RE:RE:RE:RE:RE:RE:Not sure what's new? That's exactly what poster #4335 hints at:
Sortilin receptor is associated with VM and it is needed for VM formation in TNBC (MDA-MB-231) and ovarian (ES-2) cancer cells.
Both doxorubicin (TH1904) and docetaxel (TH1902) conjugates strongly inhibit formation of VM 3D-tubular structures indicating that these new
chemical entities have different anticancer properties than their parent drugs.
Docetaxel and doxorubicin affects the VM structure only at concentrations higher than the ones tolerated in patients
Overall, results indicate that sortilin regulates VM, and that exploiting sortilin’s functions to increase drug internalization may complement current
treatments in patients with TNBC or ovarian cancer and may bypass some resistance mechanism of cancer cells.
jfm1330 wrote: If it's the case it would change the whole ball game, because if so, you would have a double anti-cancer effect, one from the introduction of a cytotoxic drug into the cancer cell, but also another effect from the peptide itself inhibiting the VM process of the tumor by interacting with the Sortilin receptors on the membrane of the cells. So it would be a double effect. Is it really the case or the IR person was just overoptimistic.
SPCEO1 wrote: - Our new data demonstrate that sortilin is a key player in the formation of VM structure - silencing sortilin stops the formation of the VM structure for both ovarian and TNBC cancer cells.