ArticleOncogene2011
c-Met-induced epithelial carcinogenesis is initiated by the serine protease matriptase.
Article in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 103 citations in OpenAlex.
- A start methionine mutation in matriptase causes the membrane anchor to be skipped and replaced by a cryptic signal peptide.The Journal of biological chemistry · 2026Article
- MMP1 and PRSS23 induce PARCommunications biology · 2026Article
- Matriptase-dependent epidermal pre-neoplasm in zebrafish embryos caused by a combination of hypotonic stress and epithelial polarity defects.PLoS genetics · 2023Article
- Understanding HAIs: Ally proteins in the fight against cancer.The FEBS journal · 2022Article
- Insufficiency of hepatocyte growth factor activator inhibitor-1 confers lymphatic invasion of tongue carcinoma cells.Cancer science · 2022Article
- Kallikrein 5 Inhibition by the Lympho-Epithelial Kazal-Type Related Inhibitor Hinders Matriptase-Dependent Carcinogenesis.Cancers · 2021Article
- Matriptase activation of Gq drives epithelial disruption and inflammation via RSK and DUOX.eLife · 2021Article
- TMPRSS13 promotes cell survival, invasion, and resistance to drug-induced apoptosis in colorectal cancer.Scientific reports · 2020Article
- A JUN N-terminal kinase inhibitor induces ectodomain shedding of the cancer-associated membrane protease Prss14/epithin via protein kinase CβII.The Journal of biological chemistry · 2020Article
- Membrane-anchored serine proteases as regulators of epithelial function.Biochemical Society transactions · 2020Review
- Entosis and apical cell extrusion constitute a tumor-suppressive mechanism downstream of Matriptase.The Journal of cell biology · 2020Article
- Loss of SPINT2 expression frequently occurs in glioma, leading to increased growth and invasion via MMP2.Cellular oncology (Dordrecht, Netherlands) · 2020Article
- Aberrant regulation favours matriptase proteolysis in neoplastic B-cells that co-express HAI-2.Journal of enzyme inhibition and medicinal chemistry · 2019Article
- Cell surface-anchored serine proteases in cancer progression and metastasis.Cancer metastasis reviews · 2019Review
- SPINT2 is hypermethylated in both IDH1 mutated and wild-type glioblastomas, and exerts tumor suppression via reduction of c-Met activation.Journal of neuro-oncology · 2019Article
- Inhibition of HGF/MET signaling decreases overall tumor burden and blocks malignant conversion in Tpl2-related skin cancer.Oncogenesis · 2019Article
- 3-Cl-AHPC inhibits pro-HGF maturation by inducing matriptase/HAI-1 complex formation.Journal of cellular and molecular medicine · 2019Article
- Expression of protease activating receptor-2 (PAR-2) is positively correlated with the recurrence of non-muscle invasive bladder cancer: an immunohistochemical analysis.Research and reports in urology · 2019Article
- Matriptase-Induced Phosphorylation of MET is Significantly Associated with Poor Prognosis in Invasive Bladder Cancer; an Immunohistochemical Analysis.International journal of molecular sciences · 2018Article
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Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The progression and negative outcome of a variety of human carcinomas are intimately associated with aberrant activity of the c-Met oncogene. The underlying cause of this dysregulation, however, remains a subject of discussion, as the majority of cancer patients do not present with activating mutations in c-Met receptor itself. In this study, we show that the oncogenic protease matriptase is ubiquitously co-expressed with the c-Met in human squamous cell carcinomas and amplifies migratory and proliferative responses of primary epithelial cells to the cognate ligand for c-Met, pro-hepatocyte growth factor/scatter factor (proHGF/SF), through c-Met and Gab1 signaling. Furthermore, the selective genetic ablation of c-Met from matriptase-expressing keratinocytes completely negates the oncogenic potential of matriptase. In addition, matriptase-dependent carcinoma formation could be blocked by the pharmacological inhibition of the Akt-mammalian target of Rapamycin (mTor) pathway. Our data identify matriptase as an initiator of c-Met-Akt-mTor-dependent signaling axis in tumors and reveal mTor activation as an essential component of matriptase/c-Met-induced carcinogenesis. The study provides a specific example of how epithelial transformation can be promoted by epigenetic acquisition of the capacity to convert a widely available paracrine growth factor precursor to its signaling competent state.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.