Literature summary for 3.4.24.B3 extracted from

Hsin, C.H.; Chou, Y.E.; Yang, S.F.; Su, S.C.; Chuang, Y.T.; Lin, S.H.; Lin, C.W.
MMP-11 promoted the oral cancer migration and Fak/Src activation (2017), Oncotarget, 8, 32783-32793 .

Search for more literature for 3.4.24.B3

Application

Application	Comment	Organism
diagnostics	association between the clinicopathological characteristics and MMP-11 expression in oral squamous cell carcinoma (OSCC) patients, expression of MMP-11 is associated with higher incidence of lymph node metastasis and worse grade of tumor differentiation, overview. The MMP-11 expression in OSCC samples can predict the progression, especially lymph node metastasis, and the survival of OSCC patients in Taiwan	Homo sapiens

Cloned(Commentary)

Cloned (Comment)	Organism
gene MMP11, quantitative enzyme expression analysis	Homo sapiens

Metals/Ions

Metals/Ions	Comment	Organism	Structure
Zn2+	a zinc-dependent endopeptidase	Homo sapiens

Organism

Organism	UniProt	Comment	Textmining
Homo sapiens	P24347	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
carcinoma cell	matrix metalloproteinase-11 is observed in most invasive human carcinomas	Homo sapiens	-
oral squamous cell carcinoma cell	immunohistochemistry analysis shows that MMP-11 expression is present in 118/279 (42.3%) cases and expression of MMP-11 is associated with higher incidence of lymph node metastasis and worse grade of tumor differentiation. Cancer distribution, overview	Homo sapiens	-

Synonyms

Synonyms	Comment	Organism
MMP-11	-	Homo sapiens

General Information

General Information	Comment	Organism
metabolism	effects of MMP-11 expression on regulation of focal adhesion kinase/Src kinase (FAK/Src) and MAP-Kinase signalling pathway, overview	Homo sapiens
physiological function	MMP-11 overexpression in OSCC cells increases in vitro cell migration. Mechanistically, MMP-11 increases the cell motility of oral squamous cell carcinoma (OSCC) cells through focal adhesion kinase/Src kinase (FAK/Src) pathway	Homo sapiens

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Release 2023.1 (January 2023)