Inhibition of Endothelial Cell Migration by Gene Transfer of Tissue Inhibitor of Metalloproteinases-1

Fernandez, Harold A.; Kallenbach, Klaus; Seghezzi, Graziano; Grossi, Eugene A.; Colvin, Stephen B.; Schneider, Robert J.; Mignatti, Paolo; Galloway, Aubrey C.

doi:10.1006/jsre.1998.5534

Cited by 72 publications

(45 citation statements)

References 26 publications

(33 reference statements)

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“…Upregulation of TIMP-1 expression by cannabinoids has also been demonstrated in cervical carcinoma and lung cancer cells [48], albeit a possible COX-2-dependent pathway was not focussed on in these cells. Moreover, the antimigratory function 21 of TIMP-1 shown here is in line with other studies demonstrating a correlation between increased TIMP-1 levels and impaired cellular migration [47,[49][50][51][52][53].…”

Section: Confirmation Of the Proposed Antimigratory Mechanism By Use supporting

confidence: 92%

Cyclooxygenase-2 and tissue inhibitor of matrix metalloproteinases-1 confer the antimigratory effect of cannabinoids on human trabecular meshwork cells

Ramer

Hinz

2010

Biochemical Pharmacology

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To cite this version:Robert Ramer, Burkhard Hinz. Cyclooxygenase-2 AND tissue inhibitor of matrix metalloproteinases-1 confer the antimigratory effect of cannabinoids on human trabecular meshwork cells. Biochemical Pharmacology, Elsevier, 2010, 80 (6) This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 3 ABSTRACTCannabinoids have received considerable attention as potential antiglaucomatous drugs.

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Section: Confirmation Of the Proposed Antimigratory Mechanism By Use supporting

confidence: 92%

Cyclooxygenase-2 and tissue inhibitor of matrix metalloproteinases-1 confer the antimigratory effect of cannabinoids on human trabecular meshwork cells

Ramer

Hinz

2010

Biochemical Pharmacology

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“…TIMPs have antiangiogenic activity either by their ability to inhibit the activity of MMPs (Fernandez et al, 1999), or by a direct e ect on endothelial cell proliferation. MMPs promote endothelial cell migration and trigger angiogenic switch.…”

Section: Paradox 2: Timps Regulate Pro-mmp Activation and Tumor Angiomentioning

confidence: 99%

“…Second, the e ect of TIMPs on tumor angiogenesis is controversial. TIMPs have antiangiogenic activity either by inhibiting the activity of MMPs or by a direct inhibitory e ect on endothelial cell proliferation (Murphy et al, 1993;Fernandez et al, 1999). However, some MMPs also play a critical role in generations of angiostatin and endostatin, potent angiogenic inhibitors (Dong et al, 1997;Wen et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Complex roles of tissue inhibitors of metalloproteinases in cancer

2002

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Matrix metalloproteinases (MMPs) is tightly associated with extracellular matrix (ECM) turnover, which plays a very active role in tumor invasion and metastasis. Tissue inhibitors of metalloproteinases (TIMPs) plays a critical role in the homeostasis of ECM by regulating the activity of MMPs. TIMPs are well-known for their ability to inhibit MMP activity thereby inhibiting tumor growth and metastasis. However, many evidences suggest that TIMPs are multifunctional proteins, which regulate cell proliferation, apoptosis, proMMP-2 activation, and angiogenesis. These e ects may be through MMPdependent or MMP-independent pathways. Recent data indicate that TIMPs have many paradoxical roles in tumorigenesis. In particular, both inhibitory e ect and stimulatory e ect on tumorigenesis have been demonstrated in many animal models in which TIMPs were overexpressed in cancer cells or in mice. Elevated TIMP levels are reported in association with cancer progression and identi®ed as poor prognostic indicators in several human tumor types. Herein, we review the complex roles of TIMPs in cancer growth and metastasis.

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“…Through the inhibition of MMPs, TIMPs can block the degradation of the extracellular matrix, tumor invasion, and metastasis (7,8). In addition, they inhibit the release of angiogenic factors from the matrix, block endothelial cell migration (9), and inhibit the formation of endothelial tube in vitro (10). Most synthetic MMP inhibitors target the catalytic site of the MMPs and act by chelating the catalytically essential zinc ion.…”

Section: Introductionmentioning

confidence: 99%

Isoginkgetin inhibits tumor cell invasion by regulating phosphatidylinositol 3-kinase/Akt–dependent matrix metalloproteinase-9 expression

Yoon

Shin

Lee³

et al. 2006

Molecular Cancer Therapeutics

103

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Matrix metalloproteinase (MMP)-9 plays a key role in tumor invasion. Inhibitors of MMP-9 were screened from Metasequoia glyptostroboides (Dawn redwood) and one potent inhibitor, isoginkgetin, a biflavonoid, was identified. Noncytotoxic levels of isoginkgetin decreased MMP-9 production profoundly, but up-regulated the level of tissue inhibitor of metalloproteinase (TIMP)-1, an inhibitor of MMP-9, in HT1080 human fibrosarcoma cells. The major mechanism of Ras-dependent MMP-9 production in HT1080 cells was phosphatidylinositol 3-kinase (PI3K)/Akt/nuclear factor-KB (NF-KB) activation. Expression of dominant-active H-Ras and p85 (a subunit of PI3K) increased MMP-9 activity, whereas dominant-negative forms of these molecules decreased the level of MMP-9. H-Ras did not increase MMP-9 in the presence of a PI3K inhibitor, LY294002, and a NF-KB inhibitor, SN50. Further studies showed that isoginkgetin regulated MMP-9 production via PI3K/Akt/NF-KB pathway, as evidenced by the findings that isoginkgetin inhibited activities of both Akt and NF-KB. PI3K/Akt is a well-known key pathway for cell invasion, and isoginkgetin inhibited HT1080 tumor cell invasion substantially. Isoginkgetin was also quite effective in inhibiting the activities of Akt and MMP-9 in MDA-MB-231 breast carcinomas and B16F10 melanoma. Moreover, isoginkgetin treatment resulted in marked decrease in invasion of these cells. In summary, PI3K/ Akt is a major pathway for MMP-9 expression and isoginkgetin markedly decreased MMP-9 expression and invasion through inhibition of this pathway. This suggests that isoginkgetin could be a potential candidate as a therapeutic agent against tumor invasion. [Mol Cancer Ther 2006;5(11):2666 -75]

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Inhibition of Endothelial Cell Migration by Gene Transfer of Tissue Inhibitor of Metalloproteinases-1

Cited by 72 publications

References 26 publications

Cyclooxygenase-2 and tissue inhibitor of matrix metalloproteinases-1 confer the antimigratory effect of cannabinoids on human trabecular meshwork cells

Cyclooxygenase-2 and tissue inhibitor of matrix metalloproteinases-1 confer the antimigratory effect of cannabinoids on human trabecular meshwork cells

Complex roles of tissue inhibitors of metalloproteinases in cancer

Isoginkgetin inhibits tumor cell invasion by regulating phosphatidylinositol 3-kinase/Akt–dependent matrix metalloproteinase-9 expression

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