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Study of Helicobater Pylori Related Genes of Gastric Cancer by Comparative Genomic Profiling

Author: WangFen
Tutor: ShenShouRong
School: Central South University
Course: Internal Medicine
Keywords: Helicobacter pylori Gastric cancer Human gastric epithelial cells Microarray Immunohistochemistry
CLC: R735.2
Type: PhD thesis
Year: 2011
Downloads: 167
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The incidence of gastric cancer in China ranks second in the various types of malignant tumors, diseases of serious harm to people's health. Since the 1980s, the population has a higher rate of infection of Helicobacter pylori (Helicobacter pylori, Hp) and gastric cancer has received extensive attention. Epidemiological confirmed, Hp chronic infection is one of the important risk factors lead to gastric cancer and gastric cancer development is closely related to the infected population risk of stomach cancer is four times higher than non-infected. Most studies have shown that chronic gastritis - gastric atrophy - intestinal metaplasia - dysplasia - Cancer \1998 Watanabe et al first reported the Hp infected Mongolian gerbils can occur gastric Hp infection may induce gastric direct evidence. In 1994, the World Health Organization International Research on Cancer (IARC) in Hp classified as a class I carcinogen of gastric cancer. Hp cause gastric mechanism has not yet been fully elucidated. The incidence of gastric cancer is more than one cause of the multi-stage process, Hp infection, the outcome may occur with chronic gastritis may also be the development of gastric cancer. Tip different strains may have different effects on gastric epithelial cells, resulting in varying degrees of disease. In this experiment, clinical isolates from gastric cancer, patients with gastritis strains of the 10 cases, respectively the proportion of different concentrations and GES-1 cells co-cultured, 12h, 24h and 48h, respectively, after the cells were harvested, MTT and flow cytometry. The results show that HP strains of different sources GES-1 cells in proliferating with significant difference between the low concentration broth can be different degrees to promote cell proliferation, high concentrations of bacterial suspension to the activity of inhibiting cell proliferation, and, with time, The low concentration broth promote cell proliferation gradually increased, the high concentration of liquid on the cell proliferation inhibition is more obvious. The Hp strains of different diseases can cause gastric epithelial cell apoptosis rate increase, but no difference between the groups was significant. With the extension of time and bacterial concentration increased, Hp strains promote gastric epithelial cell apoptosis is more significant. The proliferation of GES-1 cells were selected the most significant and a minimum of two Hp strains, respectively, and GES-1 cells co-cultured cells were harvested and RNA extraction product with whole genome microarray hybridization for statistical analysis. Hp infection GES-1 cells induced gastric epithelial cell gene expression profiles vary widely, these differences in expression of the activation or deactivation of the gene with the original oncogenes and tumor suppressor genes, cell cycle, cytoskeleton and movement, apoptosis , DNA synthesis, transcription, cell signaling, protein translation, material and energy metabolism, and other process-related. Screened closely associated with the development of tumor genes, such as TRAF1, HDAC6, ETS1, JUN, JUNB, CLDN1, CXCL2, IL-8, IRAK2 NUPR1 STC2, TP53BP1, TNFAIP3, DIO2 and SR protein family, for the next step of gene expression validation and biological function study provides new clues. Gene chip results to pick travel heterosexual larger and higher research significance, Hp-related gastric cancer pathogenesis has not been reported in the two genes: TRAF1 and HDAC6. Will be selected on the proliferation of GES-1 cells the most significant and the smallest two Hp strains, respectively, and GES-1 cells co-cultured, compared with a blank group divided into a control group, gastritis and gastric cancer groups, a total of after 24 hours incubation. The cells are harvested to extract the RNA product, reverse transcriptase cDNA by RT-PCR, and found that TRAF1 and HDAC6 were enhanced expression in the control group, gastritis, gastric cancer group, consistent with the results of the gene chip. Use taken from clinical infection with Hp chronic superficial gastritis, atrophic gastritis (pathologic examination showed intestinal metaplasia, dysplasia) and patients with gastric cancer specimens were detected by immunohistochemistry. The results showed that TRAF1 and HDAC6 in chronic superficial gastritis, intestinal metaplasia, dysplasia and gastric cancer tissues expression were enhanced; prompted TRAF1 and HDAC6 may be involved in Hp infection leads to chronic superficial gastritis, atrophic gastritis, gastric occurrence of the development process, and provide new clues to clarify the Hp induced molecular mechanism of gastric cancer, and gastric cancer molecular markers.

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CLC: > Medicine, health > Oncology > Gastrointestinal Cancer > Gastric neoplasms
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