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Elucidating the Genetic Contribution to Nasopharyngeal Carcinoma Risk Through Matrix Metalloproteinase-11 (MMP-11)
Shih-Wei Hsu1,2,3, Che-Lun Hsu4,5, Hou-Yu Shih1,6
1Graduate Institute of Biomedical Sciences, China Medical University, Taichung, Taiwan, R.O.C.
Background/Aim:
Nasopharyngeal carcinoma (NPC) is a distinct malignancy of epithelial origin with multifactorial etiology involving Epstein-Barr virus, genetic susceptibility, and environmental exposures. MMP-11, a matrix metalloproteinase implicated in extracellular matrix remodeling and cancer progression, is overexpressed in NPC tissues; however, its genetic role in NPC remains unexplored.
Materials And Methods:
This case-control study investigated four MMP-11 single nucleotide polymorphisms (SNPs), rs738791, rs2267029, rs738792, and rs28382575, in 208 patients with NPC and 416 matched cancer-free controls from a Taiwanese cohort. Genotypic distributions were tested for Hardy-Weinberg equilibrium, and logistic regression was used to evaluate associations with NPC risk. Stratified analyses assessed gene-environment interactions with smoking, alcohol drinking, and betel quid chewing.
Results:
No significant associations were found between any of the four MMP-11 genotypes and NPC risk under co-dominant or dominant models (all p>0.05). Allelic analysis further supported the lack of independent associations. However, significant gene-environment interactions were observed. The rs2267029 variant genotypes (AG+AA) conferred increased NPC risk among alcohol drinkers [odds ratio (OR)=1.90, 95% confidence interval (CI)=1.09-3.30, p=0.0326] and betel quid chewers (OR=2.50, 95%CI=1.41-4.43, p=0.0025). Similarly, rs738792 variant genotypes (CT+CC) showed a strong interaction with betel quid chewing (OR=2.15, 95%CI=1.22-3.80, p=0.0119). A borderline interaction was noted between rs738791 and smoking (OR=1.80, 95%CI=1.00-3.20, p=0.0645).
Conclusion:
While MMP-11 polymorphisms alone do not independently influence NPC susceptibility, their interaction with environmental risk factors may modulate NPC risk. These findings suggest potential roles for MMP-11 genotypes in NPC pathogenesis via gene-environment interplay and merit further investigation in diverse populations.
