Finds homozygous variant MnSOD genotype is associated with increased lung cancer risk among individuals with zero or "low" asbestos exposure score and no association among the "high" AES group.

The common Val16Ala MnSOD polymorphism does not confer increased or reduced risk of lung cancer in Chinese in Hong Kong

lung cancer cases and 141 controls were evaluated for the 58T > C and 60C > T SNPs in exon 3. All were of the wild-type homozygous genotype for both 58C and 60T in exon 3.

genetic variants may be protective against lung adenocarcinoma risk in light smokers

the Val/Val genotype of SOD2 may be associated with lung cancer in a Turkish

The polymorphism of superoxide dismutase 2 identified an association of T allele with a decreased risk of lung cancer

MnSOD expression is significantly reduced in lung adenocarcinoma and squamous cell carcinoma compared with matched normal lung tissue.

We conclude that MnSOD may promote tumor aggressiveness via upregulation of the FoxM1-MMP2 axis, and that MnSOD expression can independently predict survival and relapse in patients with resected lung adenocarcinoma.

High SOD2 expression is associated with lung adenocarcinoma.

Results suggest that MnSOD Val(16)Ala single-nucleotide polymorphism may not contribute to lung cancer susceptibility.

SOD2 C47T polymorphism is significantly associated with lung cancer.

SOD2 expression was not associated with prognosis in limited-stage small cell lung cancer.

Study suggests that tumor-associated inflammation mediates SOD-2 upregulation through NF-kappaB pathway, which may contribute to epithelial-mesenchymal transition and cell migration in AFG1-induced lung adenocarcinoma.

These findings revealed the role of forkhead box M1 upregulation by manganese superoxide dismutase overexpression in maintaining lung cancer stem-like cell properties. Therefore, inhibition of forkhead box M1 upregulation by manganese superoxide dismutase overexpression may represent an effective therapeutic strategy for non-small cell lung cancer.

miR-330-3p promoted metastasis of lung cancer cells by suppressing hSOD2b expression and unveiled a new clinical application of miR-330-3p in the therapy of lung cancer.