Inhibition of STAT3 signaling targets both tumor-initiating and differentiated cell populations in prostate cancer.

ABSTRACT: Despite of tremendous research efforts to profile prostate cancer, the genetic alterations and biological processes that correlate with disease progression remain partially elusive. In this study we show that the STAT3 small molecule inhibitor Stattic caused S-phase accumulation at low-dose levels and led to massive apoptosis at a relatively high-dose level in prostate cancer cells. STAT3 knockdown led to the disruption of the microvascular niche which tumor-initiating cells (TICs) and non-tumor initiating cells (non-TICs)depend on. Primary human prostate cancer cells and prostate cancer cell line contained high aldehyde dehydrogenase activity (ALDH(high)) subpopulations with stem cell-like characteristics, which expressed higher levels of the active phosphorylated form of STAT3 (pSTAT3) t

SUBMITTER: Han Z 

PROVIDER: S-EPMC4226693 | biostudies-literature | 2014 Sep

REPOSITORIES: biostudies-literature