Background: Quercetin is a flavonoid found ubiquitously in nature. Studies in vitroand in vivohave suggested that quercetin may have a protective role against colon cancer. Methods: We selected the human colon cancer cell line RKO to investigate the effects of quercetin in vitro. RKO cells were treated with different concentrations of quercetin. Results: In comparison to the control, quercetin was able to inhibit the growth of RKO cells, as measured using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Untreated RKO cells demonstrated almost complete methylation of the p16INK4a gene. Hypermethylation of the p16INK4a gene was successfully reversed after 120 h of treatment with quercetin. Expression of the p16INK4a gene was restored in a concentration-dependent manner. Conclusion: All these data suggest that quercetin has antitumor properties, probably via demethylation of the p16INK4a gene promoter.
CITED2 was identified as a cardiac transcription factor which is essential to the heart development. Cited2-deficient mice showed cardiac malformations, adrenal agenesis and neural crest defects. To explore the potential impact of mutations in CITED2 on congenital heart disease (CHD) in humans, we screened the coding region of CITED2 in a total of 700 Chinese people with congenital heart disease and 250 healthy individuals as controls. We found five potential disease-causing mutations, p.P140S, p.S183L, p.S196G, p.Ser161delAGC and p. Ser192_Gly193delAGCGGC. Two mammalian two-hybrid assays showed that the last four mutations significantly affected the interaction between p300CH1 and CITED2 or HIF1A. Further studies showed that four CITED2 mutations recovered the promoter activity of VEGF by decreasing its competitiveness with HIF1A for binding to p300CH1 and three mutations decreased the consociation of TFAP2C and CITED2 in the transactivation of PITX2C. Both VEGF and PITX2C play very important roles in cardiac development. In conclusion, we demonstrated that CITED2 has a potential causative impact on congenital heart disease.
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