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Activation of RAS/MEK/ERK signaling drives biliary differentiation in primary liver cancer [396UE]

ABSTRACT: RAS mutations are frequently observed in human cholangiocarcinoma (CCA), while they are relatively rare in hepatocellular carcinoma (HCC). In a genetically engineered mouse model with liver specific conditional deletion of tumor suppressors Rb and p53 together with activation of oncogenic KRAS, intrahepatic CCA develop primarily from hepatocytes. CCA show activation of PI3K/AKT and MEK/ERK signaling pathways. targeted genetic inactivation of each of these downstream pathways of KRAS leads to delayed tumor growth and profound alterations in tumor differentiation. Specifically, reduced PI3K/AKT signaling promotes the formation of well-differentiated tumors, whereas the inactivation of MEK/ERK signaling induces a differentiation switch towards a more hepatocyte-like phenotype.

ORGANISM(S): Mus musculus

PROVIDER: GSE235820 | GEO | 2025/04/30

REPOSITORIES: GEO

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Project description:Pappalardo2016 - PI3K/AKT and MAPK Signaling Pathways in Melanoma Cancer This model is described in the article: Computational Modeling of PI3K/AKT and MAPK Signaling Pathways in Melanoma Cancer. Pappalardo F, Russo G, Candido S, Pennisi M, Cavalieri S, Motta S, McCubrey JA, Nicoletti F, Libra M. PLoS ONE 2016; 11(3): e0152104 Abstract: Malignant melanoma is an aggressive tumor of the skin and seems to be resistant to current therapeutic approaches. Melanocytic transformation is thought to occur by sequential accumulation of genetic and molecular alterations able to activate the Ras/Raf/MEK/ERK (MAPK) and/or the PI3K/AKT (AKT) signalling pathways. Specifically, mutations of B-RAF activate MAPK pathway resulting in cell cycle progression and apoptosis prevention. According to these findings, MAPK and AKT pathways may represent promising therapeutic targets for an otherwise devastating disease.Here we show a computational model able to simulate the main biochemical and metabolic interactions in the PI3K/AKT and MAPK pathways potentially involved in melanoma development. Overall, this computational approach may accelerate the drug discovery process and encourages the identification of novel pathway activators with consequent development of novel antioncogenic compounds to overcome tumor cell resistance to conventional therapeutic agents. The source code of the various versions of the model are available as S1 Archive. This model is hosted on BioModels Database and identified by: MODEL1609190000. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Activation of RAS/MEK/ERK signaling drives biliary differentiation in primary liver cancer [396UE]

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