The Contribution of MMP-7 Genotypes to Colorectal Cancer Susceptibility in Taiwan

Yueh, Te Cheng; Hung, Yi Wen; Chang, Wen Shin; Fu, Chun Kai; Pei, Jen Sheng; Wu, Ming; Lai, Yu‐Hung; Lee, Yi Min; Yen, Shiou Ting; Li, Hsin Ting; Tsai, Chia Wen; Bau, Da‐Tian

doi:10.21873/cgp.20079

Cited by 20 publications

(22 citation statements)

References 35 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%

“…Genomic DNA from peripheral blood leukocytes of each participant was carefully extracted within 12 h after sample collection, then aliquoted and stored as we previously described (27). The MMP7 genotyping methodology is the same as our recently published article (28) Fisher's exact test (when any number was less than 5) was applied to compare the distribution of gender, and MMP7 genotypes and alleles between the two groups. The unpaired Student's t-test was applied for the comparison of distribution of the ages between the two groups.…”

Section: Methodsmentioning

confidence: 99%

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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%

Section: Methodsmentioning

confidence: 99%

The Association of MMP7 Genotype With Pterygium

Hu¹,

Wang²,

Liao³

et al. 2019

In Vivo

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“…Genotyping conditions for ERCC1 rs11615 and rs3212986. The extraction of genomic DNA from the peripheral blood leukocytes of each participant was conducted within 24 h after blood collection with a QIAamp Blood Mini Kit (Blossom, Taipei, Taiwan) as described previously (22,23). The DNA was then quantified, stored long-term at -80˚C, diluted and aliquoted for genotyping as a working stock at -20˚C (24)(25)(26).…”

Section: Methodsmentioning

confidence: 99%

The Significant Interaction of Excision Repair Cross-complementing Group 1 Genotypes and Smoking to Lung Cancer Risk

Chen

Shen

et al. 2020

Cancer Genomics Proteomics

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Background: The study aims to evaluate the contribution of excision repair cross-complementing group 1 (ERCC1), which plays an important role in genome integrity maintenance, to lung cancer risk. Materials and Methods: ERCC1 rs11615 and rs3212986 genotypes were identified by polymerase chain reaction-restriction fragment length polymorphism analysis and their association with lung cancer risk was examined among 358 lung cancer patients and 716 controls. Results: The proportions of CC, CT and TT for the rs11615 genotype were 43.6%, 41.6% and 14.8% in the case group and 50.0%, 41.1% and 8.9% in the control group, respectively (p for trend=0.0082). Allelic analysis showed that ERCC1 rs11615 T-allele carriers have a 1.32-fold higher risk of lung cancer than wild-type C-allele carriers [95%confidence interval (CI)=1.09-1.60, p=0.0039]. In addition, a significant interaction between the rs11615 genotype and smoking status was observed. Conclusion: The T allele of ERCC1 rs11615 jointly with smoking habits may contribute to a higher lung cancer risk in Taiwan. According to the most recent report on cancer incidence and mortality by the International Agency for Research on Cancer, lung cancer has remained as the leading cause of cancer deaths all over the world (1). An estimated 2.1 million new lung cancer cases and 1.8 million cancer-related deaths occurred worldwide in 2018 (1). The rapidly increasing cases and the high death rate have urged us to look for effective marker(s) for the prediction of the risk of lung cancer, the outcome of the prognosis and the responsiveness of patient drug treatment. The initiation and development of lung cancer is related to multiple exogenous and endogenous factors including behavioral, environmental and genetic discrepancies, among which the consumption of cigarettes is the most significant factor to be associated with lung cancer risk (2). On the other hand, the fact that about 10% to 25% of lung cancer patients are non-smokers worldwide indicates that the individual genomic influences also play a critical part for personal lung cancer etiology (3). In Taiwan, the incidence and mortality of lung cancer has been ranked on the third and first place, respectively, among different types of cancer, for several years (4). Although several biomarkers for the early detection of lung cancer are being examined during recent years (5-11), the continuous search for effective clinically practical markers and the undermining mechanisms is still largely ongoing. Our genome is regularly and frequently damaged by various kinds of endogenous and exogenous mutagens and the DNA repair systems play a vital role in protecting it from irreversible mutations that can lead to carcinogenesis (12, 13). Concerning non-small cell lung cancer, genomic instability was 571 This article is freely accessible online.

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“…Genomic DNA from the peripheral blood samples of each participant was extracted, aliquoted, and stored as described previously. 25 − 27 Seven polymorphic sites were analyzed. Briefly, the seven polymorphic sites were genotyped through conventional polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) methodology.…”

Section: Methodsmentioning

confidence: 99%

The contribution of <em>XRCC3 </em>genotypes to childhood acute lymphoblastic leukemia

Pei

Chang

Hsu

et al. 2018

CMAR

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PurposeA growing body of evidence shows an association between DNA repair protein genotypes and susceptibility to various cancers. However, few studies have assessed the contribution of the genotype of XRCC3, a homologous repair gene, to the occurrence or prognosis of childhood acute lymphoblastic leukemia (ALL). In this study, we investigated the contribution of seven XRCC3 polymorphisms to childhood ALL.Patients and methodsWe recruited 266 patients with childhood ALL and 266 healthy controls. Genomic DNA was isolated from peripheral blood samples. The XRCC3 rs1799794, rs45603942, rs1799796, rs861530, rs28903081, rs861539, and rs3212057 polymorphic genotypes of each subject were determined through conventional polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis.ResultsGenotypes with the rs861539 polymorphism were significantly associated with the risk of childhood ALL. The allelic distribution analyses suggested a significant association between the T allele at rs861539 with an increased risk of childhood ALL in the Taiwanese population. Polymorphic variants of XRCC3 at rs3212057 or rs28903081 did not exist in the study population. XRCC3 rs1799794, rs45603942, rs1799796, and rs861530 were not significantly associated with the risk of childhood ALL in the Taiwanese population.ConclusionOur findings suggest that XRCC3 genotypes with polymorphisms at rs861539 may play a role in determining individual susceptibility to childhood ALL in this Taiwanese population. The polymorphism may be a potential detector and predictor of childhood ALL.

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The Contribution of MMP-7 Genotypes to Colorectal Cancer Susceptibility in Taiwan

Cited by 20 publications

References 35 publications

The Association of MMP7 Genotype With Pterygium

The Association of MMP7 Genotype With Pterygium

The Significant Interaction of Excision Repair Cross-complementing Group 1 Genotypes and Smoking to Lung Cancer Risk

The contribution of <em>XRCC3 </em>genotypes to childhood acute lymphoblastic leukemia

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