2005•Chinese Journal of Industrial MedicineRequires access

A study of effect of trichostatin A on the expression of cell cycle related protein in K562 cell line

Tian Fan-qing

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Abstract

Objective To explore the effect of Trichostatin A(TSA) on cell proliferation and cell cycle in K562 cell lines.Method K562 cells were treated with(50-400)nmol/L Trichostatin A for 12-60 h and the growth inhibition rate of K562 cells was measured by MTT and cell apoptosis was inspected by flow cytometry(FCM).The expressions of cyclin E and retinoblastoma protein(Rb)in K562 cells was observed by immunohistochemistry at varied concentrations of TSA(100-300 nmol/L)for 24 hours.Result Proliferation of K562 cells was selectively inhibited by TSA in a dose-and time-dependent manner,with inhibitory rates of 37.83%-78.57%(P0.01)and K562 cell apoptosis rates were 14.38%-61.18% by FCM.Optical absorbance by immunochemistry for cyclin E was 0.215 4 ± 0.201 5 , 0.150 1±0.197 8 and 0.118 3±0.502 1 and that for Rb was 0.301 7±0.135 6 , 0.213 4±0.128 3 and 0.152 7±0.021 6 at varied concentrations of TSA(100-300 nmol/L),respectively,as compared to that of 0.327 4±0.109 3 and 0.418 6±0.187 0,respectively,in controls(P0.05),showing an decreasing trend with increase in TSA concentration in a dose-and time-dependent manner.Conclusion TSA could disturb the progress of cell cycle of K562 cells,with mechanisms of induction of cell apoptosis,regulation of G1/S checkpoints and down-regulation of the expression of cyclin E,leading to inhibition of the expression of Rb.

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Objective To explore the effect of Trichostatin A(TSA) on cell proliferation and cell cycle in K562 cell lines.Method K562 cells were treated with(50-400)nmol/L Trichostatin A for 12-60 h and the growth inhibition rate of K562 cells was measured by MTT and cell apoptosis was inspected by flow cytometry(FCM).The expressions of cyclin E and retinoblastoma protein(Rb)in K562 cells was observed by immunohistochemistry at varied concentrations of TSA(100-300 nmol/L)for 24 hours.Result Proliferation of K562 cells was selectively inhibited by TSA in a dose-and time-dependent manner,with inhibitory rates of 37.83%-78.57%(P0.01)and K562 cell apoptosis rates were 14.38%-61.18% by FCM.Optical absorbance by immunochemistry for cyclin E was 0.215 4 ± 0.201 5 , 0.150 1±0.197 8 and 0.118 3±0.502 1 and that for Rb was 0.301 7±0.135 6 , 0.213 4±0.128 3 and 0.152 7±0.021 6 at varied concentrations of TSA(100-300 nmol/L),respectively,as compared to that of 0.327 4±0.109 3 and 0.418 6±0.187 0,respectively,in controls(P0.05),showing an decreasing trend with increase in TSA concentration in a dose-and time-dependent manner.Conclusion TSA could disturb the progress of cell cycle of K562 cells,with mechanisms of induction of cell apoptosis,regulation of G1/S checkpoints and down-regulation of the expression of cyclin E,leading to inhibition of the expression of Rb.

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Available abstract

Objective To explore the effect of Trichostatin A(TSA) on cell proliferation and cell cycle in K562 cell lines.Method K562 cells were treated with(50-400)nmol/L Trichostatin A for 12-60 h and the growth inhibition rate of K562 cells was measured by MTT and cell apoptosis was inspected by flow cytometry(FCM).The expressions of cyclin E and retinoblastoma protein(Rb)in K562 cells was observed by immunohistochemistry at varied concentrations of TSA(100-300 nmol/L)for 24 hours.Result Proliferation of K562 cells was selectively inhibited by TSA in a dose-and time-dependent manner,with inhibitory rates of 37.83%-78.57%(P0.01)and K562 cell apoptosis rates were 14.38%-61.18% by FCM.Optical absorbance by immunochemistry for cyclin E was 0.215 4 ± 0.201 5 , 0.150 1±0.197 8 and 0.118 3±0.502 1 and that for Rb was 0.301 7±0.135 6 , 0.213 4±0.128 3 and 0.152 7±0.021 6 at varied concentrations of TSA(100-300 nmol/L),respectively,as compared to that of 0.327 4±0.109 3 and 0.418 6±0.187 0,respectively,in controls(P0.05),showing an decreasing trend with increase in TSA concentration in a dose-and time-dependent manner.Conclusion TSA could disturb the progress of cell cycle of K562 cells,with mechanisms of induction of cell apoptosis,regulation of G1/S checkpoints and down-regulation of the expression of cyclin E,leading to inhibition of the expression of Rb.

Key concepts: Trichostatin A, Apoptosis, K562 cells, Cell cycle, Cyclin B1, Cell growth, Chemistry, Molecular biology

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