Matrix Metallopeptidase 16 (Membrane-inserted) Protéines (MMP16)

Mouse (Murine) Matrix Metallopeptidase 16 (Membrane-inserted) (MMP16) interaction partners

1. miR-155 contributed to the up-regulation of MMP-16, and MMP-16 further degraded aggrecan and collagen type II, leading to the dehydration and degeneration of intervertebral discs

2. Neuronal knockdown of MT3-MMP resulted in the accumulation of NgR1 at the cell surface and reduced the accumulation of the NgR1 cleavage fragment in medium conditioned by cortical neurons

3. Study demonstrates that MT3-MMP, is expressed in mesenchymal tissues of the skeleton and in peri-skeletal soft connective tissue; and MT3-MMP-deficient mice display growth inhibition tied to a decreased viability of mesenchymal cells in skeletal tissues.

Human Matrix Metallopeptidase 16 (Membrane-inserted) (MMP16) interaction partners

1. 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.

2. MMP16 was highly expressed and correlated with poor prognosis in gastric cancer patients by promoting proliferation and invasion of gastric cancer cells

3. Findings suggest that these MMP16 rs10090371, ADAMTS3 rs788935, TLL2 rs10882807 and MMP9 rs3918251 may be promising prognostic biomarkers for cutaneous melanoma specific survival (CMSS).

4. 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.

5. more severe intervertebral disc degeneration is correlated with higher matrix metallopeptidase 16

6. 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

7. the results support a role for MMP16 in promoting invasive properties of the meningioma tumours

8. 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.

9. MMP16 is a putative indicator of adverse melanoma prognosis.

10. Expression of MMP-16 in HTB9 and T24 cells increases following transforming growth factorbeta1 treatment.

11. 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

12. Matrix metalloproteinase 16 (MMP16) was a downstream target of miR-146b-5p.

13. 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.

14. Data show that MMP16 is regulated by miR-146a in spontaneously differentiated Caco-2 cells.

15. MT3-MMP is a matrix-dependent modifier of the invasive tumor cell functions during melanoma progression

16. down-regulation of most MT-MMPs is typical for prostate carcinoma; seems to occur mainly in epithelial cells

17. 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.

18. MT3-MMP is not only important in matrix degradation but also may affect the function of focal adhesions through FAK cleavage.

19. 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.

20. Chondroitin-4-sulfate, which is expressed on tumour cell surface, can function to bind to pro-MMP-2 and facilitate its activation by MT3-MMP-expressing tumour cells to enhance invasion and metastasis