Molecular mechanism(s) of regulation(s) of c-MET/HGF signaling in head and neck cancer
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F62156489%3A43210%2F22%3A43921058" target="_blank" >RIV/62156489:43210/22:43921058 - isvavai.cz</a>
Result on the web
<a href="https://doi.org/10.1186/s12943-022-01503-1" target="_blank" >https://doi.org/10.1186/s12943-022-01503-1</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1186/s12943-022-01503-1" target="_blank" >10.1186/s12943-022-01503-1</a>
Alternative languages
Result language
angličtina
Original language name
Molecular mechanism(s) of regulation(s) of c-MET/HGF signaling in head and neck cancer
Original language description
Head and neck cancer is the sixth most common cancer across the globe. This is generally associated with tobacco and alcohol consumption. Cancer in the pharynx majorly arises through human papillomavirus (HPV) infection, thus classifying head and neck squamous cell carcinoma (HNSCC) into HPV-positive and HPV-negative HNSCCs. Aberrant, mesenchymal-epithelial transition factor (c-MET) signal transduction favors HNSCC progression by stimulating proliferation, motility, invasiveness, morphogenesis, and angiogenesis. c-MET upregulation can be found in the majority of head and neck squamous cell carcinomas. c-MET pathway acts on several downstream effectors including phospholipase C gamma (PLCγ), cellular Src kinase (c-Src), phosphotidylinsitol-3-OH kinase (PI3K), alpha serine/threonine-protein kinase (Akt), mitogen-activated protein kinase (MAPK), and wingless-related integration site (Wnt) pathways. c-MET also establishes a crosstalk pathway with epidermal growth factor receptor (EGFR) and contributes towards chemoresistance in HNSCC. In recent years, the signaling communications of c-MET/HGF in metabolic dysregulation, tumor-microenvironment and immune modulation in HNSCC have emerged. Several clinical trials have been established against c-MET/ hepatocyte growth factor (HGF) signaling network to bring up targeted and effective therapeutic strategies against HNSCC. In this review, we discuss the molecular mechanism(s) and current understanding of c-MET/HGF signaling and its effect on HNSCC.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
10601 - Cell biology
Result continuities
Project
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Continuities
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Others
Publication year
2022
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Molecular Cancer
ISSN
1476-4598
e-ISSN
1476-4598
Volume of the periodical
21
Issue of the periodical within the volume
26 January
Country of publishing house
DE - GERMANY
Number of pages
16
Pages from-to
31
UT code for WoS article
000749248800002
EID of the result in the Scopus database
2-s2.0-85123586457