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Effects of 17-AAG on the cell cycle and apoptosis of H446 cells and the associated mechanisms.

Zhao X, Wang J, Xiao L, Xu Q, Zhao E, Zheng X, Zheng H, Zhao S, Ding S - Mol Med Rep (2016)

Bottom Line: As a heat shock protein 90 inhibitor, 17-allylamino-17‑demethoxygeldanamycin (17-AAG) has been studied in numerous types of cancer, however the effects of 17-AAG on apoptosis and the cell cycle of H446 cells remain unclear.With treatment of 3.125, 6.25 and 12.5 mg/l 17‑AAG for 48 h, significant apoptosis and cell cycle arrest was observed.The results indicated that the gene and protein expression levels of STAT3, survivin and cyclin D1 were downregulated, and cyt‑C, caspase 9 and caspase 3 were upregulated by 17‑AAG in a dose-dependent manner when the cells were treated with 3.125 and 6.25 mg/l 17-AAG for 48 h.

View Article: PubMed Central - PubMed

Affiliation: Department of Immunology, Chengde Medical University, Chengde, Hebei 067000, P.R. China.

ABSTRACT
As a heat shock protein 90 inhibitor, 17-allylamino-17‑demethoxygeldanamycin (17-AAG) has been studied in numerous types of cancer, however the effects of 17-AAG on apoptosis and the cell cycle of H446 cells remain unclear. In the current study, the MTT method was used to evaluate the inhibitory effects of different durations and doses of 17‑AAG treatment on the proliferation of H446 cells. The cells were stained with Annexin-fluorescein isothiocyanate/propidium iodide and measured by flow cytometry, and the gene and protein expression levels of signal transducer and activator of transcription 3 (STAT3), survivin, cyclin D1, cyt‑C, caspase 9 and caspase 3 were determined by reverse transcription‑quantitative polymerase chain reaction and western blot analysis. The results indicated that with treatment with 1.25‑20 mg/l 17‑AAG for 24 and 48 h, significant inhibition of H446 cell proliferation was observed in a time‑ and dose‑dependent manner. With treatment of 3.125, 6.25 and 12.5 mg/l 17‑AAG for 48 h, significant apoptosis and cell cycle arrest was observed. The results indicated that the gene and protein expression levels of STAT3, survivin and cyclin D1 were downregulated, and cyt‑C, caspase 9 and caspase 3 were upregulated by 17‑AAG in a dose-dependent manner when the cells were treated with 3.125 and 6.25 mg/l 17-AAG for 48 h. The results indicated that 17‑AAG is able to inhibit the cell proliferation, induce apoptosis and G2/M arrest and downregulate the gene and protein expression levels of STAT3, survivin and cyclin D1, and upregulate gene and protein expression of cyt‑C, caspase 9, caspase 3.

No MeSH data available.


Related in: MedlinePlus

Inhibitory effects of different concentration of 17-AAG. 17-AAG, 17-allylamino-17-demethoxygeldanamycin.
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f2-mmr-14-02-1067: Inhibitory effects of different concentration of 17-AAG. 17-AAG, 17-allylamino-17-demethoxygeldanamycin.

Mentions: The MTT assay results indicated that 1.25~20 mg/l 17-AAG had a clear inhibitory effect on H446 proliferation, with a significant concentration-dependent correlation. The cell number of the drug groups was significantly less than in the control group, and abnormal morphology was observed (Fig. 1). The proliferation inhibition rate of 17-AAG on cells at 48 h (IC50, 12.61 mg/l) was higher than that at 24 h (IC50, 27.54 mg/l) (Table II, Fig. 2).


Effects of 17-AAG on the cell cycle and apoptosis of H446 cells and the associated mechanisms.

Zhao X, Wang J, Xiao L, Xu Q, Zhao E, Zheng X, Zheng H, Zhao S, Ding S - Mol Med Rep (2016)

Inhibitory effects of different concentration of 17-AAG. 17-AAG, 17-allylamino-17-demethoxygeldanamycin.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4940086&req=5

f2-mmr-14-02-1067: Inhibitory effects of different concentration of 17-AAG. 17-AAG, 17-allylamino-17-demethoxygeldanamycin.
Mentions: The MTT assay results indicated that 1.25~20 mg/l 17-AAG had a clear inhibitory effect on H446 proliferation, with a significant concentration-dependent correlation. The cell number of the drug groups was significantly less than in the control group, and abnormal morphology was observed (Fig. 1). The proliferation inhibition rate of 17-AAG on cells at 48 h (IC50, 12.61 mg/l) was higher than that at 24 h (IC50, 27.54 mg/l) (Table II, Fig. 2).

Bottom Line: As a heat shock protein 90 inhibitor, 17-allylamino-17‑demethoxygeldanamycin (17-AAG) has been studied in numerous types of cancer, however the effects of 17-AAG on apoptosis and the cell cycle of H446 cells remain unclear.With treatment of 3.125, 6.25 and 12.5 mg/l 17‑AAG for 48 h, significant apoptosis and cell cycle arrest was observed.The results indicated that the gene and protein expression levels of STAT3, survivin and cyclin D1 were downregulated, and cyt‑C, caspase 9 and caspase 3 were upregulated by 17‑AAG in a dose-dependent manner when the cells were treated with 3.125 and 6.25 mg/l 17-AAG for 48 h.

View Article: PubMed Central - PubMed

Affiliation: Department of Immunology, Chengde Medical University, Chengde, Hebei 067000, P.R. China.

ABSTRACT
As a heat shock protein 90 inhibitor, 17-allylamino-17‑demethoxygeldanamycin (17-AAG) has been studied in numerous types of cancer, however the effects of 17-AAG on apoptosis and the cell cycle of H446 cells remain unclear. In the current study, the MTT method was used to evaluate the inhibitory effects of different durations and doses of 17‑AAG treatment on the proliferation of H446 cells. The cells were stained with Annexin-fluorescein isothiocyanate/propidium iodide and measured by flow cytometry, and the gene and protein expression levels of signal transducer and activator of transcription 3 (STAT3), survivin, cyclin D1, cyt‑C, caspase 9 and caspase 3 were determined by reverse transcription‑quantitative polymerase chain reaction and western blot analysis. The results indicated that with treatment with 1.25‑20 mg/l 17‑AAG for 24 and 48 h, significant inhibition of H446 cell proliferation was observed in a time‑ and dose‑dependent manner. With treatment of 3.125, 6.25 and 12.5 mg/l 17‑AAG for 48 h, significant apoptosis and cell cycle arrest was observed. The results indicated that the gene and protein expression levels of STAT3, survivin and cyclin D1 were downregulated, and cyt‑C, caspase 9 and caspase 3 were upregulated by 17‑AAG in a dose-dependent manner when the cells were treated with 3.125 and 6.25 mg/l 17-AAG for 48 h. The results indicated that 17‑AAG is able to inhibit the cell proliferation, induce apoptosis and G2/M arrest and downregulate the gene and protein expression levels of STAT3, survivin and cyclin D1, and upregulate gene and protein expression of cyt‑C, caspase 9, caspase 3.

No MeSH data available.


Related in: MedlinePlus