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Matrix metalloproteinase-2 -1306 C>T gene polymorphism is associated with reduced risk of cancer: a meta-analysis
Shafiul Haque1, Naseem Akhter, Mohtashim Lohani
1Research and Scientific Studies Unit, College of Nursing and Allied Health Sciences, Jazan University, Jazan, Saudi Arabia
Abstract:
Matrix metalloproteinase-2 (MMP2) is an endopeptidase, mainly responsible for degradation of extracellular matrix components, which plays an important role in cancer disease. A single nucleotide polymorphism (SNP) at -1306 disrupts a Sp1-type promoter site. The results from the published studies on the association between MMP2 -1306 C>T polymorphism and cancer risk are contradictory and inconclusive. In the present study, a meta-analysis was therefore performed to evaluate the strength of any association between the MMP2 -1306 C>T polymorphism and risk of cancer. We searched all eligible studies published on association between MMP2 -1306 C>T polymorphism and cancer risk in PubMed (Medline), EMBASE and Google Scholar online web databases until December 2013. Genotype distribution data were collected to calculate the pooled odds ratios (ORs) and 95% confidence intervals (95%CIs) to examine the strength of the association. A total of 8,590 cancer cases and 9,601 controls were included from twenty nine eligible case control studies. Overall pooled analysis suggested significantly reduced risk associated with heterozygous genotype (CT vs CC: OR=0.758, 95%CI=0.637 to 0.902, p=0.002) and dominant model (TT+CT vs CC: OR=0.816, 95%CI=0.678 to 0.982, p=0.032) genetic models. However, allelic (T vs C: OR=0.882, 95%CI=0.738 to 1.055, p=0.169), homozygous (TT vs CC: OR=1.185, 95%CI=0.825 to 1.700, p=0.358) and recessive (TT vs CC+CT: OR=1.268, 95%CI=0.897 to 1.793, p=0.179) models did not show any risk. No evidence of publication bias was detected during the analysis. The results of present meta-analysis suggest that the MMP2 -1306 C>T polymorphism is significantly associated with reduced risk of cancer. However, further studies with consideration of different populations will be required to evaluate this relationship in more detail.
Insights
The MMP2 -1306 C>T polymorphism is linked to a reduced risk of cancer. This meta-analysis found a significant association with heterozygous and dominant genetic models, suggesting a protective effect for certain genotypes.
Area of Science:
- Genetics
- Oncology
- Molecular Biology
Background:
- Matrix metalloproteinase-2 (MMP2) is crucial for extracellular matrix degradation and plays a role in cancer progression.
- A single nucleotide polymorphism (SNP) at the -1306 position in the MMP2 gene promoter affects Sp1-type binding sites.
- Previous studies on the association between the MMP2 -1306 C>T polymorphism and cancer risk have yielded conflicting results.
Purpose of the Study:
- To conduct a meta-analysis to evaluate the association between the MMP2 -1306 C>T polymorphism and cancer risk.
- To consolidate evidence from published studies to determine the overall strength of the association.
Main Methods:
- A comprehensive literature search was performed in PubMed, EMBASE, and Google Scholar databases until December 2013.
- Data on genotype distributions from eligible case-control studies were collected.
- Pooled odds ratios (ORs) and 95% confidence intervals (95%CIs) were calculated to assess the association under various genetic models.
Main Results:
- The meta-analysis included 29 case-control studies with 8,590 cancer cases and 9,601 controls.
- A significantly reduced risk of cancer was observed for the heterozygous genotype (CT vs CC: OR=0.758) and the dominant genetic model (TT+CT vs CC: OR=0.816).
- Allelic, homozygous, and recessive models did not show a significant association with cancer risk. No publication bias was detected.
Conclusions:
- The MMP2 -1306 C>T polymorphism is significantly associated with a reduced risk of cancer, particularly in heterozygous and dominant models.
- The findings suggest a potential protective role of certain MMP2 genotypes against cancer development.
- Further research in diverse populations is recommended to elucidate the detailed relationship between this polymorphism and cancer risk.
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