Show simple item record

dc.contributor.authorRaj, Sibi
dc.contributor.authorKesari, Kavindra Kumar
dc.contributor.authorKumar, Arun
dc.contributor.authorRathi, Brijesh
dc.contributor.authorSharma, Ashok
dc.contributor.authorGupta, Piyush Kumar
dc.contributor.authorJha, Saurabh Kumar
dc.contributor.authorJha, Niraj Kumar
dc.contributor.authorSláma, Petr
dc.contributor.authorRoychoudhury, Shubhadeep
dc.contributor.authorKumar, Dhruv
dc.date.accessioned2023-03-17T01:03:03Z
dc.date.available2023-03-17T01:03:03Z
dc.date.issued2022
dc.identifier.issn1476-4598 Sherpa/RoMEO, JCR
dc.identifier.urihttps://repozitar.mendelu.cz/xmlui/handle/20.500.12698/1654
dc.description.abstractHead 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.en
dc.format31
dc.publisherSpringer-Verlag GmbH
dc.relation.ispartofMolecular Cancer
dc.relation.urihttps://doi.org/10.1186/s12943-022-01503-1
dc.rightsCC BY 4.0
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectHead and neck squamous cell carcinomaen
dc.subjectC-METen
dc.subjectEGFRen
dc.subjectHepatocyte growth factoren
dc.subjectChemoresistanceen
dc.subjectMonoclonal antibodyen
dc.titleMolecular mechanism(s) of regulation(s) of c-MET/HGF signaling in head and neck canceren
dc.typeJ_ČLÁNEK
dc.date.updated2023-03-17T01:03:03Z
dc.description.versionOA
local.identifier.doi10.1186/s12943-022-01503-1
local.identifier.scopus2-s2.0-85123586457
local.identifier.wos000749248800002
local.number26 January
local.volume21
local.identifier.obd43922499
local.identifier.e-issn1476-4598
dc.identifier.orcidSláma, Petr 0000-0003-0570-259X
local.contributor.affiliationAF


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record

CC BY 4.0
Except where otherwise noted, this item's license is described as CC BY 4.0