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CCR9-CCL25 interactions promote cisplatin resistance in breast cancer cell through Akt activation in a PI3K-dependent and FAK-independent fashion
BACKGROUND: Chemotherapy heavily relies on apoptosis to kill breast cancer (BrCa) cells. Many breast tumors respond to chemotherapy, but cells that survive this initial response gain resistance to subsequent treatments. This leads to aggressive cell variants with an enhanced ability to migrate, inva...
Αποθηκεύτηκε σε:
| Κύριοι συγγραφείς: | , , , , , |
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| Μορφή: | Artigo |
| Γλώσσα: | Inglês |
| Έκδοση: |
BioMed Central
2011
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| Θέματα: | |
| Διαθέσιμο Online: | https://ncbi.nlm.nih.gov/pmc/articles/PMC3110128/ https://ncbi.nlm.nih.gov/pubmed/21539750 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1186/1477-7819-9-46 |
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