MMP16

MMP16

A gene on chromosome 8q21.3 that encodes matrix metalloproteinase 16, an endopeptidase that degrades components of the extracellular matrix, including collagen III and fibronectin, and activates progelatinase A. Unlike other matrix metalloproteinases, which are secreted as inactive proproteins and activated when cleaved by extracellular proteinases, MMP16 is a transmembrane protein that is activated from its precursor by furin endopeptidase cleavage. It is expressed in the heart, brain, placenta, ovaries and small intestine.

Molecular pathology
Interaction of MMP16 and CSPG4 may trigger degradation and invasion of type-I collagen by melanomas.
References in periodicals archive ?
Of the other four MMPs expressed at moderate levels in hMSCs at day 0 (MMP14, MMP16, MMP19, and MMP24), only MMP14 can degrade collagen type I, FN, and LN [30-32].
MMP16 was upregulated in 3D/Col1 bioprinted prisms.
Yu et al., "miR-146b-5p inhibits glioma migration and invasion by targeting MMP16," Cancer Letters, vol.
To date, there are 28 MMP family members described, including the collagenase subfamily (MMP-1, MMP-8, and MMP-13), the gelatinase subfamily (MMP-2 and MMP-9), the stromelysin subfamily (MMP-3, MMP-10, and MMP11), membrane-associated MMPs (MMP-14, MMP-15, MMP16, MMP-17, MMP-23, MMP-24, and MMP-25), and other MMPs, all of which possess a Zn ion-dependent endopeptidase activity homologue domain [18-20].
MMP2 (collagenase IV) and MMP16 (activates MMP2) expression was significantly upregulated at all time points, suggesting a detrimental role in wound healing processes [93].
Due to structural and substrate specificity, MMPs are currently divided into seven classes: collagenases (MMP1, MMP8, MMP13, and MMP18), gelatinases (MMP2 and MMP9), stromelysins (MMP3, MMP10), stromelysin like (MMP11 and MMP12), matrilysins (MMP7 and MMP26), membrane type (MMP14, MMP15, MMP16, MMP17, MMP24, and MMP25), and others (MMP19, MMP20, MMP21, MMP22, MMP23, MMP27, and MMP28) [18, 27, 28].
MMPs can be divided into 4 main subtypes: collagenases (MMP-1, MMP-8, and MMP13), stromelysins (MMP-3, MMP-10, and MMP-11), gelatinases (MMP-2 and MMP-9), and membrane-type matrix metalloproteinases (MT-MMP, MMP-14, MMP-15, MMP16, MMP-17, MMP-24, and MMP-25) [6].
Primers and probes were designed and validated by Applied Biosystems for 18SRNA (4308329), MMP1 (Hs00899658_m1), MMP2 (Hs00234422_m1), MMP3 (Hs00968308_m1), MMP8 (Hs01029057_m1), MMP9 (Hs00234579_m1), MMP13 (Hs00233992_m1), MMP14 (Hs00237119_m1), MMP16 (Hs00254755_m1) MMP24 (Hs00198580_m1), MMP25 (Hs01554789_m1), TIMP1 (Hs99999139_m1), and TIMP3 (Hs00165949_m1).
For MMP16, expression was not detected in the majority of the SG samples (17/22), except in 5/22 samples which presented low levels of this transcript; in GC, this protease was expressed at low levels in 8/17 samples, while the other 9/17 samples presented no expression.
hasmiR-546b-5p had inhibitory effect on pancreatic cancer cell migration and invasion by targeting MMP16 [31].
Genes for which some or all of the 267 measurements were nondetectable due to values <10 molecules/[10.sup.6] ACTB molecules included MMP16, TPBG, LGALS9, CDC20, RAG1, and IFNG.
Membrane-anchored MMPs include MT1-MMP (MMP14), MT2-MMP (MMP15), MT3-MMP (MMP16), MT4-MMP (MMP17), MT5-MMP (MMP24), MT6-MMP (MMP25), and MMP23.