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Effects Of Arsenic On HELF Cell’s β-catenin, Axin,C-myc Gene MRNA Expression

Posted on:2015-08-23Degree:MasterType:Thesis
Country:ChinaCandidate:B L ChenFull Text:PDF
GTID:2284330434961325Subject:Public health
Abstract/Summary:PDF Full Text Request
Objective:In order to understand arsenic exposure on the incidence of lung cancer, lung oxidative stress and the changes of WNT signal pathway, which provides new ideas for the further understanding of the pathogenic mechanism of arsenic. Method:In order to find out the effect of arsenic exposure on lung cancer meta analysis were used. The cells of experimental were used, cell morphology change by using microscope, cell growth change by useing MTT methods, alterations in oxidative stress by detect kit; cell cycle, cell apoptosis was detected by using flow cytometry; mRNA expression by using reverse transcription PCR. Results:(1) Meta analysis found that arsenic exposure increases the risk of lung cancer (OR=2.19,95%CI=1.60-3.01);(2) arsenic exposure can makes cell morphology changes, cell deformation and nucleus becomes larger;(3) arsenic exposure dose or time increase can cause the cell inhibition rate increased;(4) compared with the control group, the concentration ratio of the sodium arsenite exposure of HELF cells in G2+M phase were increased; HELF cell percentage of G2+M phase in the exposure of24,48h were decreased.(5) HELF apoptosis ratio in the exposure of24,48,72h were positively correlated with Aresinc concentration (24h:r=0.927, P<0.05;48h: r=0.921, P<0.05,72h:r=0.989, P<0.05).(6) After exposure for24,48,72h, superoxide dismutase were decreased (P<0.05); the cell active oxygen were increased (P<0.05); the GSH-PX concentration decreased (P<0.05).(7) Compared with the control group, the concentration of sodium arsenite exposure of24,48,72h after intracellular expression of mRNA p-catenin were decreased (P<0.05); the expression of Axin in mRNA cells were increased (P<0.05); the expression of C-myc in mRNA cells were decreased (P<0.05) Conclusion:Arsenic exposure increased relative risk of lung cancer. The mechanism of arsenic induced pulmonary lesion and WNT/beta-catenin pathway inhibition has certain relevance, research shows, WNT/beta-catenin path way maybe the underline mechanism of cell differentiation, replication and cell cycle and apoptosis.
Keywords/Search Tags:Arsenic, lung cancer, beta catenin signaling pathway, WNT, cell cycle, apoptosis, human embryonic hmg fibroblasts
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