TO901317 suppresses FOXM1 expression and proliferation in HepG2 cells
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TO901317 suppresses FOXM1 expression and proliferation in HepG2 cells
Journal of Army Medical UniversityVol. 33, Issue 22, Pages: 2345-2348(2011)
作者机构:
第三军医大学基础医学部生物化学与分子生物学教研室
作者简介:
基金信息:
DOI:
CLC:R394.3;R735.7;R730.23
Published:2011,
Published Online:30 November 2011,
稿件说明:
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HU CHANGJIANG, ZHANG YAN, HUANG GANG, et al. TO901317 suppresses FOXM1 expression and proliferation in HepG2 cells. [J]. Journal of army medical university, 2011, 33(22): 2345-2348.
DOI:
HU CHANGJIANG, ZHANG YAN, HUANG GANG, et al. TO901317 suppresses FOXM1 expression and proliferation in HepG2 cells. [J]. Journal of army medical university, 2011, 33(22): 2345-2348.DOI:
TO901317 suppresses FOXM1 expression and proliferation in HepG2 cells
Objective To investigate the effect of treatment of live X receptors specific agonist TO901317 on the expression of FOXM1 and the cell cycle and proliferation in HepG2 cells. Methods HepG2 cells were treated for 24 h with DMSO and 0.5 or 5 μmol/L TO901317.
RT-PCR and Western blotting was taken to detect the FOXM1 expression at mRNA and protein levels. Cell cycle analysis was examined by flow cytometry and cell proliferation was determined by cell counting kit-8 (CCK-8). Results FOXM1 mRNA and protein expression were remarkably reduced after the treatment of TO901317 at different concentrations (
P
<
0.05). The percentage of cells at G
1
stage were (61.32±2.36)% and (70.40±4.65)% respectively after 0.5 and 5 μmol/L TO901317 treatment
significantly higher than that of the control group (
P
<
0.05). The OD value at 450 nm was 1.25±0.09 and 1.06±0.06 respectively after 0.5 and 5 μmol/L TO901317 treatment
significantly lower than the control group (1.53±0.07
P
<
0.05). TO901317 notablely inhibited the HepG2 cells proliferation. Conclusion TO901317 could suppress HepG2 proliferation and induce cell arrest at G
1
cycle in a does-dependent manner
and it may be result from the downregulation of FOXM1
which is one of the key transcription regulators of cell cycle proteins.
Dihydromyricetin improves triglyceride accumulation in HepG2 cells by regulating SIRT1 signaling pathway
Mibefradil improves insulin-resistance HepG2 cells by down-regulating FoxO1 expression
Resveratrol improves lipid droplet lipolysis via up-regulating PKA-PLIN2 pathway in HepG2 cells
CD36 knockdown alleviates lipid accumulation induced by tumor necrosis factor-α and interleukin-6 in HepG2 cells
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Related Institution
Department of Biochemistry and Molecular Biology, College of Basic Medical Sciences, Army Medical University (Third Military Medical University)
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State Key Laboratory of Trauma, Burns and Combined Injury, Department 1, Institute of Surgery Research, Daping Hospital, Third Military Medical University
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Department for Nutrition and Food Safety, Chongqing Center of Medical Nutrition, Chongqing Key Laboratory of Nutrition and Food Safety, College of Military Preventive Medicine, Third Military Medical University