Correction: Corrigendum: Beta 1-integrin–c-Met cooperation reveals an inside-in survival signalling on autophagy-related endomembranes

Barrow-McGee, Rachel; Kishi, Naoki; Joffre, Carine; Ménard, Ludovic; Hervieu, Alexia; Bakhouche, Bakhouche A.; Noval, Alejandro J.; Mai, Anja; Guzmán, Camilo; Robbez-Masson, Luisa; Iturrioz, Xavier; Hulit, James; Brennan, Caroline H.; Hart, Ian R.; Parker, Peter J.; Ivaska, Johanna; Kermorgant, Stéphanie

doi:10.1038/ncomms12392

Cited by 9 publications

(26 citation statements)

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“…Events such as c-Met gene mutation, overexpression, and amplification may be closely related to aberrant activation of HGF/c-Met signaling in human cancers (Barrow-Mcgee et al, 2016;Bahrami et al, 2017). Increasing preclinical evidence has allowed for development of specific molecular inhibitors, including anti-c-Met monoclonal antibodies and small molecule tyrosine kinase inhibitors (TKIs).…”

Section: Mirna Lncrna-based Therapeutics In C-met-related Cancermentioning

confidence: 99%

“…Amplification of c-Met was detected in patients with advanced solid cancers (Jardim et al, 2014). Furthermore, mutations, overexpression, or amplification of the MET gene in some tumor types resulted in aberrant HGF/c-Met axis activity, which induced cell motility and proliferation, promoted tumor development, and led to resistance to radiotherapy and targeted drug therapy in multiple cancers (Minuti et al, 2012;Barrow-Mcgee et al, 2016;Bahrami et al, 2017). Clinical trials of drug monotherapies targeted to c-Met have shown promising outcomes against multiple cancer types (Spigel et al, 2013;Solomon et al, 2014;Kogita et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

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MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers

Zhan

Zhang

et al. 2020

Front. Cell Dev. Biol.

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MicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are components of many signaling pathways associated with tumor aggressiveness and cancer metastasis. Some lncRNAs are classified as competitive endogenous RNAs (ceRNAs) that bind to specific miRNAs to prevent interaction with target mRNAs. Studies have shown that the hepatocyte growth factor/mesenchymal-epithelial transition factor (HGF/c-Met) pathway is involved in physiological and pathological processes such as cell growth, angiogenesis, and embryogenesis. Overexpression of c-Met can lead to sustained activation of downstream signals, resulting in carcinogenesis, metastasis, and resistance to targeted therapies. In this review, we evaluated the effects of anti-oncogenic and oncogenic non-coding RNAs (ncRNAs) on c-Met, and the interactions among lncRNAs, miRNAs, and c-Met in cancer using clinical and tissue chromatin immunoprecipition (ChIP) analysis data. We summarized current knowledge of the mechanisms and effects of the lncRNAs/miR-34a/c-Met axis in various tumor types, and evaluated the potential therapeutic value of lncRNAs and/or miRNAs targeted to c-Met on drug-resistance. Furthermore, we discussed the functions of lncRNAs and miRNAs in c-Met-related carcinogenesis and potential therapeutic strategies.

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Section: Mirna Lncrna-based Therapeutics In C-met-related Cancermentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers

Zhan

Zhang

et al. 2020

Front. Cell Dev. Biol.

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“…In many cancers, Met is mostly overexpressed rather than mutated. We have shown that, in several cancer cell lines expressing endogenous nonmutated Met, HGF stimulation triggers a rapid internalization of Met (Kermorgant et al, 2003 , 2004 ; Kermorgant and Parker, 2008 ; Ménard et al, 2014 ; Barrow-McGee et al, 2016 ). Interestingly, Met remains bound to HGF and activated on endosomes.…”

Section: The Receptor Tyrosine Kinase Metmentioning

confidence: 99%

“…Furthermore, the optimal activation by Met of signals, such as ERK1/2, STAT3, and Rac1 requires an intact endocytosis machinery (Kermorgant et al, 2004 ). Met was shown to signal in several types of endosomes: the early endosome, the late endosome, and a novel endosome decorated by LC3 that we named “Autophagy Related Endomembrane, ARE” (Kermorgant et al, 2004 ; Kermorgant and Parker, 2008 ; Joffre et al, 2011 ; Ménard et al, 2014 ; Barrow-McGee et al, 2016 ).…”

Section: The Receptor Tyrosine Kinase Metmentioning

confidence: 99%

“…Increasing amounts of studies suggest the importance of the localization of the receptors and their signals within the cell, such as on various endomembranes, to regulate cell functions (Joffre et al, 2011 ; Ménard et al, 2014 ; Barrow-McGee et al, 2016 ). Recent studies suggest that Met can activate the PI3K pathway from endosomes.…”

Section: The Pi3k Signaling Pathwaymentioning

confidence: 99%

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The Role of PI3K in Met Driven Cancer: A Recap

Hervieu

Kermorgant

2018

Front. Mol. Biosci.

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The Receptor Tyrosine Kinase (RTK) Met, overexpressed or mutated in cancer, plays a major role in cancer progression and represents an attractive target for cancer therapy. However RTK inhibitors can lead to drug resistance, explaining the necessity to develop therapies that target downstream signaling. Phosphatidylinositide 3-kinase (PI3K) is one of the most deregulated pathways in cancer and implicated in various types of cancer. PI3K signaling is also a major signaling pathway downstream of RTK, including Met. PI3K major effectors include Akt and “mechanistic Target of Rapamycin” (mTOR), which each play key roles in numerous and various cell functions. Advancements made due to the development of molecular and pharmaceutical tools now allow us to delve into the roles of each independently. In this review, we summarize the current understanding we possess of the activation and role of PI3K/Akt/mTOR, downstream of Met, in cancer.

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A PI3K- and GTPase-independent Rac1-mTOR mechanism mediates MET-driven anchorage-independent cell growth but not migration

et al. 2020

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Receptor tyrosine kinases (RTKs) are often overexpressed or mutated in cancers and drive tumor growth and metastasis. In the current model of RTK signaling, including that of MET, downstream phosphatidylinositol 3-kinase (PI3K) mediates both cell proliferation and cell migration, whereas the small guanosine triphosphatase (GTPase) Rac1 mediates cell migration. However, in cultured NIH3T3 and glioblastoma cells, we found that class I PI3K mediated oncogenic MET–induced cell migration but not anchorage-independent growth. In contrast, Rac1 regulated both processes in distinct ways. Downstream of PI3K, Rac1 mediated cell migration through its GTPase activity, whereas independently of PI3K, Rac1 mediated anchorage-independent growth in a GTPase-independent manner through an adaptor function. Through its RKR motif, Rac1 formed a complex with the kinase mTOR to promote its translocation to the plasma membrane, where its activity promoted anchorage-independent growth of the cell cultures. Inhibiting mTOR with rapamycin suppressed the growth of subcutaneous MET-mutant cell grafts in mice, including that of MET inhibitor–resistant cells. These findings reveal a GTPase-independent role for Rac1 in mediating a PI3K-independent MET-to-mTOR pathway and suggest alternative or combined strategies that might overcome resistance to RTK inhibitors in patients with cancer.

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Correction: Corrigendum: Beta 1-integrin–c-Met cooperation reveals an inside-in survival signalling on autophagy-related endomembranes

Abstract: The original version of this Article contained an error in the spelling of the author Luisa Robbez-Masson, which was incorrectly given as Luisa Robert-Masson. This has now been corrected in both the PDF and HTML versions of the Article.

Cited by 9 publications

References 1 publication

MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers

MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers

The Role of PI3K in Met Driven Cancer: A Recap

A PI3K- and GTPase-independent Rac1-mTOR mechanism mediates MET-driven anchorage-independent cell growth but not migration

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