![]() By exploring the transgenic mouse model of hepatic tumorigenesis induced by liver-specific expression of H-ras12V more » oncogene, the activation of RAS/ERK, the mRNA expression levels of retinoid metabolism-related genes, the contents of retinoid metabolites, and phosphorylation of RXRα were determined. However, the relationships among them still remained to be elucidated. Abstract: Activation of RAS/ERK signaling pathway, depletion of retinoid, and phosphorylation of retinoid X receptor alpha (RXRα) are frequent events found in liver tumors and thought to play important roles in hepatic tumorigenesis. The atRA has no effect on preventing hepatic tumorigenesis or curing the developed hepatic nodules.The retinoid metabolism-related genes are down-regulated by ras oncogene.The activation of RAS/ERK is insufficient to inhibit RXRα function and deplete RA.Our results elucidated the molecular mechanism of RA-induced neuroblastoma cellular differentiation, which may be important for developing novel therapeutic strategy against poorly differentiated neuroblastoma. Importantly, we found that the PI3K/AKT pathway is required for RA-induced neuroblastoma cell differentiation. Interestingly, RA promoted cell survival during the differentiation process, hence suggesting a potential mechanism for neuroblastoma resistance to RA therapy. =, which inhibit cell proliferation by blocking cell cycle progression at G1/S phase, increased after RA treatment.
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