Aim: Evolution of gene expression change of intestine tissue in celiac patients to find a new molecular prospective of disease is the aim of this study. Background: Celiac disease (CD) as an autoimmune disease is known as an immune reaction response to the gluten in patients. It is reported that genetic and environmental conditions are important in onset and progress of CD. Methods: gene expression profiles of intestinal tissue in 12 celiac patients and 12 healthy controls from gene expression omnibus (GEO) were downloaded and verified by boxplot analysis. The significant and selected differentially expressed genes (DEGs) were included protein-protein interaction (PPI) network analysis. The central nodes were identified by network analyzer. Results: The network was constructed from 161 query DEGs and 50 additional neighbors. GTF2H1, VEGFA, SUMO1, RAD51, MED21, BBP4, LEP, and MAP2K7 as potent hub nodes LRP5, RABGEF1, BCAS2, DYRK1B, AOC3, RABL2A, CRTAP, VEGFA, and SPOPL as potent bottlenecks are introduced as crucial nodes. Conclusion: Among the crucial DEGs, Vascular endothelial growth factor A (VEGFA) was highlighted as an important biomarker candidate for follow up of celiac patients.

Angiogenesis is closely related to the development and progression of hepatocellular carcinoma (HCC). Angiogenic factors have been confirmed to be overexpressed in HCC. The hepatitis B virus preS2 domain is a transactivator that plays an important role in hepatitis B virus (HBV)-related HCC. Here, we aimed to investigate the potential of the preS2 domain in inducing angiogenesis in HCC. A total of 25 cases of pathologically confirmed HCC were screened. The levels of preS2, CD34, and vascular endothelial growth factor A (VEGFA) inHCCsamples were evaluated by immunohistochemistry (IHC). The proliferation of vascular endothelial cells was detected by CCK-8. Besides, VEGFA was analyzed by Western blot in HCC cells. The effect of preS2 on the VEGFA promoter was measured by dual-luciferase reporter assays. We found that preS2 domain-positive HCCs had significantly higher microvessel density (MVD) and VEGFA expression than preS2 domain-negative HCCs. Overexpression of preS2 upregulated VEGFA expression in HepG2 and activated vascular endothelial cell proliferation. However, blocking preS2 expression reduced VEGFA expression in HepG2. 2. 15 and inhibited the proliferation of vascular endothelial cells. In addition, a dual-luciferase assay indicated that the preS2 domain could activate VEGFA promoter activity. In conclusion, we showed that the expression of the preS2 domain promotes angiogenesis by transactivating the VEGFA promoter in HCC.