Cancer stem cells act as highly-adaptable tumor-initiating cells, which colonize tumor growth in secondary metastatic sites. CSCs may arise naturally from dedifferentiated adult cells, yet, in tumors, the epithelial-to-mesenchymal transition (EMT) has been shown to yield CSCs. It may be through this de-differentiation transition that cancer cells gain their stemness, making EMT an attractive process to target in the attempts to eliminate CSCs. Our work seeks to understand the EMT-associated mechanisms responsible for sensitization to a fungus-derived natural product, driving further insights into the effect of small-molecule inhibition of EMT/CSC-driven phenotypes in reducing chemoresistance in TNBC metastases.

Funded by CPRIT #RP180771