2009•Huazhong yixue zazhiRequires access

Effect of trichostatin A on the expression of HDAC2 in HEC-1B cells.

Wang Ze-hu

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Abstract

Objective To investigate the depressant effect and mechanism of trichostatin A(TSA) on proliferation and being induced apoptosis of Histone deacetylase 2(HDAC2) and p53 in human endometrial cancer-1B cell line(HEC-1B).Methods Three levels concentration of TSA(100,200,400 nmol/L) on HEC-1B at different time duration(0,24,48,72 hours) were applied.The expression of HDAC2 in HEC-1B was examined using Western Blot and the data was analyzed with different concentrations of TSA at various treating time duration.The proliferation and apoptotic rates of HEC-1B and the effect of TSA on them were determined using MTT method.At the same testing condition,the expression level of HDAC and p53 in HEC-1B and the effect of TSA were determined using reverse transcription-polymerase chain reaction(RT-PCR).Results TSA has significant inhibition effect on proliferation of HEC-1B,which shows the trend of time duration dependency.With the increasing of TSA dose and time duration,expression of HDAC2 in cancer cells attenuated,but that of p53 increased.Conclusion TSA had the HDAC inhibitor's character,which could inhibit the expression of HDAC2 and promote activation and expression of p53,inhibit proliferation of HEC-1B at the same time.

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Objective To investigate the depressant effect and mechanism of trichostatin A(TSA) on proliferation and being induced apoptosis of Histone deacetylase 2(HDAC2) and p53 in human endometrial cancer-1B cell line(HEC-1B).Methods Three levels concentration of TSA(100,200,400 nmol/L) on HEC-1B at different time duration(0,24,48,72 hours) were applied.The expression of HDAC2 in HEC-1B was examined using Western Blot and the data was analyzed with different concentrations of TSA at various treating time duration.The proliferation and apoptotic rates of HEC-1B and the effect of TSA on them were determined using MTT method.At the same testing condition,the expression level of HDAC and p53 in HEC-1B and the effect of TSA were determined using reverse transcription-polymerase chain reaction(RT-PCR).Results TSA has significant inhibition effect on proliferation of HEC-1B,which shows the trend of time duration dependency.With the increasing of TSA dose and time duration,expression of HDAC2 in cancer cells attenuated,but that of p53 increased.Conclusion TSA had the HDAC inhibitor's character,which could inhibit the expression of HDAC2 and promote activation and expression of p53,inhibit proliferation of HEC-1B at the same time.

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Available abstract

Objective To investigate the depressant effect and mechanism of trichostatin A(TSA) on proliferation and being induced apoptosis of Histone deacetylase 2(HDAC2) and p53 in human endometrial cancer-1B cell line(HEC-1B).Methods Three levels concentration of TSA(100,200,400 nmol/L) on HEC-1B at different time duration(0,24,48,72 hours) were applied.The expression of HDAC2 in HEC-1B was examined using Western Blot and the data was analyzed with different concentrations of TSA at various treating time duration.The proliferation and apoptotic rates of HEC-1B and the effect of TSA on them were determined using MTT method.At the same testing condition,the expression level of HDAC and p53 in HEC-1B and the effect of TSA were determined using reverse transcription-polymerase chain reaction(RT-PCR).Results TSA has significant inhibition effect on proliferation of HEC-1B,which shows the trend of time duration dependency.With the increasing of TSA dose and time duration,expression of HDAC2 in cancer cells attenuated,but that of p53 increased.Conclusion TSA had the HDAC inhibitor's character,which could inhibit the expression of HDAC2 and promote activation and expression of p53,inhibit proliferation of HEC-1B at the same time.

Key concepts: Trichostatin A, Chemistry, Histone deacetylase 2, Apoptosis, Cell growth, Molecular biology, Western blot, Real-time polymerase chain reaction

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Effect of trichostatin A on the expression of HDAC2 in HEC-1B cells. — Research Paper | ScholarLens