Published on February 16, 2013 at 1:29 AM
In this study, the researchers also reported for the first time that IKBKE is a target of STAT3, a transcription factor that plays a key role in many cellular processes, such as cell growth and programmed cell death.
According to the researchers, STAT3 is frequently activated in various types of human cancers and, when activated, STAT3 increases IKBKE overexpression and protein levels. In non-small cell lung cancer, nicotine-induced IKBKE depends on STAT3.
The authors noted that the activation stage of STAT3 represents an attractive therapeutic potential because IKBKE is a STAT3 target. While IKBKE induces chemotherapy resistance, knocking down IKBKE sensitizes cancer cells to chemotherapy and reduces cancer cell survival.
"Since the IKBKE kinase overexpression is induced by tobacco smoke and IKBKE levels increase in response to nicotine and nicotine-derived nitrosamine ketone, this evidence can be potentially used to develop a non-small cell lung cancer intervention strategy that targets IKBKE," concluded Cheng.
Source: Moffitt Cancer Center