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- W2148281664 abstract "Abstract Clusterin is a stress-activated, cytoprotective chaperone that confers broad-spectrum treatment resistance in cancer. However, the molecular mechanisms mediating CLU transcription following anticancer treatment stress remain incompletely defined. We report that Y-box binding protein-1 (YB-1) directly binds to CLU promoter regions to transcriptionally regulate clusterin expression. In response to endoplasmic reticulum stress inducers, including paclitaxel, YB-1 is translocated to the nucleus to transactivate clusterin. Furthermore, higher levels of activated YB-1 and clusterin are seen in taxane-resistant, compared with parental, prostate cancer cells. Knockdown of either YB-1 or clusterin sensitized prostate cancer cells to paclitaxel, whereas their overexpression increased resistance to taxane. Clusterin overexpression rescued cells from increased paclitaxel-induced apoptosis following YB-1 knockdown; in contrast, however, YB-1 overexpression did not rescue cells from increased paclitaxel-induced apoptosis following clusterin knockdown. Collectively, these data indicate that YB-1 transactivation of clusterin in response to stress is a critical mediator of paclitaxel resistance in prostate cancer. Mol Cancer Res; 9(12); 1755–66. ©2011 AACR." @default.
- W2148281664 created "2016-06-24" @default.
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- W2148281664 date "2011-12-01" @default.
- W2148281664 modified "2023-10-16" @default.
- W2148281664 title "Clusterin Is a Critical Downstream Mediator of Stress-Induced YB-1 Transactivation in Prostate Cancer" @default.
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- W2148281664 doi "https://doi.org/10.1158/1541-7786.mcr-11-0379" @default.
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