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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

Effects of 17-AAG on protein expression. 17-AAG, 17-allylamino-17-demethoxygeldanamycin; STAT3, signal transducer and activator of transcription 3.
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f6-mmr-14-02-1067: Effects of 17-AAG on protein expression. 17-AAG, 17-allylamino-17-demethoxygeldanamycin; STAT3, signal transducer and activator of transcription 3.

Mentions: RT-qPCR and western blot analysis results indicated that the expression of STAT3, cyclin D1 and survivin in the drug groups were significantly reduced compared with the control group, while expression levels of cyt-C, caspase 9 and caspase 3 were significantly increased compared with the control group. The increases in cyt-C, caspase 9 and caspase 3 observed were concentration-dependent. Comparisons were performed between drug groups and control groups (Tables IV and V, Figs. 5 and 6).


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)

Effects of 17-AAG on protein expression. 17-AAG, 17-allylamino-17-demethoxygeldanamycin; STAT3, signal transducer and activator of transcription 3.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f6-mmr-14-02-1067: Effects of 17-AAG on protein expression. 17-AAG, 17-allylamino-17-demethoxygeldanamycin; STAT3, signal transducer and activator of transcription 3.
Mentions: RT-qPCR and western blot analysis results indicated that the expression of STAT3, cyclin D1 and survivin in the drug groups were significantly reduced compared with the control group, while expression levels of cyt-C, caspase 9 and caspase 3 were significantly increased compared with the control group. The increases in cyt-C, caspase 9 and caspase 3 observed were concentration-dependent. Comparisons were performed between drug groups and control groups (Tables IV and V, Figs. 5 and 6).

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