Matrix metalloproteinase-2 (MMP2) is an endopeptidase, mainly responsible for degradation of extracellularmatrix 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 betweenMMP2 -1306 C>T polymorphism and cancer risk are contradictory and inconclusive. In the present study, ameta-analysis was therefore performed to evaluate the strength of any association between the MMP2 -1306C>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 webdatabases 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 cancercases and 9,601 controls were included from twenty nine eligible case control studies. Overall pooled analysissuggested significantly reduced risk associated with heterozygous genotype (CT vs CC: OR=0.758, 95%CI=0.637to 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) geneticmodels. 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 ofpresent meta-analysis suggest that the MMP2 -1306 C>T polymorphism is significantly associated with reducedrisk of cancer. However, further studies with consideration of different populations will be required to evaluatethis relationship in more detail.