Abstract
Background: Cancer Stem Cells (CSCs) are highly tumourigenic in the undifferentiated state only. As such, forced differentiation of CSCs is a potential clinical CSC-targeting mechanism. Historically, treatment with Retinoic Acid (RA) has yielded strong forcedifferentiation results in pre-clinical studies but its use does not translate to the clinic. We have previously described a role for Toll-Like Receptor (TLR) Signaling modulator MyD88 in malignancy pluripotency. The aim of this study was to further elucidate this mechanism with a view towards developing improved methods of forced differentiation. Approach: MyD88 was inhibited (peptide-inhibitor) in nullipotent embryonal carcinoma (EC) CSC cell line 2102Ep [nullipotent] and resulting cell types isolated and analysed via flow cytometry. Results: Initial studies indicated that inhibition of MyD88 forced 2102Ep CSCs to transition in to a ‘Primed Undifferentiated State …