BTF3 sustains cancer stem-like phenotype of prostate cancer via stabilization of BMI1

Jing Hu,Feifei Sun,Weiwen Chen,Jing Zhang,Zhang Tao,M. Qi,T. Feng,Hui Liu,Xinjun Li,Yuan-xin Xing,Xueting Xiong,B. Shi,Geng-yin Zhou,B. Han

Published 2019 in Journal of experimental & clinical cancer research : CR

ABSTRACT

Cancer stem-like traits contribute to prostate cancer (PCa) progression and metastasis. Deciphering the novel molecular mechanisms underlying stem-like traits may provide important insight for developing novel therapeutics. Immunohistochemistry and immunofluorescence assays in prostatic tissues; gain- and loss-of-function analyses using ectopic overexpression and shRNAs in PCa cell lines; measurements of tumorigenic and stemness properties, and transcription in vitro and in vivo; transcriptional analysis in public databases. We identified that overexpression of BTF3 in PCa tissues and BTF3 expression highly correlates to stem-like traits. Cancer stem-like characteristics in PCa including self-renewal and metastatic potential were impaired by BTF3 loss and promoted by BTF3 overexpression. Mechanistically, BTF3 could stabilize BMI1, which is a crucial regulator of prostate stem cell self-renewal. More importantly, our data revealed that BTF3 is highly predictive of poor prognosis and may help in risk stratification of PCa patients. BTF3 promotes PCa progression though modeling stem-like traits in PCa. BTF3 represents a stratification marker in PCa progression and outcomes.

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