The Possible Role And Mechanism Of Transcriptional Factor GATA4 In Mouse Fetal Liver Development And Hepatocarcinogenesis

Transcriptional factor GATA4 is rarely reported to be expressed in heaptocarcinoma though it is indispensable in liver development. We aimed to detect GATA4 expression in fetal liver, heaptocarcinoma tissue chips and cell lines and explore its relationship with hepatocyte differentiation. We found that GATA4 was highly expressed in fetal liver, tissue chips and cell lines of heaptocarcinoma and was negatively correlated with hepatocyte differentiation and more sensitve than AFP in heaptocarcinoma tissue chips. After transfected into normal liver cell lines, GATA4 was found to promote cell proliferation, up-regulate PCNA, apoptosis inhibiting gene Bcl-2 and Bcl-X_L and down-regulate E-cadherin. With the decrement of GATA4 after use of doxorubicine in live cancer cell lines, the increasing apoptotic cells and the declining expression of AFP, Bcl-2 and Bcl-X_L were lagged behind GATA4 changes. It is implied that GATA4 may facilitate hepatocarcinogenesis by up-regulating AFP, attenuating cell adherence and inhibiting cell apoptosis.