An let-7 KRAS rs712 polymorphism increases hepatocellular carcinoma risk

KRAS, also known as V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog, acts as an intracellular signal transducer. The oncogenic KRAS mutation is an essential step in the development of many types of human cancers, including hepatocellular carcinoma. Here we aimed to investigate the relationship between KRAS rs712 polymorphisms and hepatocellular carcinoma susceptibility. Five-hundred-and-fourteen participants were enrolled in a case-control study (262 cases and 252 normal subjects). The variants were distinguished using polymerase chain reaction-restriction fragment length polymorphism. Significantly increased HCC risk was observed to be associated with the T allele of the rs712 locus (P = 0.049, OR = 1.35, 95%CI = 1.01-1.78). Further, HCC risk with the GT genotype (P = 0.015, OR = 1.64, 95%CI = 1.08-2.50) and the TT genotype (P = 0.015, OR = 2.56, 95%CI = 1.05-6.25) in a codominant model was significantly higher than that with the GG genotype. In a dominant model, significantly increased HCC susceptibility was also associated with T allele carriers (P = 0.006, OR = 1.75, 95%CI = 1.16-2.63). Moreover, we found that the frequency of the KRAS rs712 TT genotype was significantly higher in HBV-positive HCC patients than in HBV-negative HCC patients.