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- W2789780705 abstract "Abstract Prostate cancer stem-like cells (PCSCs) are not only enriched in the CD44 + PSA −/lo subpopulation but also employ androgen-independent signaling mechanisms for survival. CD44 + PCSCs defy androgen deprivation, resist chemo- and radiotherapy and are highly tumorigenic. Human prostate tissue microarray (TMA) staining revealed an increased membranous staining of CD44 in the luminal compartment in higher grade G7-G9 tumors versus staining of the basal layer in benign hyperplasia. To uncover tyrosine kinase/s critical for the survival of the CD44 + PSA −/lo subpopulation, we performed an unbiased screen targeting 87 tyrosine kinases with gene specific siRNAs. Among a subset of tyrosine kinases crucial for PCSC survival, was a non-receptor tyrosine kinase, ACK1/TNK2, a critical regulator of castration resistant prostate cancer (CRPC) growth. Consistently, activated ACK1 as measured by phosphorylation at Tyr284 was significant in the CD44 + PSA −/lo population. Conversely, pharmacological inhibition by ACK1 inhibitor, ( R )- 9b MS mitigated CD44 + PSA −/lo sphere formation, overcame resistance to radiation-induced cell death, induced significant apoptosis in PCSCs and inhibited CD44 + PSA −/lo xenograft tumor growth in castrated mice suggesting dependency of PCSCs on ACK1 for survival. Thus, blockade of ACK1/TNK2 could be a new therapeutic modality to target recalcitrant PCSCs." @default.
- W2789780705 created "2018-03-29" @default.
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- W2789780705 date "2018-01-31" @default.
- W2789780705 modified "2023-10-12" @default.
- W2789780705 title "Blockade of ACK1/TNK2 To Squelch the Survival of Prostate Cancer Stem-like Cells" @default.
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- W2789780705 doi "https://doi.org/10.1038/s41598-018-20172-z" @default.
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