Analysis of proteolytic mechanisms of GATA-6 as novel molecular target of chemotherapy for colorectal cancer

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GATA-6 is transcription factor essential for differentiation or proliferation of early embryonic cells. Recently it is reported that GATA-6 involved proliferation and surviving of gastrointestinal tumor cells. In this study, I configured the research theme, "How effective is the degradation of GATA-6 as novel molecular target of chemotherapy for colorectal cancer". Especially I focused on two issues, (1) Identification of signal transduction pathway for degradation of GATA-6, and (2) Estimation of effectiveness of degradation of GATA-6 as novel anti-tumor chemotherapy. Experiment for (1) resulted that novel kinase pathway activating JNK involved degradation of GATA-6 via nuclear export pathway. The other experiment for (2) showed that JNK activator inducing proteolysis of GATA-6 arrested the cell cycle at G2/M phase, and suppressed proliferation of colorectal cancer cells.