CD44 and CD24 coordinate the reprogramming of nasopharyngeal carcinoma cells towards a cancer stem cell phenotype through STAT3 activation.

摘要: Cell surface proteins such as CD44 and CD24 are used to distinguish cancer stem cells (CSCs) from the bulk-tumor population. However, molecular functionalities of CD44, how these two molecules coordinate in CSCs remain poorly understood. We found that nasopharyngeal carcinoma (NPC) with high expression presented pronounced CSC properties. Accordingly, a subpopulation NPC co-expression were specially enriched high-stage clinical samples. Furthermore, ectopically expressing epithelial-mesenchymal transition (EMT) regulator Twist was able upregulate stemness factors, vice versa. This indicates reciprocal regulation EMT. Intriguingly, we this differentially orchestrated by CD24, only simultaneous silencing led broad-spectrum suppression Oppositely, overexpression induced reprogramming parental into through STAT3 activation, which could be blunted inhibition, indicating collaboratively drive STAT3-mediated EMT activation. Consequently, targeting CD44/CD24/STAT3 axis may provide potential therapeutic paradigm for treatment repressing activities.