ABSTRACT
<p><b>INTRODUCTION</b>We aimed to examine the turnover of chronic atrophic gastritis (CAG) pathologically and endoscopically and explore its potential causes.</p><p><b>METHODS</b>A retrospective analysis was conducted of prospective data collected from 1,592 patients who underwent gastroscopy three times or more during the period 1985-2009 at Renji Hospital, Shanghai, China. Pathological and endoscopic findings were analysed. Data collected included gender, age, length of follow-up period, family history, past medical history, history of Helicobacter (H.) pylori infection, drug history for the use of proton pump inhibitors (PPIs), antacids and non-steroidal anti-inflammatory drugs [NSAIDs], and lifestyle history, including the patients' eating habits.</p><p><b>RESULTS</b>23 (1.44%) patients presented with gastric cancers resulting from CAG and 349 (21.92%) patients had dysplasia. Pathological and endoscopic findings suggested that the proportion of patients with worsening gastric mucosa during the atrophic and intestinal metaplasia (IM) phases was over 35% with increasing age. Gastric mucosa was found to be pathologically aggravated by carbonated drinks and fast food, and pathologically degenerated by H. pylori infection. Smoking deteriorated the gastric mucosa. Side dishes of vegetables may benefit the gastric mucosa even in the atrophic and IM phases.</p><p><b>CONCLUSION</b>Our findings support the consensus that CAG is a progressive disease. Potential factors that were found to affect the state of the gastric mucosa in our patient group were gender, H. pylori infection, use of PPIs or NSAIDs, and intake of vegetable side dishes, spicy food, carbonated drinks and fast food.</p>
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Age Distribution , Biopsy , China , Epidemiology , Disease Progression , Follow-Up Studies , Gastric Mucosa , Pathology , Gastritis, Atrophic , Diagnosis , Epidemiology , Gastroscopy , Medical Records , Morbidity , Prognosis , Retrospective Studies , Severity of Illness Index , Sex Factors , Time FactorsABSTRACT
<p><b>OBJECTIVE</b>To evaluate the effect of PKC-delta inhibitor Rottlerin on human colon cancer cells and its mechanism.</p><p><b>METHODS</b>Human colon cancer cell line SW1116 cells were treated with Rottlerin. The transcriptional level of DNA methyltransferase (Dnmt)1, Dnmt3a and Dnmt3b was detected by real-time RT-PCR. Cell cycle distribution was evaluated by flow cytometry (FCM). In addition, cellular morphological changes were examined by light microscopy.</p><p><b>RESULTS</b>PKC-delta inhibitor decreased the expression of Dnmt1, Dnmt3a mRNA, up-regulated APC, p21(WAF1) and p16(INK4A) mRNA. Demonstarted by flow cytometry, Rottlerin increased the percentage of cell cycle G0/G1 phase cell numbers (P = 0.02) and decreased the percentage of cell cycle G2/M phase cell numbers (P = 0.01). Remarkable changes of cellular morphology were observed under light microscope: The volume and cytoplasm of cells treated with Rottlerin were increased. The cell contour was not very clear, and mitotic figures were less frequently seen.</p><p><b>CONCLUSION</b>PKC-delta inhibitor Rottlerin inhibites cell division and proliferation of the colon cancer SW1116 cells through regulating DNA methylation and blocking the signaling pathway of mitogen-activated protein kinase (MAPK).</p>
Subject(s)
Humans , Acetophenones , Pharmacology , Adenomatous Polyposis Coli Protein , Genetics , Benzopyrans , Pharmacology , Cell Cycle , Cell Line, Tumor , Cell Proliferation , Colonic Neoplasms , Genetics , Metabolism , Pathology , Cyclin-Dependent Kinase Inhibitor p16 , Genetics , Cyclin-Dependent Kinase Inhibitor p21 , Genetics , DNA (Cytosine-5-)-Methyltransferase 1 , DNA (Cytosine-5-)-Methyltransferases , Genetics , Flow Cytometry , Gene Expression Regulation, Neoplastic , Protein Kinase C-delta , RNA, Messenger , Genetics , Metabolism , Reverse Transcriptase Polymerase Chain Reaction , Signal TransductionABSTRACT
Objective To analyze the effect of eukaryotic plasmids containing wild (sense) or anti- sense methylenetetrahydrofolate reductase (MTHFR) gene on cell viability and transcription level of tumor related genes in human gastric cancer cell line.Methods Human gastric cancer cell line MKN-45 was cultured.Recombinant plasmids containing wild MTHFR (W) or antisense MTHFR (A) gene, pCMV-W and pCMV-A,were constructed.Then pCMV-W,pCMV-A and pCMV blank plasmid were transfected into MKN45 cells respectively by using lipofect.Cell viability was analyzed by 3-(4,5-bime- thylthiazolyl-2)-2,5-diphenyhetrazolium dromide(MTT).The transcription levels of Dnmt 1,c-myc, p21~(WAF1) and hMLH1 genes were detected by real-time polymerase chain reaction(PCR).Results Cell vi- ability remarkably increased in those transfected with wild MTHFR (P＜0.01),which was contrary to those transfected with antisense MTHFR(P＜0.01).The expression of those tumor related genes mRNAs were all remarkably decreased in the MKN45-W cells in comparison with those in the MKN45-pCMV cells.No significant difference in the expressions of those tumor related genes mRNAs were found between the MKN45 cells transfected with pCMV-A and blank pCMV.Conclusion MTHFR influences cell viability and the expres- sion level of tumor related genes in human gastric cancer cell line MKN45.