HSP27 expression in primary colorectal cancers is dependent on mutation of KRAS and PI3K/AKT activation status and is independent of TP53.

摘要: Abstract Colorectal adenomas display features of senescence, but these are often lost upon progression to carcinoma, indicating that oncogene induced senescence (OIS) could be a roadblock in colorectal cancer (CRC) development. Heat shock proteins (HSPs) have been implicated the prognosis CRC and HSP based therapy is current interest for drug Recent cell culture studies suggested absence TP53 mutation, OIS mediated by PI3K/AKT activation can circumvented high expression HSPs. Furthermore, while KRAS mutations independent inducers OIS, suppress -induced when both present cultured cells. As mutations, all common CRC, it possible requirement inhibit dependent on mutation spectrum tumour. However, work utilised profiled human tumour tissues has limited. Here, we characterised two major (HSP27 72) immunohistochemistry (IHC), status , PIK3CA genes direct sequencing AKT IHC cohort unselected primary (n = 74). We compare our data with findings generated from cell-based studies. Expression HSP27 HSP72 was correlated clinicopathological survival no significant association found. also established panel. did not detect any associations between or status. CRCs strongly associated co-presence wildtype activated (p = 0.004), role overcoming tumours. Our suggest using archival validating hypotheses investigations.