Ron Kinase Transphosphorylation Sustains <i>MET</i> Oncogene Addiction

Benvenuti, Silvia; Lazzari, Luca; Arnesano, Addolorata; Chiavi, Giulia Li; Gentile, Alessandra; Comoglio, Paolo M.

doi:10.1158/0008-5472.can-10-2100

Cited by 66 publications

(74 citation statements)

References 49 publications

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“…Crosstalk between c-MET and other RTKs has also been studied in great depth because of its potential importance in the development of [Benvenuti et al 2011]. Recently, transactivation between c-Met and both platelet-derived growth factor receptor (PDGFR) and Axl was found to play a role in bladder cancer [Yeh et al 2011].…”

Section: Hgf/c-met Signalingmentioning

confidence: 99%

An overview of the c-MET signaling pathway

2011

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c-MET is a receptor tyrosine kinase that, after binding with its ligand, hepatocyte growth factor, activates a wide range of different cellular signaling pathways, including those involved in proliferation, motility, migration and invasion. Although c-MET is important in the control of tissue homeostasis under normal physiological conditions, it has also been found to be aberrantly activated in human cancers via mutation, amplification or protein overexpression. This paper provides an overview of the c-MET signaling pathway, including its role in the development of cancers, and provides a rationale for targeting the pathway as a possible treatment option.

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Section: Hgf/c-met Signalingmentioning

confidence: 99%

An overview of the c-MET signaling pathway

2011

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“…Several kinase inhibitors such as imatinib and geftinib have been very successful in the clinics due to the phenomenon of oncogene addiction. Recently it is shown that cross-talk between RON and MET sustains the oncogene addiction of MET [69]. Thus study of the phenomenon of oncogene addiction with reference to RON activation in colon cancer will further strengthen the avenues for therapeutic utilization of RON RTK.…”

Section: Future Directionsmentioning

confidence: 97%

RON - The Con in Colorectal Carcinoma

Tarang

Wang²

2012

TOCOLCJ

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Abstract:The recepteur d'origine nantais (RON) is a member of MET family of receptor tyrosine kinase (RTKs), an overexpression of which has been observed in several cancers. The expression of RON gene is required during embryonic development and also plays critical roles in regulating macrophage inflammatory response. In CRC, the overexpression of moderate RON activity contributes to their oncogenic potential by regulating several key processes such as proliferation, motility and resistance to apoptosis. Interestingly, an aberrant RON expression is often associated with the generation of several splice variants with unique transforming activities. The targeting of RON signaling pathway by the use of monoclonal antibodies and small-molecule inhibitors has shown promising therapeutic results in animal models. The present article aims at summarizing the current understanding of RON kinase in CRC.

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“…RON and Met concomitant overexpression is detected in many tumor types. 65,68 Lee et al 66 found that overexpression of RON and c-Met in CRC is associated with a remarkably poor clinical outcome and short-term disease-free survival. Various mechanisms underlay on abnormal expression and activation of c-Met and RON such as gene amplification, enhanced TK activity due to point mutations, and aberrant splicing of RON.…”

Section: C-met and Ron Receptorsmentioning

confidence: 99%

“…c-Met and RON signaling pathways mostly rely on activation of PI3K and MAPK as key adaptor proteins which result in PI3K/AKT, Src, STAT3, NF-κB, FAK, and β-catenin activation, leading to critical cellular responses including cytoskeletal changes, EMT, stemness, invasion, resistance to apoptosis, angiogenesis, and proliferation. 64 Benvenuti et al 65 …”

Section: C-met and Ron Receptorsmentioning

confidence: 99%

The c-Met receptor: Implication for targeted therapies in colorectal cancer

et al. 2017

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c-Met (mesenchymal-epithelial transition factor) is a tyrosine kinase receptor activated by hepatocyte growth factor and regulates multiple biological processes, such as cell scattering, survival, and proliferation. Aberrant c-Met signaling has been implicated in a variety of cancer types, including colorectal cancer. c-Met is genetically altered through various mechanisms that is associated with colorectal cancer progression and metastasis. Especially, in colorectal cancer, preclinical evidence for the aberrant activation of the c-Met signaling exists. Accordingly, molecular targeting of c-Met receptor could be a promising strategy, in the treatment of colorectal cancer patients. Recently, it was also shown that crosstalk between c-Met and other cell surface receptors attributes to tumorigenesis and development of therapeutic resistance. Characterization of the molecular mechanisms through which c-Met crosstalks with other receptors in favor of tumor formation and progression remains to explore. This review will describe the mechanisms of aberrant c-Met signaling in colorectal cancer and discuss on additional roles for c-Met receptor through crosstalk with other tyrosine kinase receptors and cell surface proteins in colorectal cancer. Novel therapeutic approaches for c-Met pathway targeting will also be discussed.

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Ron Kinase Transphosphorylation Sustains MET Oncogene Addiction

Cited by 66 publications

References 49 publications

An overview of the c-MET signaling pathway

An overview of the c-MET signaling pathway

RON - The Con in Colorectal Carcinoma

The c-Met receptor: Implication for targeted therapies in colorectal cancer

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