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| http://purl.uniprot.org/citations/28108260 | http://www.w3.org/2000/01/rdf-schema#comment | "About 40,000 American women die from metastatic breast cancer each year despite advancements in treatment. Approximately, 15% of breast cancers are triple-negative for estrogen receptor, progesterone receptor, and HER2. Triple-negative cancer is characterized by more aggressive, harder to treat with conventional approaches and having a greater possibility of recurrence. Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid signaling mediator has emerged as a key regulatory molecule in breast cancer progression. Therefore, we investigated whether cytosolic sphingosine kinase type 1 (SphK1) and nuclear sphingosine kinase type 2 (SphK2), the enzymes that make S1P are critical for growth and PI3K/AKT, ERK-MAP kinase mediated survival signaling of lung metastatic variant LM2-4 breast cancer cells, generated from the parental triple-negative MDA-MB-231 human breast cancer cell line. Similar with previous report, SphKs/S1P signaling is critical for the growth and survival of estrogen receptor positive MCF-7 human breast cancer cells, was used as our study control. MDA-MB-231 did not show a significant effect of SphKs/S1P signaling on AKT, ERK, and p38 pathways. In contrast, LM2-4 cells that gained lung metastatic phenotype from primary MDA-MB-231 cells show a significant effect of SphKs/S1P signaling requirement on cell growth, survival, and cell motility. PF-543, a selective potent inhibitor of SphK1, attenuated epidermal growth factor (EGF)-mediated cell growth and survival signaling through inhibition of AKT, ERK, and p38 MAP kinase pathways mainly in LM2-4 cells but not in parental MDA-MB-231 human breast cancer cells. Moreover, K-145, a selective inhibitor of SphK2, markedly attenuated EGF-mediated cell growth and survival of LM2-4 cells. We believe this study highlights the importance of SphKs/S1P signaling in metastatic triple-negative breast cancers and targeted therapies."xsd:string |
| http://purl.uniprot.org/citations/28108260 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.cellsig.2017.01.021"xsd:string |
| http://purl.uniprot.org/citations/28108260 | http://purl.uniprot.org/core/author | "Takabe K."xsd:string |
| http://purl.uniprot.org/citations/28108260 | http://purl.uniprot.org/core/author | "Hait N.C."xsd:string |
| http://purl.uniprot.org/citations/28108260 | http://purl.uniprot.org/core/author | "Maiti A."xsd:string |
| http://purl.uniprot.org/citations/28108260 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
| http://purl.uniprot.org/citations/28108260 | http://purl.uniprot.org/core/name | "Cell Signal"xsd:string |
| http://purl.uniprot.org/citations/28108260 | http://purl.uniprot.org/core/pages | "85-92"xsd:string |
| http://purl.uniprot.org/citations/28108260 | http://purl.uniprot.org/core/title | "Metastatic triple-negative breast cancer is dependent on SphKs/S1P signaling for growth and survival."xsd:string |
| http://purl.uniprot.org/citations/28108260 | http://purl.uniprot.org/core/volume | "32"xsd:string |
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