Infiltrating mast cells increase prostate cancer chemotherapy and radiotherapy resistances via modulation of p38/p53/p21 and ATM signals.

摘要: Early studies indicated that mast cells in prostate tumor microenvironment might influence cancer (PCa) progression. Their impacts to PCa therapy, however, remained unclear. Here we found could recruit more than normal epithelial then alter chemotherapy and radiotherapy sensitivity, leading resistant these therapies. Mechanism dissection revealed infiltrated increase p21 expression via modulation of p38/p53 signals, interrupting p38-p53 signals siRNAs p53 or reverse cell-induced docetaxel resistance PCa. Furthermore, recruited also the phosphorylation ATM at ser-1981 site, inhibition activity resistance. The vivo mouse model with xenografted C4-2 co-cultured confirmed activating p38/p53/p21 signaling. Together, our results provide a new mechanism showing sensitivity modulating signaling ATM. Targeting this newly identified may help us better suppress