by fluorescence analysis. Extracellular sphingosine-1-phosphate (S1P) was detected using an ELISA kit. Associations between SphK1 and metastasis potential were analyzed by Transwell assay. RESULTS Levels of SphK1 in TNBC patients were significantly higher than levels in other patients with other breast tumors. The expression of SphK1 was positively correlated with poor overall survival (OS) and progression-free survival (PFS), as well as poor response to 5-FU and doxorubicin. The depression of SphK1 thus could repress the Notch signaling pathway, reduce migration, and invasion of TNBC cells in vivo and in vitro. Furthermore, silencing of SphK1 by Ad-SPHK1-siRNA or SphK1 inhibitor PF543 sensitized TNBCs to 5-FU and doxorubicin. Our results also indicated that SphK1 inhibition could effectively counteracts tumors metastasis via Notch signaling pathways, indicating a potentially anti-tumor strategy in TNBC. CONCLUSIONS We found that elevated levels of pSphK1 were positive correlation with high expression of S1P, which in turn promoted metastasis of TNBC through S1P/S1PR3/Notch signaling pathway.</description><identifier>ISSN: 1643-3750</identifier><identifier>ISSN: 1234-1010</identifier><identifier>EISSN: 1643-3750</identifier><identifier>DOI: 10.12659/msm.905833</identifier><identifier>PMID: 29605826</identifier><language>eng</language><publisher>United States: International Scientific Literature, Inc</publisher><subject>Animals ; Cell Line, Tumor ; Doxorubicin - pharmacology ; Drug Synergism ; Female ; Fluorouracil - pharmacology ; Heterografts ; Humans ; Lab/In Vitro Research ; Lysophospholipids - metabolism ; MCF-7 Cells ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Middle Aged ; Neoplasm Metastasis ; Neoplasm Recurrence, Local - enzymology ; Neoplasm Recurrence, Local - metabolism ; Neoplasm Recurrence, Local - pathology ; Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors ; Phosphotransferases (Alcohol Group Acceptor) - biosynthesis ; Phosphotransferases (Alcohol Group Acceptor) - metabolism ; Pyrrolidines - pharmacology ; Receptor, ErbB-2 - biosynthesis ; Receptor, ErbB-2 - genetics ; Receptors, Lysosphingolipid - metabolism ; Receptors, Notch - metabolism ; Signal Transduction ; Sphingosine - analogs & derivatives ; Sphingosine - metabolism ; Sulfones - pharmacology ; Triple Negative Breast Neoplasms - drug therapy ; Triple Negative Breast Neoplasms - genetics ; Triple Negative Breast Neoplasms - metabolism ; Triple Negative Breast Neoplasms - pathology ; Up-Regulation</subject><ispartof>Medical science monitor, 2018-04, Vol.24, p.1912-1923</ispartof><rights>Med Sci Monit, 2018 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c489t-f0338506d7ecbe8d80d796a73dd6cc4b8b80aaaf087806fed31ce2630899a4cc3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5894569/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5894569/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29605826$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Shushu</creatorcontrib><creatorcontrib>Liang, Yueyang</creatorcontrib><creatorcontrib>Chang, Wenxiao</creatorcontrib><creatorcontrib>Hu, Baoquan</creatorcontrib><creatorcontrib>Zhang, Yi</creatorcontrib><title>Triple Negative Breast Cancer Depends on Sphingosine Kinase 1 (SphK1)/Sphingosine-1-Phosphate (S1P)/Sphingosine 1-Phosphate Receptor 3 (S1PR3)/Notch Signaling for Metastasis</title><title>Medical science monitor</title><addtitle>Med Sci Monit</addtitle><description>BACKGROUND Triple negative breast cancer (TNBC) has a more aggressive recurrence. Previous reports have demonstrated that sphingosine kinase 1 (SphK1) is a crucial regulator of breast cancer progression. However, the correlation of SphK1 with clinical prognosis has been poorly investigated. Thus, we aimed to elaborate the role of SphK1 in TNBC metastasis. MATERIAL AND METHODS We first determined the level of SphK1 in breast cancer tissue samples and breast cancer cells. Furthermore, the expression of HER2 and phosphor-SphK1 (pSphK1) in human breast cancer tissue samples was determined by immunohistochemical analysis. Associations between SphK1 and clinical parameters of tumors were analyzed. The activity of SphK1 was measured by fluorescence analysis. Extracellular sphingosine-1-phosphate (S1P) was detected using an ELISA kit. Associations between SphK1 and metastasis potential were analyzed by Transwell assay. RESULTS Levels of SphK1 in TNBC patients were significantly higher than levels in other patients with other breast tumors. The expression of SphK1 was positively correlated with poor overall survival (OS) and progression-free survival (PFS), as well as poor response to 5-FU and doxorubicin. The depression of SphK1 thus could repress the Notch signaling pathway, reduce migration, and invasion of TNBC cells in vivo and in vitro. Furthermore, silencing of SphK1 by Ad-SPHK1-siRNA or SphK1 inhibitor PF543 sensitized TNBCs to 5-FU and doxorubicin. Our results also indicated that SphK1 inhibition could effectively counteracts tumors metastasis via Notch signaling pathways, indicating a potentially anti-tumor strategy in TNBC. CONCLUSIONS We found that elevated levels of pSphK1 were positive correlation with high expression of S1P, which in turn promoted metastasis of TNBC through S1P/S1PR3/Notch signaling pathway.</description><subject>Animals</subject><subject>Cell Line, Tumor</subject><subject>Doxorubicin - pharmacology</subject><subject>Drug Synergism</subject><subject>Female</subject><subject>Fluorouracil - pharmacology</subject><subject>Heterografts</subject><subject>Humans</subject><subject>Lab/In Vitro Research</subject><subject>Lysophospholipids - metabolism</subject><subject>MCF-7 Cells</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>Mice, SCID</subject><subject>Middle Aged</subject><subject>Neoplasm Metastasis</subject><subject>Neoplasm Recurrence, Local - enzymology</subject><subject>Neoplasm Recurrence, Local - metabolism</subject><subject>Neoplasm Recurrence, Local - pathology</subject><subject>Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors</subject><subject>Phosphotransferases (Alcohol Group Acceptor) - biosynthesis</subject><subject>Phosphotransferases (Alcohol Group Acceptor) - metabolism</subject><subject>Pyrrolidines - pharmacology</subject><subject>Receptor, ErbB-2 - biosynthesis</subject><subject>Receptor, ErbB-2 - genetics</subject><subject>Receptors, Lysosphingolipid - metabolism</subject><subject>Receptors, Notch - metabolism</subject><subject>Signal Transduction</subject><subject>Sphingosine - analogs & derivatives</subject><subject>Sphingosine - metabolism</subject><subject>Sulfones - pharmacology</subject><subject>Triple Negative Breast Neoplasms - drug therapy</subject><subject>Triple Negative Breast Neoplasms - genetics</subject><subject>Triple Negative Breast Neoplasms - metabolism</subject><subject>Triple Negative Breast Neoplasms - pathology</subject><subject>Up-Regulation</subject><issn>1643-3750</issn><issn>1234-1010</issn><issn>1643-3750</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc1u3CAURlHVqvnrqvuKZaLKGTAGw6ZSOm3aKJk0yqRrxODrMZUNLngi5aH6jkGZNJqsLuIcPq70IfSRklNaCq5mQxpOFeGSsTdon4qKFazm5O3OeQ8dpPSHkFIKwt-jvVLlKUuxj_7dRTf2gK9hbSZ3D_hrBJMmPDfeQsTfYATfJBw8Xo6d8-uQnAd86bxJgCk-zreX9GS2Awta3HQhjZ2ZIHN684riXXoLFsYpRMyexFt2MrsOk-3w0q296fMb3Ga6gCmvZJJLR-hda_oEH57nIfp9_v1u_rO4-vXjYn52VdhKqqloCWOSE9HUYFcgG0maWglTs6YR1lYruZLEGNMSWUsiWmgYtVAKRqRSprKWHaIv29xxsxqgseCnaHo9RjeY-KCDcfo18a7T63CvuVQVFyoHHD8HxPB3A2nSg0sW-t54CJukS1ISKTmndVY_b1UbQ0oR2pdvKNFPBevFcqG3BWf70-5mL-7_Rtkj8-KiwQ</recordid><startdate>20180401</startdate><enddate>20180401</enddate><creator>Wang, Shushu</creator><creator>Liang, Yueyang</creator><creator>Chang, Wenxiao</creator><creator>Hu, Baoquan</creator><creator>Zhang, Yi</creator><general>International Scientific Literature, Inc</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180401</creationdate><title>Triple Negative Breast Cancer Depends on Sphingosine Kinase 1 (SphK1)/Sphingosine-1-Phosphate (S1P)/Sphingosine 1-Phosphate Receptor 3 (S1PR3)/Notch Signaling for Metastasis</title><author>Wang, Shushu ; Liang, Yueyang ; Chang, Wenxiao ; Hu, Baoquan ; Zhang, Yi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c489t-f0338506d7ecbe8d80d796a73dd6cc4b8b80aaaf087806fed31ce2630899a4cc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Cell Line, Tumor</topic><topic>Doxorubicin - pharmacology</topic><topic>Drug Synergism</topic><topic>Female</topic><topic>Fluorouracil - pharmacology</topic><topic>Heterografts</topic><topic>Humans</topic><topic>Lab/In Vitro Research</topic><topic>Lysophospholipids - metabolism</topic><topic>MCF-7 Cells</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>Mice, SCID</topic><topic>Middle Aged</topic><topic>Neoplasm Metastasis</topic><topic>Neoplasm Recurrence, Local - enzymology</topic><topic>Neoplasm Recurrence, Local - metabolism</topic><topic>Neoplasm Recurrence, Local - pathology</topic><topic>Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors</topic><topic>Phosphotransferases (Alcohol Group Acceptor) - biosynthesis</topic><topic>Phosphotransferases (Alcohol Group Acceptor) - metabolism</topic><topic>Pyrrolidines - pharmacology</topic><topic>Receptor, ErbB-2 - biosynthesis</topic><topic>Receptor, ErbB-2 - genetics</topic><topic>Receptors, Lysosphingolipid - metabolism</topic><topic>Receptors, Notch - metabolism</topic><topic>Signal Transduction</topic><topic>Sphingosine - analogs & derivatives</topic><topic>Sphingosine - metabolism</topic><topic>Sulfones - pharmacology</topic><topic>Triple Negative Breast Neoplasms - drug therapy</topic><topic>Triple Negative Breast Neoplasms - genetics</topic><topic>Triple Negative Breast Neoplasms - metabolism</topic><topic>Triple Negative Breast Neoplasms - pathology</topic><topic>Up-Regulation</topic><toplevel>online_resources</toplevel><creatorcontrib>Wang, Shushu</creatorcontrib><creatorcontrib>Liang, Yueyang</creatorcontrib><creatorcontrib>Chang, Wenxiao</creatorcontrib><creatorcontrib>Hu, Baoquan</creatorcontrib><creatorcontrib>Zhang, Yi</creatorcontrib><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>PubMed Central (Full Participant titles)</collection><jtitle>Medical science monitor</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Shushu</au><au>Liang, Yueyang</au><au>Chang, Wenxiao</au><au>Hu, Baoquan</au><au>Zhang, Yi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Triple Negative Breast Cancer Depends on Sphingosine Kinase 1 (SphK1)/Sphingosine-1-Phosphate (S1P)/Sphingosine 1-Phosphate Receptor 3 (S1PR3)/Notch Signaling for Metastasis</atitle><jtitle>Medical science monitor</jtitle><addtitle>Med Sci Monit</addtitle><date>2018-04-01</date><risdate>2018</risdate><volume>24</volume><spage>1912</spage><epage>1923</epage><pages>1912-1923</pages><issn>1643-3750</issn><issn>1234-1010</issn><eissn>1643-3750</eissn><abstract>BACKGROUND Triple negative breast cancer (TNBC) has a more aggressive recurrence. Previous reports have demonstrated that sphingosine kinase 1 (SphK1) is a crucial regulator of breast cancer progression. However, the correlation of SphK1 with clinical prognosis has been poorly investigated. Thus, we aimed to elaborate the role of SphK1 in TNBC metastasis. MATERIAL AND METHODS We first determined the level of SphK1 in breast cancer tissue samples and breast cancer cells. Furthermore, the expression of HER2 and phosphor-SphK1 (pSphK1) in human breast cancer tissue samples was determined by immunohistochemical analysis. Associations between SphK1 and clinical parameters of tumors were analyzed. The activity of SphK1 was measured by fluorescence analysis. Extracellular sphingosine-1-phosphate (S1P) was detected using an ELISA kit. Associations between SphK1 and metastasis potential were analyzed by Transwell assay. RESULTS Levels of SphK1 in TNBC patients were significantly higher than levels in other patients with other breast tumors. The expression of SphK1 was positively correlated with poor overall survival (OS) and progression-free survival (PFS), as well as poor response to 5-FU and doxorubicin. The depression of SphK1 thus could repress the Notch signaling pathway, reduce migration, and invasion of TNBC cells in vivo and in vitro. Furthermore, silencing of SphK1 by Ad-SPHK1-siRNA or SphK1 inhibitor PF543 sensitized TNBCs to 5-FU and doxorubicin. Our results also indicated that SphK1 inhibition could effectively counteracts tumors metastasis via Notch signaling pathways, indicating a potentially anti-tumor strategy in TNBC. CONCLUSIONS We found that elevated levels of pSphK1 were positive correlation with high expression of S1P, which in turn promoted metastasis of TNBC through S1P/S1PR3/Notch signaling pathway.</abstract><cop>United States</cop><pub>International Scientific Literature, Inc</pub><pmid>29605826</pmid><doi>10.12659/msm.905833</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Cell Line, Tumor Doxorubicin - pharmacology Drug Synergism Female Fluorouracil - pharmacology Heterografts Humans Lab/In Vitro Research Lysophospholipids - metabolism MCF-7 Cells Mice Mice, Inbred NOD Mice, SCID Middle Aged Neoplasm Metastasis Neoplasm Recurrence, Local - enzymology Neoplasm Recurrence, Local - metabolism Neoplasm Recurrence, Local - pathology Phosphotransferases (Alcohol Group Acceptor) - antagonists & inhibitors Phosphotransferases (Alcohol Group Acceptor) - biosynthesis Phosphotransferases (Alcohol Group Acceptor) - metabolism Pyrrolidines - pharmacology Receptor, ErbB-2 - biosynthesis Receptor, ErbB-2 - genetics Receptors, Lysosphingolipid - metabolism Receptors, Notch - metabolism Signal Transduction Sphingosine - analogs & derivatives Sphingosine - metabolism Sulfones - pharmacology Triple Negative Breast Neoplasms - drug therapy Triple Negative Breast Neoplasms - genetics Triple Negative Breast Neoplasms - metabolism Triple Negative Breast Neoplasms - pathology Up-Regulation |
| title | Triple Negative Breast Cancer Depends on Sphingosine Kinase 1 (SphK1)/Sphingosine-1-Phosphate (S1P)/Sphingosine 1-Phosphate Receptor 3 (S1PR3)/Notch Signaling for Metastasis |
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