Abstract
The cancer stem cell (CSC) hypothesis has arisen from the molecular concept of cancer progression. The stem cell generation seems temporally to correspond with epithelial mesenchymal transition (EMT) activation and tumour progression. Hedgehog, Wnt, Notch, Akt/mTOR and miRNAs signalling are associated with EMT activation and CSC development. Hence targeting stem cells and suppressing the resistance to therapy by interfering with these signalling pathways could be viable approaches. Salinomycin, a putative CSC inhibitor, targets Hedgehog signalling. Vismodegib and rapamycin also suppress Hedgehog and mTOR pathways and synergistically inhibit CSCs. CSCs display tissue-specific tropism. This could provide a road to targeted delivery of drugs and antibodies to tumours. The benefits of combining chemotherapy with stem cell therapy have been disputed, but there are reports of response. Some transcription factors involved with CSCs have been suggested as therapeutic targets. Of note are Sp1 and the Ets family transcription factors. The bHLH (basic helix loop helix) neurogenins have also attracted much attention. Stem cell therapy is still in its infancy.
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