The Contribution of <i>MMP-7</i> Promoter Polymorphisms to Taiwan Lung Cancer Susceptibility

Chen, Guan Liang; Shen, Te Chun; Chang, Wen Shin; Tsai, Chia Wen; Li, Hsin Ting; Chuang, Chih Liang; Lai, Yu‐Hung; Yueh, Te Cheng; Hsia, Te‐Chun; Wang, Shou Cheng; Bau, Da‐Tian

doi:10.21873/anticanres.12903

Cited by 28 publications

(26 citation statements)

References 38 publications

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“…In literature, the A-181G genotypes of MMP7 have been examined for their association with various types of cancer, including oral, breast, esophageal, gastric, colorectal, gallbladder, bladder, cervical cancer, leukemia and renal cell carcinoma (28,(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45)(46). The lack of association of MMP7 genotype with pterygium in the current study, together with those in bladder (34), renal cell (44), oral (35), colorectal (28), and lung (46) cancer in Taiwan supports the concept that MMP7 may influence Taiwanese susceptibility to these diseases via other mechanisms, such as regulation of translation or protein-protein interaction, and simply not through the regulation at the transcriptional level via polymorphic variations in the promoter region. Notably, while the AG genotype at MMP7 promoter A-181G was associated with an OR of 1.22 (95% CI=0.91-1.63, p=0.2235), the GG genotype had an OR of 2.84 (95% CI=1.64-7.48, p=0.0007) compared to those carrying the AA wild-type genotype among a very large Taiwan population with 1,232 patients with breast cancer and 1,232 non-cancer controls (32).…”

Section: Discussionmentioning

confidence: 99%

The Association of MMP7 Genotype With Pterygium

Hu¹,

Wang²,

Liao³

et al. 2019

In Vivo

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Background/Aim: In literature, few studies have examined the diagnostic or prognostic potential of matrix metalloproteinases (MMP) in pterygium, whose formation and progression are closely related to imbalance in the extracellular microenvironment. In this study, we investigated the contribution of MMP7 promoter (A-181G and C-153T) polymorphic genotypes to pterygium risk. Materials and Methods: A total of 134 cases and 268 controls were collected and their MMP7 genotypes at A-181G and C-153T were examined by polymerase chain reaction-restriction fragment length polymorphism methodology. Results: The AA, AG and GG genotypes at MMP7 promoter A-181G were nonsignificantly differentially distributed between the two groups at 85.8, 11.2 and 3.0%, respectively, in pterygium cases and 88.4, 9.7 and 1.9% in controls, respectively (p for trend=0.6822). There was no polymorphic genotype for MMP7 C-153T among our Taiwanese cohort. Conclusion: A-181G and C-153T genotypes at MMP7 do not have a direct role in determining Taiwanese susceptibility to pterygium. Pterygium is a disease presenting an abnormal wing-shaped outgrowth of fibrovascular conjunctival tissues invading the clear cornea. The etiology of pterygium is still largely unclear. The incidence of pterygium is epidemiologically due to several factors, such as overexposure to sunshine, UV light, heat, dust, and other particles in the atmosphere (1-3). In the past two decades, mounting evidence has supported the concept that variations in our genome play a critical role in the determination of the etiology and development of pterygium (4-11). Many theories for pterygium have been proposed, such as imbalances in immunological mechanisms, growth factors, cytokines, apoptosis, angiogenesis (12-15), and most interestingly but complicatedly, an imbalance in the extracellular microenvironment and the involvement of matrix metalloproteinases (MMPs) (16-19). MMPs are a group of zinc-binding endopeptidases responsible for regulating the components of the extracellular matrix microenvironment (20). The activation of MMPs generally takes place in the extracellular space, and interacts with various other proteases, teaming up to regulate the behaviors of cancer cells including viability, cell differentiation, programmed cell death, angiogenesis, immune surveillance, invasiveness and migration capacity (21, 22). The smallest MMP member, MMP7 (matrilysin), is responsible for the metabolism of a broad spectrum of substrates including fibronectin, vitronectin, elastin, collagen IV, aggrecan, and proteoglycans (23). In addition, MMP7 is involved in inflammatory responses via its capacity to promote cell-surface processing of cytokines such as tumor necrosis factor a (24). MMP7 activation was first proposed to be involved in the pathogenesis of pterygium as early as 2001 by Girolamo and colleagues (25). In their analysis of cultured pterygial and conjunctival tissues from eight pterygium cases at Wales hospital in Sydney, basal and activated MMP7 levels were 1.4-and 2.7-fold higher, resp...

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Section: Discussionmentioning

confidence: 99%

The Association of MMP7 Genotype With Pterygium

Hu¹,

Wang²,

Liao³

et al. 2019

In Vivo

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“…Genotyping processes. The genomic DNA was extracted from the peripheral blood leucocytes of each participant within 24 h after their donation, and stored at −80˚C until processed as per our previous studies (30)(31)(32). In this study, the genotypes at -1306 and -735 polymorphic sites in the MMP-2 promoter region were determined for all the subjects in both the control and oral cancer patient groups.…”

Section: Methodsmentioning

confidence: 99%

Association of Matrix Metallopeptidase-2 Promoter Polymorphisms With the Risk of Childhood Leukemia

et al. 2019

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Background/Aim: The association of matrix metalloproteinase-2 (MMP-2) genotypes with adult leukemia has been reported only once, but never for childhood leukemia. This study aimed to determine the role of MMP-2 promoter-1306 (rs243865) and-735 (rs2285053) genotypes in childhood leukemia risk. Materials and Methods: This case-control study included 266 patients and 266 age-and gender-matched healthy controls. The polymorphic sites of MMP-2 were genotyped by typical polymerase chain reaction-restriction fragment length polymorphism. Results: The CC, CT and TT of rs243865 genotype were 75.2, 23.7 and 1.1% in the case group and 69.2, 28.9 and 1.9% in the control group, respectively. The CT and TT genotypes caused a 0.75-and 0.55-fold increase in the risk of childhood leukemia, respectively. There was no differential distribution of rs2285053 genotypes. Allelic frequency analysis showed that the T allele of MMP-2 promoter-1306 and-735 conferred lower susceptibility than the C allele. Conclusion: The MMP-2 promoter genotypes play a minor role in determining personal susceptibility to childhood leukemia among the Taiwanese.

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“…In our body, MMP-7 has been shown to be constitutively produced by the mammary and parotid glands, pancreas, liver, prostate and lung peribronchial glands (16). In the past years, accumulating evidence indicated that the functional polymorphisms of MMPs may contribute to inter-individual differences in susceptibility to several types of cancer (17)(18)(19)(20)(21)(22)(23)(24)(25)(26). Furthermore, the basal promoter activity was higher in promoter constructs harboring the combination of the two rare alleles of MMP-7 at A-181G (rs11568818) and C-153T (rs11568819) (27).…”

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Association of Matrix Metalloproteinase-7 Genotypes with the Risk of Bladder Cancer

Liao

Chang

Tsai

et al. 2018

In Vivo

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Background/Aim: The breakage of matrix metalloproteinases (MMPs) has been reported to be one of the mechanisms required for tumor invasion, and the expression of MMP-7 in serum is correlated with poor prognosis of urinary bladder cancer patients. However, the role of the MMP-7 genotypes has been seldom examined among bladder cancer patients. Therefore, this study aimed at examining the promoter polymorphic MMP-7 genotypes A-181G and C-153T among Taiwanese bladder cancer patients and evaluate the contribution of the genotypic variants of MMP-7 to bladder cancer risk in Taiwan. Materials and Methods: Three hundred and seventy-five bladder cancer patients and the same number of gender-and age-matched healthy controls were genotyped for A-181G and C-153T in the promoter of MMP-7 via polymerase chain reaction-restriction fragment length polymorphism methodology. Results: The frequencies of AA, AG and GG at A-181G of the promoter of MMP-7 were 89.1, 8.8 and 2.1% in the bladder cancer patient group and 87.5, 10.9 and 1.6% in the matched healthy control group, respectively (p for trend=0.5475). There was no polymorphic genotype for MMP-7 C-153T among the Taiwanese population. The comparisons in allelic frequency distribution also support the findings that the G allele may not be the determinant allele for bladder cancer in Taiwan. In addition, the results showed that there is no significant association of the bladder risk with the MMP-7 A-181G genotype, even after adjustment for the possible confounding factors. Furthermore, there is no interaction of the genotypes of MMP-7 with age, gender, smoking and alcohol consumption on bladder cancer risk. Conclusion: The results of this study suggest that the two MMP-7 polymorphisms,-A-181G and C-153T, do not play a major role in determining personal susceptibility to bladder cancer in Taiwan. Bladder cancer is the 2nd most common urological malignancy worldwide, contributing to about 5% of cancer deaths and is estimated to cost four million dollars each year (1). According to the statistical data provided by the International Agency for Research on Cancer, there were an estimated 429,800 new cases of bladder cancer and 165,100 deaths in 2012 worldwide, and males are four times more likely to develop the disease than females (1, 2). In Taiwan, bladder cancer ranks seventh in incidence and mortality among the common types of cancer (3, 4). Tumorigenesis of bladder cancer is a complex, multistep and multifactorial process being the result of interactions of lifestyle, environmental and genetic factors (3-9). The matrix metalloproteinases (MMPs, matrixins) are a family of endopeptidases that have been reported to play a key role in maintaining the homeostasis of extracellular matrix (ECM) components and the processes of inflammation, carcinogenesis and cancer cell migration (10, 11). Since the 1045 This article is freely accessible online.

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The Contribution of MMP-7 Promoter Polymorphisms to Taiwan Lung Cancer Susceptibility

Cited by 28 publications

References 38 publications

The Association of MMP7 Genotype With Pterygium

The Association of MMP7 Genotype With Pterygium

Association of Matrix Metallopeptidase-2 Promoter Polymorphisms With the Risk of Childhood Leukemia

Association of Matrix Metalloproteinase-7 Genotypes with the Risk of Bladder Cancer

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