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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Animals, Antineoplastic Agents, Cell Line, Tumor, Cell Proliferation, Cell Self Renewal, Cell Survival, Cell Transformation, Neoplastic, Humans, Male, Mice, Mice, Inbred NOD, Mice, SCID, Neoplastic Stem Cells, Polycomb Repressive Complex 1, Prostatic Neoplasms, Receptors, Androgen, Xenograft Model Antitumor Assays.
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Does bMI-1 Targeting interfere with Patient-Derived Tumor-Initiating Cell Survival and Tumor Growth in Prostate Cancer? Context: 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. We have previously developed a combined immunophenotypic and time-of-adherence assay to identify CD49b 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 in vitro and attenuated tumor initiation in vivo, thereby functionally diminishing the frequency of TICs, particularly in cells resistant to proliferation- and androgen receptor-directed therapies, without toxic effects on normal tissues.
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Our data offer a paradigm for targeting TICs and support the development of BMI-1-targeting therapy for a more effective prostate cancer treatment. Clin Cancer Res; 1-16. ©2016 AACR. Final Decision: yes