Genetic polymorphism of the kinesin-like protein KIF1B gene and the risk of hepatocellular carcinoma

PLoS One. 2013 Apr 25;8(4):e62571. doi: 10.1371/journal.pone.0062571. Print 2013.

Abstract

Background: Frequent deletions of the kinesin-like protein gene 1B (KIF1B) have been reported in neural tumors. Recently, a genome-wide association study revealed an association between polymorphisms in the KIF1B gene and the risk of hepatocellular carcinoma (HCC), and several case-control studies have further investigated this relationship. However, these studies have yielded controversial results. We therefore performed a meta-analysis to derive a more precise estimation of the association between the KIF1B gene polymorphisms and HCC risk.

Methodology/principal finding: PubMed, EMBASE, the ISI Web of Science and the CNKI databases were systematically searched to identify relevant studies. A total of 5 studies containing 13 cohorts with 5,773 cases and 6,404 controls were included. Odds ratios (ORs) with corresponding 95% confidence intervals (CIs) were used to assess the strength of the associations. Subgroup analyses were conducted based on ethnicities, sample sizes and quality scores. Overall, the G allele at rs17401966 of the KIF1B gene was associated with a significantly decreased risk for HCC (OR = 0.81, 95%CI: 0.70-0.93; P = 0.003). Furthermore, subgroup analyses showed that the G allele at rs17401966 of the KIF1B gene significantly reduced the risk for HCC in Chinese cohorts (OR = 0.76, 95%CI: 0.64-0.90; P = 0.002), large-sample-size cohorts (OR = 0.80, 95%CI: 0.73-0.88, P<0.01) and high-quality cohorts (OR = 0.78, 95%CI: 0.71-0.87, P<0.01). However, no significant associations were found in small-sample-size cohorts, studies with low-quality scores and when excluding the cohorts from the study reporting the original discovery.

Conclusion/significance: These findings demonstrate that the presence of the G allele at rs17401966 of the KIF1B gene may decrease the risk for HCC and suggest that KIF1B may play a critical role in the development of HCC. High-quality studies with larger sample sizes and different ethnic populations will be of great value to further confirm these findings.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Carcinoma, Hepatocellular / enzymology*
  • Carcinoma, Hepatocellular / genetics*
  • Cohort Studies
  • Genetic Predisposition to Disease / genetics*
  • Humans
  • Kinesins / genetics*
  • Liver Neoplasms / enzymology*
  • Liver Neoplasms / genetics*
  • Polymorphism, Genetic*

Substances

  • KIF1B protein, human
  • Kinesins

Grants and funding

This work was supported by the Major Program of NSFC (No.81030038), National Key Sci-Tech Project (2012ZX10002011-002), China National Funds for Distinguished Young Scientists (No. 812250125), National Natural Science Foundation of China (Nos. 81071992, 81272725), FANEDD (No. 201183), the Fok Ying-Tong Education Foundation (No. 132029). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.