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- W4361946602 abstract "<div>Abstract<p><b>Purpose:</b> Current prostate cancer management calls for identifying novel and more effective therapies. Self-renewing tumor-initiating cells (TICs) hold intrinsic therapy resistance and account for tumor relapse and progression. As BMI-1 regulates stem cell self-renewal, impairing BMI-1 function for TIC-tailored therapies appears to be a promising approach.</p><p><b>Experimental Design:</b> We have previously developed a combined immunophenotypic and time-of-adherence assay to identify CD49b<sup>hi</sup>CD29<sup>hi</sup>CD44<sup>hi</sup> cells as human prostate TICs. We utilized this assay with patient-derived prostate cancer cells and xenograft models to characterize the effects of pharmacologic inhibitors of BMI-1.</p><p><b>Results:</b> We demonstrate that in cell lines and patient-derived TICs, BMI-1 expression is upregulated and associated with stem cell–like traits. From a screened library, we identified a number of post-transcriptional small molecules that target BMI-1 in prostate TICs. Pharmacologic inhibition of BMI-1 in patient-derived cells significantly decreased colony formation <i>in vitro</i> and attenuated tumor initiation <i>in vivo</i>, thereby functionally diminishing the frequency of TICs, particularly in cells resistant to proliferation- and androgen receptor–directed therapies, without toxic effects on normal tissues.</p><p><b>Conclusions:</b> Our data offer a paradigm for targeting TICs and support the development of BMI-1–targeting therapy for a more effective prostate cancer treatment. <i>Clin Cancer Res; 22(24); 6176–91. ©2016 AACR</i>.</p></div>" @default.
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- W4361946602 date "2023-03-31" @default.
- W4361946602 modified "2023-10-16" @default.
- W4361946602 title "Data from BMI-1 Targeting Interferes with Patient-Derived Tumor-Initiating Cell Survival and Tumor Growth in Prostate Cancer" @default.
- W4361946602 doi "https://doi.org/10.1158/1078-0432.c.6527079" @default.
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