Two-Step Forward Genetic Screen in Mice Identifies the Ral Pathway as a Central Drug Target in Hepatocellular Carcinoma

Teufel, Andreas; Dufour, Jean–François

doi:10.1053/j.gastro.2016.06.034

Cited by 1 publication

(1 citation statement)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Rals regulate tumorigenesis and cancer progression in three ways: (1) through activation of Ral effector proteins such as RalBP1 and kinase Aurora A, (2) via activation of several signaling pathways such as phosphaolipase D1, Src, JNK, NF‐kB, and cyclin D, and (3) by phosphorylation of Ral proteins . Ral activation was shown to be involved in a number of different tumor types such as lung , colorectal , melanoma , pancreatic , squamous cell carcinoma , hepatocellular carcinoma , prostate , ovarian , bladder , chronic myelogenous leukemia , peripheral nerve sheath tumors , and medulloblastoma . Studies have even been completed showing Ral‐A autoantibodies as a potentially useful serum biomarker for prostate adenocarcinoma .…”

Section: Ral Signaling In Cancermentioning

confidence: 99%

Ral signaling pathway in health and cancer

et al. 2017

View full text Add to dashboard Cite

The Ral (Ras‐Like) signaling pathway plays an important role in the biology of cells. A plethora of effects is regulated by this signaling pathway and its prooncogenic effectors. Our team has demonstrated the overactivation of the RalA signaling pathway in a number of human malignancies including cancers of the liver, ovary, lung, brain, and malignant peripheral nerve sheath tumors. Additionally, we have shown that the activation of RalA in cancer stem cells is higher in comparison with differentiated cancer cells. In this article, we review the role of Ral signaling in health and disease with a focus on the role of this multifunctional protein in the generation of therapies for cancer. An improved understanding of this pathway can lead to development of a novel class of anticancer therapies that functions on the basis of intervention with RalA or its downstream effectors.

show abstract