| http://purl.uniprot.org/citations/29555978 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/29555978 | http://www.w3.org/2000/01/rdf-schema#comment | "Semaphorin 4C (Sema4C) expression in human breast cancers correlates with poor disease outcome. Surprisingly, upon knock-down of Sema4C or its receptor PlexinB2 in diverse mammary carcinoma cells (but not their normal counterparts), we observed dramatic growth inhibition associated with impairment of G2/M phase transition, cytokinesis defects and the onset of cell senescence. Mechanistically, we demonstrated a Sema4C/PlexinB2/LARG-dependent signaling cascade that is required to maintain critical RhoA-GTP levels in cancer cells. Interestingly, we also found that Sema4C upregulation in luminal-type breast cancer cells drives a dramatic phenotypic change, with disassembly of polarity complexes, mitotic spindle misorientation, cell-cell dissociation and increased migration and invasiveness. We found that this signaling cascade is dependent on the PlexinB2 effectors ErbB2 and RhoA-dependent kinases. Moreover, Sema4C-overexpressing luminal breast cancer cells upregulated the transcription factors Snail, Slug and SOX-2, and formed estrogen-independent metastatic tumors in mice. In sum, our data indicate that Sema4C/PlexinB2 signaling is essential for the growth of breast carcinoma cells, featuring a novel potential therapeutic target. In addition, elevated Sema4C expression enables indolent luminal-type tumors to become resistant to estrogen deprivation, invasive and metastatic in vivo, which could account for its association with a subset of human breast cancers with poor prognosis."xsd:string |
| http://purl.uniprot.org/citations/29555978 | http://purl.org/dc/terms/identifier | "doi:10.1038/s41418-018-0097-4"xsd:string |
| http://purl.uniprot.org/citations/29555978 | http://purl.uniprot.org/core/author | "Lanzetti L."xsd:string |
| http://purl.uniprot.org/citations/29555978 | http://purl.uniprot.org/core/author | "Pupo E."xsd:string |
| http://purl.uniprot.org/citations/29555978 | http://purl.uniprot.org/core/author | "Tamagnone L."xsd:string |
| http://purl.uniprot.org/citations/29555978 | http://purl.uniprot.org/core/author | "Gurrapu S."xsd:string |
| http://purl.uniprot.org/citations/29555978 | http://purl.uniprot.org/core/author | "Franzolin G."xsd:string |
| http://purl.uniprot.org/citations/29555978 | http://purl.uniprot.org/core/date | "2018"xsd:gYear |
| http://purl.uniprot.org/citations/29555978 | http://purl.uniprot.org/core/name | "Cell Death Differ"xsd:string |
| http://purl.uniprot.org/citations/29555978 | http://purl.uniprot.org/core/pages | "1259-1275"xsd:string |
| http://purl.uniprot.org/citations/29555978 | http://purl.uniprot.org/core/title | "Sema4C/PlexinB2 signaling controls breast cancer cell growth, hormonal dependence and tumorigenic potential."xsd:string |
| http://purl.uniprot.org/citations/29555978 | http://purl.uniprot.org/core/volume | "25"xsd:string |
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