Cross-talk between the proto-oncogenes Met and Ron

Follenzi, Antonia; Bakovic, Silvia; Gual, Philippe; Stella, Maria Cristina; Longati, Paola; Comoglio, Paolo M.

doi:10.1038/sj.onc.1203620

Cited by 166 publications

(160 citation statements)

References 74 publications

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“…In addition, somatic mutations in the tyrosine kinase domain have been detected in childhood HCCs (30%) but not in adult HCCs (Park et al, 1999). Furthermore, receptor transactivation by EGF receptor (EGFR) and RON (Follenzi et al, 2000;Jo et al, 2000) or cell/cell contact ) represent potential molecular mechanisms for ligand-independent activation of this signaling pathway. Similarly, HGF has been shown to be over represented in HCCs as compared to the normal liver; however, it is not expressed by tumor cells themselves (Selden et al, 1994;Noguchi et al, 1996).…”

Section: Transforming Growth Factor B Signaling Axismentioning

confidence: 99%

Dysregulation of growth factor signaling in human hepatocellular carcinoma

2006

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Section: Transforming Growth Factor B Signaling Axismentioning

confidence: 99%

Dysregulation of growth factor signaling in human hepatocellular carcinoma

2006

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“…Ligandindependent RON activation was observed in various physiological and pathological conditions (15)(16)(17). Aberrant RON expression also results in receptor phosphorylation and kinase activation (16)(17)(18), which contributes to the pathogenesis and malignancy of epithelial tumors. The present investigation was undertaken to determine the role and the mechanisms of RON in EMT in MadinDarby canine kidney (MDCK) cells.…”

Section: Introductionmentioning

confidence: 99%

“…Binding of macrophage stimulating protein (MSP) to extracellular sequences of RON leads to receptor homo-dimerization, which is a typical example of ligand-induced RON activation (13,14). Ligandindependent RON activation was observed in various physiological and pathological conditions (15)(16)(17). Aberrant RON expression also results in receptor phosphorylation and kinase activation (16)(17)(18), which contributes to the pathogenesis and malignancy of epithelial tumors.…”

Section: Introductionmentioning

confidence: 99%

Mechanisms of RON-mediated epithelial-mesenchymal transition in MDCK cells through the MAPK pathway

Qian

Zhang

et al. 2011

Braz J Med Biol Res

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“…A bidirectional transphosphorylation occurs between MET and MST1R after exposure of cells to either HGF or macrophagestimulating protein. 61 Although MST1R is less efficient than MET as a kinase, the formation of MET/MST1R complexes leads to a more efficient MST1R transphosphorylation by MET, resulting in a more sustained signal than that induced by the MST1R/MST1R homodimer. Activation of both MET and MST1R may induce a cooperative or synergistic response to their ligands.…”

Section: Discussionmentioning

confidence: 99%

MET and MST1R as prognostic factors for classical Hodgkin's lymphoma

et al. 2013

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MST1R (RON) and MET are receptor tyrosine kinase gene family members that form a noncovalent complex on the cell surface, a critical step in tumor progression. A recent study suggested a prognostic role of MET expression in Hodgkin/Reed-Sternberg (HRS) cells in classical Hodgkin's lymphoma (cHL). The purpose of this study was to examine the prognostic significance of MET and MST1R expression in cHL. The prognostic impact of MET and MST1R was examined in 100 patients with cHL (median age: 32 years) by immunohistochemistry and mRNA in situ hybridization. The median follow-up time was 95 months (interquartile range: 42-126 months). MET or MST1R protein expression was associated with high MET or MST1R mRNA expression, respectively. Thirty-eight patients (38%) expressed MET protein in HRS cell, which was associated with better overall survival (P ¼ 0.004). Twenty-six patients (26%) expressed MST1R protein, which was associated with better overall survival (P ¼ 0.022) and event-free survival (P ¼ 0.021). Multivariate analysis identified MET protein as an independent prognostic factor for overall survival and MST1R protein as an independent prognostic factor for event-free survival. Subgroup analysis according to Ann Arbor stage showed that expressions of MET and MST1R protein have prognostic impact in the advanced stage only. In particular, coexpression of MST1R and MET protein was associated with a better survival outcome than MET or MST1R expression alone or no expression. This study suggests that MET and MST1R are independent prognostic factors in classical cHL, and may allow the identification of a subgroup of cHL patients who require more intensive therapy.

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Cross-talk between the proto-oncogenes Met and Ron

Cited by 166 publications

References 74 publications

Dysregulation of growth factor signaling in human hepatocellular carcinoma

Dysregulation of growth factor signaling in human hepatocellular carcinoma

Mechanisms of RON-mediated epithelial-mesenchymal transition in MDCK cells through the MAPK pathway

MET and MST1R as prognostic factors for classical Hodgkin's lymphoma

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