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Articles by H. Y Chung
Total Records ( 2 ) for H. Y Chung
  J. G Kim , S. K Sohn , Y. S Chae , J. H Moon , S. N Kim , B. W Kang , G. C Kim , M. H Lee , S. W Jeon , H. Y Chung and W. Yu
  Objective

The present study analyzed the functional insertion/deletion polymorphism in the promoter region of NFKB1 gene and their impact on the prognosis for patients with gastric adenocarcinoma.

Methods

Four hundred and seventy two consecutive patients with curatively resected gastric adenocarcinoma were enrolled in the present study. The genomic DNA was extracted from paraffin-embedded tissue and the –94 insertion/deletion ATTG polymorphism of NFKB1 determined using a polymerase chain reaction–restriction fragment length polymorphism assay.

Results

The NFKB1 promoter gene polymorphism was successfully amplified in 97.8% of the cases. There were no sexual differences in relation to the genotype and allele. No correlation was observed between the frequency of the genotype or allele and the T, N or M stage. The multivariate survival analysis showed no association between the NFKB1 –94 insertion/deletion promoter polymorphism and the disease-free survival or overall survival of the patients with gastric cancer.

Conclusions

The functional NFKB1 promoter polymorphism was not found to be a prognostic marker for Korean patients with surgically resected gastric adenocarcinoma.

  A. Y Kim , Y. S Lee , K. H Kim , J. H Lee , H. K Lee , S. H Jang , S. E Kim , G. Y Lee , J. W Lee , S. A Jung , H. Y Chung , S Jeong and J. B. Kim
 

In obesity, dysregulation of adipocytokines is involved in several pathological conditions including diabetes and certain cancers. As a member of the adipocytokines, adiponectin plays crucial roles in whole-body energy homeostasis. Recently, it has been reported that the level of plasma adiponectin is reduced in several types of cancer patients. However, it is largely unknown whether and how adiponectin affects colon cancer cell growth. Here, we show that adiponectin suppresses the proliferation of colon cancer cells including HCT116, HT29, and LoVo. In colon cancer cells, adiponectin attenuated cell cycle progression at the G1/S boundary and concurrently increased expression of cyclin-dependent kinase inhibitors such as p21 and p27. Adiponectin stimulated AMP-activated protein kinase (AMPK) phosphorylation whereas inhibition of AMPK activity blunted the effect of adiponectin on the proliferation of colon cancer cells. Furthermore, knockdown of adiponectin receptors such as AdipoR1 and AdipoR2 relieved the suppressive effect of adiponectin on the growth of colon cancer cells. In addition, adiponectin repressed the expression of sterol regulatory element binding protein-1c, which is a key lipogenic transcription factor associated with colon cancers. These results suggest that adiponectin could inhibit the growth of colon cancer cells through stimulating AMPK activity.

 
 
 
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