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. 2020 Jul 27;12(8):2063. doi: 10.3390/cancers12082063

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Hypothesized mechanism of PDGF-BB/PDGFR-β communication between ovarian CSC and CA-MSC with Hedgehog downstream signaling. PDGF-BB is secreted by CA-MSC and binds to PDGFR-β receptor, which are expressed by ovarian CSC. Binding between PDGFR-β and PDGF-BB directly causes an increase in CSC markers, platinum resistance and EMT markers in ovarian CSC. Additionally, PDGF-BB binding is shown to be upstream of Hedgehog as it leads to an increase in Hedgehog ligand secretion. Hedgehog is known to also cause an increase in CSC markers, platinum resistance and EMT markers in ovarian CSC through PTCH, SMO and GLI1. Treatment with sunitinib, a PDGFR-β inhibitor, leads to decrease in the CSC and EMT marker expression, and increase in sensitivity to platinum. These phenotypes are direct result of inhibition of the PDGF-BB/PDGFR-β and Hedgehog signaling pathways.