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The Effection of Arsenic Trioxide in Human Lung Adenocarcinoma A549 Cell Line Proliferation and c-Myc Gene Expression
Author: HeXiaoLong
Tutor: MaBaiLin
School: Yan'an University
Course: Respiration within the science
Keywords: Arsenic trioxide As2O3 Human lung adenocarcinoma A-549 cell line Cell Cycle Apoptosis c-Myc gene
CLC: R734.2
Type: Master's thesis
Year: 2011
Downloads: 21
Quote: 0
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Abstract
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Objective: To observe arsenic trioxide (As 2 O 3 ) on the growth of human lung adenocarcinoma cell line A-549, proliferation, cell cycle, apoptosis and other aspects of the impact and to explore its mechanism. Methods: The human lung carcinoma A-549 cell line for cell culture, take the logarithmic growth phase cells, set the negative control group, treated with different concentrations of As 2 O 3 the role of a certain period of time after trypan blue staining, light microscope counting, describing the cell growth curve, calculate the cell population doubling time; MTT assay cell growth and proliferation inhibition rate; cell cycle was determined by flow cytometry (FCM) (CC ), apoptosis rate; inverted phase contrast microscope dynamic observation of morphological changes of the A-549 cells; immunohistochemistry (SABC) analysis the different concentrations As 2 O 3 c-Myc gene expression. Results: As 2 O 3 on the in vitro growth of human lung adenocarcinoma A-549 cell line growth and proliferation was significantly inhibited, this effect is a time-and dose-dependent manner (- efficiency and dose - response relationship); As of 2 O 3 A-549 cell cycle regulation: 0.5μmol/LAs 2 sub > the O 3 the role of A-549 cells after 72 hours of S phase arrest, but p gt; 0.05, with the control group was not statistically significant; 1.0,2.0,4.0 μmol / L As the 2 the O 3 group performance of the target cells for the G 2 / M-phase arrest, ie the G 2 / M phase increased with the control group was statistically significant (p lt; 0.05), but no significant difference between the two groups; 8.0μmol/LAs 2 O 3 group , results are presented in S phase, p lt; 0.05. As 2 O 3 A-549 cell growth and proliferation, different concentrations of group performance for the induction of apoptosis or necrosis induced by 0.5 micromol / L group no significant wither apoptosis and necrosis, compared with the control group, no significant difference; 1.0, 2.0, 4.0 mol / L As 2 O 3 the role of A-549 cells after induction of apoptosis, apoptosis rate in this concentration range with the concentration increases; 8.0μmol / L induced necrosis. Different dose groups As 2 O 3 has a downward effect on the A-549 cells c-Myc gene expression, the amount of 0.5 to 4.0μmol / L concentration groups - effect relationship, p lt; of 0.01,4.0 mol / L most significant decline in 8.0μmol / L and 4.0μmol / L group no significant difference (p GT; 0.05) Conclusion: arsenic trioxide on the growth of human lung adenocarcinoma cell line A-549, significantly inhibited the proliferation and cell cycle regulation, in 1.0 to 4.0μmol / L concentration range of inhibition mechanism pro-apoptotic initial suggesting that induction of apoptosis is the inhibition of c-Myc gene expression, indicating As 2 O 3 is a valuable role in the anti-lung cancer drug. We believe that 0.5 to 4.0μmol / L concentration is the As 2 O 3 in vivo experiments safe and effective range to fully carry out the toxic effects observed in the safe range, changing the dosage form and to drug, and in combination with other classic chemotherapy drugs is the focus and direction of future research.
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CLC: > Medicine, health > Oncology > Respiratory system tumors > Lung tumors
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