Cluster of differentiation (CD) 133<sup>+</sup>/CD44<sup>+</sup> prostate CSCs and CD 44<sup>+</sup>/CD24 breast CSCs were isolated from the DU-145 human prostate cancer and MCF-7 human breast cancer cell lines, respectively, using FACSAria flow cytometry cell sorting.
We observed preferential accumulation of anti-CD24 conjugated NPs (encapsulating docetaxel) compared to the non-conjugated NPs 24 hours after a single injection into luciferase-expressing PC3M prostate cancer tumor.
Our data suggest a significant association of CD24 genetic variants with prostate cancer onset and progression, which provides new insight into molecular genetics of prostate cancer; however, these findings need to be validated in multiple independent cohorts.
Silencing of CD24 enhanced restoration of PRIMA-1-induced mutant p53 in endogenous TP53(P223L/V274F) DU145 cells and in PC3 cells transfected with TP53(R273H) CONCLUSIONS: In human prostate cancers, there is CD24-dependent inactivation of mutant p53.
In support of the functional interaction between CD24 and p53, in silico analyses reveal that TP53 mutates at a higher rate among glioma and prostate cancer samples with higher CD24 mRNA levels.
CD44+CD133+α2β1Integrin+CD24- population was isolated from mock or TGF-β treated (7 days) prostate cancer cell line, LNCaP, through fluorescent activated cell sorting.
Therefore, CD44+CD24(-) LNCaP prostate cells offer an attractive model system to both explore the biology important to the maintenance and differentiation of prostate cancer stem cells as well as to develop the therapeutics, as the gene expression pattern in these cells is consistent with poor survival in prostate cancer patients.