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Aims: To investigate the impact of AdipoQ polymorphisms, and their additional interactions with smoking and drinking on coronary heart disease (CHD) risk based on Chinese population. Methods: Hardy‒Weinberg equilibrium (HWE) was performed using SNPStats (available online at http://bioinfo.iconcologia.net/SNPstats). Generalized multifactor dimensionality reduction (GMDR) model was used to screen the best gene‒gene and gene‒environment interaction combinations. Logistic regression was performed to investigate association between four single-nucleotide polymorphisms (SNPs) and CHD and the interaction effect between rs1501299 and smoking. Results: Logistic analysis showed that CHD risks were higher in carriers with homozygous mutant of rs1501299 and rs2241766 than those with wild-type homozygotes, odds ratio (ORs) (95%CI) were 1.49 (1.19–1.95) and 1.71 (1.33–2.24), respectively, but CHD risks were lower in carriers with homozygous mutant of rs7649121 than those with wild-type homozygotes, OR (95%CI) was 0.72 (0.51–0.96). GMDR model indicated that there was a significant two-locus model (p = 0.0107) involving rs1501299 and current smoking, indicating a potential gene–environment interaction between rs1501299 and current smoking. Overall, the cross-validation consistency of this model was 9/10, and the testing accuracy was 60.11% (p = 0.0010). T-allele carriage had 42% prevalence, and one-quarter of them were current smokers. Smokers with rs1501299-GT or TT genotype have the highest CHD risk, compared to never-smokers with rs1501299-GG genotype, OR (95%CI) was 3.56 (1.91–5.42), after adjustment for gender, age, alcohol status, and body mass index. But we did not find any significant gene–gene and gene–drinking interaction combinations in GMDR models. Conclusions: Polymorphisms in rs1501299 and rs2241766, and their additional interactions between rs1501299 and smoking were associated with increased CHD risks: polymorphism in rs7649121 was associated with decreased CHD risks.

Nestin, a member of type VI intermediate filament protein family, is widely expressed in mammalian nervous tissue and stem/precursor cells of non-neuronal normal tissues. Nestin has also been investigated to determine possible tumor-promoting functions. However, whether Nestin is involved in colorectal cancer (CRC) cells remains unclear. In this report, Nestin expression was upregulated in stromal cells of human CRC tissues. Endogenous Nestin expression in CRC cell lines SW480 and HCT116 was knocked down by a lentivirus. MTT and colony formation assays revealed that Nestin deletion significantly inhibits the proliferation of CRC cell lines; flow cytometer analysis showed that Nestin deletion causes cell cycle arrest at S phase. Transwell chamber and wound healing scratch assays also revealed that Nestin deletion suppresses cell migration. Our findings indicated that Nestin plays an essential role in CRC progression; thus, Nestin can be applied as a therapeutic target of CRC.