Clusterin knockdown sensitizes prostate cancer cells to taxane by modulating mitosis

ABSTRACT: Clusterin (CLU) is a stress-activated molecular chaperone that confers treatment resistance to taxanes when highly expressed. While CLU inhibition potentiates activity of taxanes and other anti-cancer therapies in preclinical models, progression to treatment resistant disease still occurs implicating additional compensatory survival mechanisms. Taxanes are believed to selectively target cells in mitosis, a complex mechanism controlled in part by balancing antagonistic roles of Cdc25C and Wee1 in mitosis progression. Our data indicate that CLU silencing induces a constitutive activation of Cdc25C, which delays mitotic exit and hence sensitizes cancer cells to mitotic-targeting agents such taxanes. Unchecked Cdc25C activation leads to mitotic catastrophe and cell death unless cells upregulat

ORGANISM(S): Homo sapiens

SUBMITTER: Shawn Anderson 

PROVIDER: E-GEOD-67256 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress