Oxidative Stress and Prostate Cancer Progression Are Elicited by Membrane-Type 1 Matrix Metalloproteinase

Nguyen, Hoang-Lan; Zucker, Stanley; Zarrabi, Kevin; Kadam, Pournima; Schmidt, Cathleen; Cao, Jian

doi:10.1158/1541-7786.mcr-11-0033

Cited by 41 publications

(31 citation statements)

References 50 publications

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“…16 Moreover, MT1-MMP can activate the latent TGFβ and trigger tissue fibrosis, [35][36][37] can activate several pro-MMPs, such as MMP2 38 and MMP13, 39 and has been associated with oxidative stress in the myocardium 40 and reactive oxygen species production. 41 In TIMP4-deficient mice, TIMP1, but not TIMP2 or TIMP3, was markedly elevated post-I/R. TIMP1 has been strongly linked to fibrosis in multiple organs, 26,42,43 as well as to myocardial diastolic dysfunction in different cardiomypathies.…”

Section: Discussionmentioning

confidence: 97%

Myocardial Recovery From Ischemia–Reperfusion Is Compromised in the Absence of Tissue Inhibitor of Metalloproteinase 4

Takawale

Fan

Basu

et al. 2014

Circ: Heart Failure

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Background-Myocardial reperfusion after ischemia (I/R), although an effective approach in rescuing the ischemic myocardium, can itself trigger several adverse effects including aberrant remodeling of the myocardium and its extracellular matrix. Tissue inhibitor of metalloproteinases (TIMPs) protect the extracellular matrix against excess degradation by matrix metalloproteinases (MMPs). TIMP4 levels are reduced in myocardial infarction; however, its causal role in progression of post-I/R injury has not been explored. Methods and Results-In vivo I/R (20-minute ischemia, 1-week reperfusion) resulted in more severe systolic and diastolic dysfunction in TIMP4 −/− mice with enhanced inflammation, oxidative stress (1 day post-I/R), hypertrophy, and interstitial fibrosis (1 week). After an initial increase in TIMP4 (1 day post-I/R), TIMP4 mRNA and protein decreased in the ischemic myocardium from wild-type mice by 1 week post-I/R and in tissue samples from patients with myocardial infarction, which correlated with enhanced activity of membrane-bound MMP, membrane-type 1 MMP. By 4 weeks post-I/R, wild-type mice showed no cardiac dysfunction, elevated TIMP4 levels (to baseline), and normalized membranetype 1 MMP activity. TIMP4-deficient mice, however, showed exacerbated diastolic dysfunction, sustained elevation of membrane-type 1 MMP activity, and worsened myocardial hypertrophy and fibrosis. Ex vivo I/R (20-or 30-minute ischemia, 45-minute reperfusion) resulted in comparable cardiac dysfunction in wild-type and TIMP4 −/− mice. Conclusions-TIMP4 is essential for recovery from myocardial I/R in vivo, primarily because of its membrane-type 1 MMP inhibitory function. TIMP4 deficiency does not increase susceptibility to ex vivo I/R injury. Replenishment of myocardial TIMP4 could serve as an effective therapy in post-I/R recovery for patients with reduced TIMP4. (Circ Heart Fail. 2014;7:652-662.)

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Section: Discussionmentioning

confidence: 97%

Myocardial Recovery From Ischemia–Reperfusion Is Compromised in the Absence of Tissue Inhibitor of Metalloproteinase 4

Takawale

Fan

Basu

et al. 2014

Circ: Heart Failure

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“…Membrane type 1-MMP (MT1-MMP) with the capacity for pro-MMP-2 activation is a vital agent and involved in the remodeling of the ECM. The central role of MT1-MMP in inducing oxidative stress in prostate cancer was proven by Nguyen et al (18). Reis et al investigated the expression levels of MMPs and TIMPs in 2 independent studies (19,20).…”

Section: Discussionmentioning

confidence: 99%

Polymorphisms in MMP-2 and TIMP-2 in Turkish patients with prostate cancer

Yaykaşlı¹,

Kayikçi²,

Yamak³

et al. 2014

Turk J Med Sci

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Prostate cancer is the most commonly diagnosed malignancy and the second most common cause of cancer deaths in the Western male population. Matrix metalloproteinases (MMPs) and tissue inhibitors of MMPs (TIMPs) modulate the remodeling of the extracellular matrix (ECM). The imbalance between MMPs and TIMPs may lead to an emergence of pathological processes such as cancer. In this study, the association between TIMP-2 (-418 G/C) and MMP-2 (-1306 C/T) polymorphisms and prostate cancer in the Turkish population was investigated.Materials and methods: Sixty-one prostate cancer patients and 46 healthy subjects were included in the study. DNA was isolated from 2 mL of peripheral blood taken from subjects, and genotypes were analyzed by the polymerase chain reaction-restriction fragment length polymorphism method. Results:The TIMP-2 -418 (GC) genotype was found in 15 cases (32.6%) in the control group and in 9 cases (14.8%) in the patients group, and statistical significance was determined (P = 0.037, OR = 0.346). The MMP-2 -1306 (CT) genotype was found 2.17 times more in the patient group than in the control group (P = 0.149, OR = 2.17). Conclusion:Our results show that the TIMP-2 -418 (GC) genotype had a putative protective effect against prostate cancer.

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“…MMP-2 activation by overexpression of manganese superoxide dismutase in human breast cancer MCF-7 is mediated by H 2 O 2 (Zhang et al 2002). Recently, oxidative stress due to ROS, including H 2 O 2 , and cancer progression were reported to be elicited by MT1-MMP (Nguyen et al 2011). Culture medium with a negative redox potential (e.g., -180 mV) suppresses tumor invasion, revealing that the extra-and intra-cellular redox balance regulates the invasion of cancer cells (Ortega et al 2010;Chaiswing et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Suppressive effects of electrochemically reduced water on matrix metalloproteinase-2 activities and in vitro invasion of human fibrosarcoma HT1080 cells

Kinjo

Yan

et al. 2012

Cytotechnology

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It has been demonstrated that hydrogen peroxide (H(2)O(2)) is directly associated with elevated matrix metalloproteinase-2 (MMP-2) expression in several cell lines. Electrochemically reduced water (ERW), produced near the cathode during electrolysis, and scavenges intracellular H(2)O(2) in human fibrosarcoma HT1080 cells. RT-PCR and zymography analyses revealed that when HT1080 cells were treated with ERW, the gene expression of MMP-2 and membrane type 1 MMP and activation of MMP-2 was repressed, resulting in decreased invasion of the cells into matrigel. ERW also inhibited H(2)O(2)-induced MMP-2 upregulation. To investigate signal transduction involved in MMP-2 downregulation, mitogen-activated protein kinase (MAPK)-specific inhibitors, SB203580 (p38 MAPK inhibitor), PD98059 (MAPK/extracellular regulated kinase kinase 1 inhibitor) and c-Jun NH(2)-terminal kinase inhibitor II, were used to block the MAPK signal cascade. MMP-2 gene expression was only inhibited by SB203580 treatment, suggesting a pivotal role of p38 MAPK in regulation of MMP-2 gene expression. Western blot analysis showed that ERW downregulated the phosphorylation of p38 both in H(2)O(2)-treated and untreated HT1080 cells. These results indicate that the inhibitory effect of ERW on tumor invasion is due to, at least in part, its antioxidative effect.

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Oxidative Stress and Prostate Cancer Progression Are Elicited by Membrane-Type 1 Matrix Metalloproteinase

Cited by 41 publications

References 50 publications

Myocardial Recovery From Ischemia–Reperfusion Is Compromised in the Absence of Tissue Inhibitor of Metalloproteinase 4

Myocardial Recovery From Ischemia–Reperfusion Is Compromised in the Absence of Tissue Inhibitor of Metalloproteinase 4

Polymorphisms in MMP-2 and TIMP-2 in Turkish patients with prostate cancer

Suppressive effects of electrochemically reduced water on matrix metalloproteinase-2 activities and in vitro invasion of human fibrosarcoma HT1080 cells

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