Inhibition of DDR1 reduces invasive features of human A375 melanoma, HT29 colon carcinoma and SK-HEP hepatoma cells.
Biomarkers, Tumor
/ metabolism
Carcinoma, Hepatocellular
/ metabolism
Cell Adhesion
Cell Adhesion Molecules
/ metabolism
Cell Line, Tumor
Cell Movement
Cell Proliferation
Chemotaxis
Collagen Type I
/ metabolism
Colonic Neoplasms
/ metabolism
Discoidin Domain Receptor 1
/ antagonists & inhibitors
Gene Silencing
Humans
Liver Neoplasms
/ metabolism
MAP Kinase Signaling System
Matrix Metalloproteinase 9
/ metabolism
Melanoma
/ metabolism
Neoplasm Invasiveness
Phosphorylation
Proto-Oncogene Proteins c-akt
/ metabolism
RNA, Messenger
/ genetics
RNA, Small Interfering
/ metabolism
Melanoma
adhesion
collagen receptor
colon carcinoma
discoidin domain receptor 1
hepatocarcinoma
invasion
matrix metalloproteinases
migration
proliferation
silencing
Journal
Cell adhesion & migration
ISSN: 1933-6926
Titre abrégé: Cell Adh Migr
Pays: United States
ID NLM: 101469464
Informations de publication
Date de publication:
12 2020
12 2020
Historique:
pubmed:
25
2
2020
medline:
2
6
2021
entrez:
25
2
2020
Statut:
ppublish
Résumé
DDR1 is a receptor tyrosine kinases for collagen and an adverse prognostic factor in primary and metastatic tumors.Despite this, DDR1 signaling and its functional consequences in tumor development remain unclear. RT-PCR and Western blot show that A375, colon carcinoma HT29 and liver carcinoma SK-HEP human cell lines express functional DDR1 that phosphorylates in response to collagen type I. Chemical inhibition of DDR1 phosphorylation or DDR1 mRNA silencing reduced AKT and ERK phosphorylation, expression of ICAM1 and VCAM1, Ki67 and secretion of MMP9. DDR1 silenced cells showed reduced adhesion to collagen type I, MMP-dependent invasion, and chemotactic and proliferative responses to collagen type I. Our work indicates an essential role for DDR1 signaling in key prometastatic features of collagen type I in human carcinoma cells.
Identifiants
pubmed: 32090682
doi: 10.1080/19336918.2020.1733892
pmc: PMC7153652
doi:
Substances chimiques
Biomarkers, Tumor
0
Cell Adhesion Molecules
0
Collagen Type I
0
RNA, Messenger
0
RNA, Small Interfering
0
Discoidin Domain Receptor 1
EC 2.7.10.1
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Matrix Metalloproteinase 9
EC 3.4.24.35
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
69-81Références
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