05). Conclusion: ①

Smad4 gene promoter hypermethylation was Participate in esophageal cancer both in Kazak esophageal cancer and Han nationality esophageal cancer and may be used as diagnostic markers. ② Smad4 gene promoter hypermethylation in CpG Unit 15 may connected with the Kazakh esophageal cancer. Hypermethylation Deforolimus price in CpG units 1, units 16–19, units 27–28, units 31–33 may be the early events and connected with the Kazakh esophageal cancer. Smad4 gene promoter hypermethylation in CpG Unit 6, Unit 16–19 may the reason that High incidence of Kazakh esophageal cancer than Han nationality esophageal cancer. Key Word(s): 1. Han nationality; 2. Kazak; 3. smad4 gene; 4. esophageal cancer; Presenting Author: YANXIANG LV Additional Authors: SHUHUI LIANG, QIN ZHANG, QUANXIN FENG, SHUJUN LI, KAICHUN WU, JIE DING Corresponding Author: SHUHUI LIANG, JIE DING Objective: To investigate the mechanisms of angiogenesis inhibition

of GEBP11 in gastric cancer. Methods: The cellular mechanisms of angiogenesis inhibition of GEBP11 were clarified by proliferation assay, cellular cycle and apoptosis analysis, invasion and migration assay and adherence assay. The differential expression genes in Co-HUVECs treated by GEBP11 or not were screened by microarray to explore the molecular mechanisms, and verified by RT-PCR and Western blot. Results: Proliferation assay, cellular cycle and apoptosis analysis, invasion and migration assay and adherence assay showed that GEBP11 could inhibit the proliferation of Co-HUVECs APO866 and HUVECs, induce the apoptosis most of ECs, but not alter the cell cycle

of ECs. Additionally, GEBP11 appeared to inhibit the ECM degradation, migration and adhere of ECs. Microarray revealed that there were 1202 down-regulated genes and 2104 up-regulated genes in Co-HUVECs treated by GEBP11. And there were 579 down-regulated genes and 194 up-regulated genes in Co-HUVECs vs. HUVECs. Some expression changes which induced by co-culture were reversed after peptide treatment. For example, the expression of MMP1, CDH11, TNFSF18, VCAM1 was up-regulated 5, 2.5, 2, 4 times respectively by co-culture, and then down-regulated 32, 21, 16, 4 times respectively after peptide treatment. PT-PCR showed that the expression of MMPs, CXCR4, CAMs, IL18, KDR were down-regulated in Co-HUVECs treated by GEBP11 on transcriptional level. The expression of MMPs, KDR, Bcl-2/Bax were down-regulated on protein level which was confirmed by western-blot. Conclusion: GEBP11 may come true its inhibition effects on the proliferation, invasion, migration and adherence of ECs and induce apoptosis by down-regulate the expression of MMPs, CAMs, KDR, Bcl-2/Bax, and realize its angiogenesis inhibition function finally. Key Word(s): 1. Gastric cancer; 2. Angiogenesis; 3. GEBP11; 4.