Cell surface binding and activation of gelatinase A induced by expression of membrane‐type‐1‐matrix metalloproteinase (MT1‐MMP)

Sato, Hiroshi; Takino, Takahisa; Kinoshita, Takeshi; Imai, Kazushi; Okada, Yasunori; Stetler-Stevenson, William G.; Seiki, Motoharu

doi:10.1016/0014-5793(96)00389-4

Cited by 171 publications

(127 citation statements)

References 23 publications

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“…A recent biochemical analysis demonstrated that TIMP-2 contributed to the activation of MMP-2. [25][26][27] In the MMP-2 activation mechanism, pro-MMP-2 secreted by fibroblasts or tumor cells binds to TIMP-2 complexed with membrane Type 1 MMP (MT1-MMP) on the tumor cell surface, and the pro-MMP-2/TIMP-2/ MT1-MMP ternary complex is formed. Pro-MMP-2 in the ternary complex is activated by MT1-MMP that is free from TIMP-2.…”

Section: Discussionmentioning

confidence: 99%

“…Pro-MMP-2 in the ternary complex is activated by MT1-MMP that is free from TIMP-2. [25][26][27] Recently, some studies reported that TIMP-2 plays a positive role in invasion and metastasis in carcinoma of the breast, 28 lung, 29 colon, 30 and bladder. 31 The current study demonstrated that both MMP-2 and TIMP-2 were detected mostly on the tumor cell surface and cytoplasm of thymomas and that they stained more strongly in border areas between the tumor and the stroma, which was the invasive area, compared with the central area of the tumor.…”

Section: Discussionmentioning

confidence: 99%

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Characteristics of primary care physicians and their practices associated with mammography rates for older women

Harrison

Janz

Wolfe

et al. 2003

Cancer

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BACKGROUND Mammography screening rates are below national recommendations for older women. Understanding the relation between the characteristics of primary care physicians (PCPs) and mammography rates for older women can help to target screening improvement efforts. METHODS Subjects were 2527 PCPs practicing in Michigan between 1997 and 1998. A cross‐sectional design used Medicare data to identify women age 68 years or older in 1998 whom PCPs treated in 1997–1998 and to determine whether these women had a mammogram between 1996 and1998. Eligible women were Medicare beneficiaries age 65 years or older by 1996, residing in Michigan from 1996 to 1998, without specified comorbidities likely to affect decisions regarding mammography. Correlations and multiple regressions examined the relation between this score and characteristics of both PCPs and their practice populations of older women. RESULTS Mammography rates across physicians' practices ranged from 3–100% (mean = 59%, standard deviation = 17%). Five predictors accounted for 55% of the variance in mammography rates across practices. Higher mammography rates were found to be independently related to physicians who have: a lower mean age for female Medicare patients, a higher mean number of physicians billing for patients' care, a lower mean number of inpatient admissions, obstetrics/gynecology practices, and a higher mean education level in patient's zip code (beta weights ≥ 0.25, P < 0.0001). CONCLUSIONS PCPs vary substantially with regard to mammography rates for older women. Mammography rates vary more with the population of patients in physicians' practices than with commonly measured personal characteristics of physicians. Mammography rates should be adjusted for patient population to target individual PCPs with low mammography rates for interventions. Cancer 2003. © 2003 American Cancer Society.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Characteristics of primary care physicians and their practices associated with mammography rates for older women

Harrison

Janz

Wolfe

et al. 2003

Cancer

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“…MMP2 is mainly regulated by its zymogen inhibitor, tissue inhibitor of metalloproteinase 2 (TIMP2), and by its major activator, membrane type-1 MMP (MT1-MMP), also known as MMP14. MT1-MMP specifically activates the pro-gelatinase, MMP2, on the tumor cell surface in vitro through the formation of a complex with TIMP2 (6). IL8 upregulates MMP2 in tumor cells, which is thought to be responsible for its angiogenic activity (7).…”

Section: Introductionmentioning

confidence: 99%

Underexpression of MMP-2 and its regulators, TIMP2, MT1-MMP and IL-8, is associated with prostate cancer

et al. 2012

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Prostate cancer (PCa) is a common disease with a multifactorial and complex etiology. It is the most common malignancy in the male and the second leading cause of death in many countries, including Brazil. Estimates for 2011 indicate that 903,500 new cases and 258,400 deaths relatVol. 38 (2): 167-174; March -April, 2012 Objective: Extracellular matrix homeostasis is strictly maintained by a coordinated balance between the expression of metalloproteinases (MMPs) and their regulators. The purpose of this study was to investigate whether MMP-2 and its specifi c regulators, TIMP-2, MT1-MMP and IL-8, are expressed in a reproducible, specifi c pattern and if the profi les are related to prognosis and clinical outcome of prostate cancer (PCa). Materials and Methods: MMP-2, TIMP-2, MT1-MMP and IL-8 expression levels were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR) in freshly frozen malignant and benign tissue specimens collected from 79 patients with clinically localized PCa who underwent radical prostatectomies. The control group consisted of 11 patients with benign prostate hyperplasia (BPH). The expression profi le of the MMP-2 and its regulators were compared using Gleason scores, pathological stage, pre-operative PSA levels and the fi nal outcome of the PCa. Results: The analysis of 79 specimens of PCa revealed that MMP-2, TIMP-2, MT1-MMP and IL-8 were underexpressed at 60.0%, 72.2%, 62.0% and 65.8%, respectively, in malignant prostatic tissue in relation to BPH samples. Considering the prognostic parameters, we demonstrated that high Gleason score tumors (≥ 7) overexpressed MMP-2 (p = 0.048) and TIMP-2 (p = 0.021), compared to low Gleason score tumors (< 7). Conclusion: We have demonstrated that MMP-2 and its regulators are underexpressed in PCa. Alternatively, overexpression of MMP-2 and TIMP-2 was related to higher Gleason score tumors. We postulate that alterations in metalloproteinase expression may be important in the control of tissue homeostasis related to prostate carcinogenesis and tumor behavior. Underexpression of MMP-2 and its

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“…Sato and co-workers have identified MT1-MMP (membrane type 1 MMP or MMP-14): a MMP possessing a hydrophobic C-terminal transmembrane domain, which is considered as a physiological MMP-2 activator [22][23][24][25]. The active form of MT1-MMP, which is generated through a furin-dependent mechanism [26,27], binds TIMP-2 through the interaction of the N-terminal domains of each protein, thereby docking soluble TIMP-2 to the cell surface [20,[28][29][30].…”

Section: Introductionmentioning

confidence: 99%

Type IV Collagen Induces Matrix Metalloproteinase 2 Activation in HT1080 Fibrosarcoma Cells

Maquoi

Frankenne

Noël

et al. 2000

Experimental Cell Research

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Matrix metalloproteinase 2 (MMP-2) activation has been described as a "master switch" which triggers tumor spread and metastatic progression. We show here that type IV collagen, a major component of basement membranes, promotes MMP-2 activation by HT1080 cells. When plated on plastic, HT1080 cells constitutively processed the 66-kDa pro-MMP-2 into a 62-kDa intermediate activated form, most probably through a membrane type (MT) 1 MMP-dependent mechanism. In the presence of type IV collagen, part of this intermediate form was further processed to fully activated 59-kDa MMP-2. This activation was prevented by tissue inhibitor of MMP (TIMP)-2 and a broad-spectrum hydroxamic acid-based synthetic MMP inhibitor (GI129471). Type IV collagen-mediated pro-MMP-2 activation did not involve either a transcriptional modulation of MMP-2, MT1-MMP, or TIMP-2 expression nor any alteration of MT1-MMP protein synthesis or processing. An inverse relationship between MMP-2 activation and the concentration of secreted TIMP-2 was observed. This is consistent with our previous report that TIMP-2 degradation is probably linked to the MT1-MMP-dependent MMP-2 activation mechanism. Because invasive tumor cells must breach basement membranes at different steps of the metastatic dissemination, the ability of HT1080 cells to activate pro-MMP-2 in the presence of type IV collagen might represent a key regulatory mechanism for the acquisition of an invasive potential.

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Cell surface binding and activation of gelatinase A induced by expression of membrane‐type‐1‐matrix metalloproteinase (MT1‐MMP)

Cited by 171 publications

References 23 publications

Characteristics of primary care physicians and their practices associated with mammography rates for older women

Characteristics of primary care physicians and their practices associated with mammography rates for older women

Underexpression of MMP-2 and its regulators, TIMP2, MT1-MMP and IL-8, is associated with prostate cancer

Type IV Collagen Induces Matrix Metalloproteinase 2 Activation in HT1080 Fibrosarcoma Cells

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