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HOXA11-AS could promote renal cancer cells growth and invasion by modulating miR-146b-5p-MMP16 axis.
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Overexpression of MMP2 and MMP16 in endometrial cancerous tissues corresponded to down-regulation of miR-377, miR-382 and miR-410, while decreased expression of TIMP2 was associated with miR-200b up-regulation.
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MMP16 was highly expressed and correlated with poor prognosis in gastric cancer patients by promoting proliferation and invasion of gastric cancer cells
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Findings suggest that these MMP16 rs10090371, ADAMTS3 rs788935, TLL2 rs10882807 and MMP9 rs3918251 may be promising prognostic biomarkers for cutaneous melanoma specific survival (CMSS).
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the present findings indicate that MT3-MMP is down-regulated in ESCC, which correlates to lymph node metastasis and poor survival of patients with this disease.
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more severe intervertebral disc degeneration is correlated with higher matrix metallopeptidase 16
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results suggest that miR-145 functions as a tumor metastasis suppressor gene by down-regulating MMP16 and may be a potential target in osteosarcoma treatment
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the results support a role for MMP16 in promoting invasive properties of the meningioma tumours
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These results demonstrate that the MT3-MMP promoter is frequently hypermethylated in colorectal cancer and that downregulation of MT3-MMP may be important for cell migration in colorectal cancer.
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MMP16 is a putative indicator of adverse melanoma prognosis.
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Expression of MMP-16 in HTB9 and T24 cells increases following transforming growth factorbeta1 treatment.
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E2F1 acts as a transcriptional activator for MMPs and directly enhances MMP transcription by binding to E2F1 binding sequences in the promoter, or indirectly activates MMPs (MMP-9 and MMP-16)through enhanced Sp1 and NF-kappa B
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Matrix metalloproteinase 16 (MMP16) was a downstream target of miR-146b-5p.
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The overexpression of miR-146b-5p in glioblastoma cell lines led to MMP16 mRNA silencing, MMP2 inactivation, and the inhibition of tumour cell migration and invasion.
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Data show that MMP16 is regulated by miR-146a in spontaneously differentiated Caco-2 cells.
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MT3-MMP is a matrix-dependent modifier of the invasive tumor cell functions during melanoma progression
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down-regulation of most MT-MMPs is typical for prostate carcinoma; seems to occur mainly in epithelial cells
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Results report the structure of the catalytic domain (cd) of the membrane-type matrix metalloproteinase MT3-MMP/MMP-16 in complex with the hydroxamic acid inhibitor batimastat.
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MT3-MMP is not only important in matrix degradation but also may affect the function of focal adhesions through FAK cleavage.
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Type-3 metalloproteinases, are identified as the triggering agents that independently confer cancer cells with the ability to proteolytically efface the BM scaffolding, initiate the assembly of invasive pseudopodia, and propagate transmigration.