2008Zhonghua jianyan yixue zazhiRequires access

Effect of DNA methyltransferase 5-aza-2'-deoxycytidine on proliferation of human esophageal squamous cancer cell line Eca109 in vitro

Ting Yang, Aerziguli·Tuerxun, Xiaomei Lü

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Abstract

Objective To explore the effect of the DNA methyltransferase 5-aza-2'-deoxycytidine (5-aza-CdR)on human esophageal squamous cancer Ecal09 cells.nethods Human esophageal squamous cell cancer(ESCC)Eca109 cells were treated by 5-aza-CdR with 10-7,10-6,1O-5,10-4,0 mol/L. Respectively.Consequently,the growth rate of the cells was detected by MTT assay and morphological structure Was observed.Meanwhile,cell apoptosis and cell cycle were analyzed by flow cytometry method. (FCM).ResulIs The proliferation of Eea109 cells Was inhibited by 5-aza-CdR from 10-7 to 10-4 mol/L Moreover,the inhibition rate showed time-and-concentration-dependent manner(24~96 h,F=160.06,P=0.000,10-7~10-4 mol/L,F:60.95,P:0.000).The maximum rate of inhibitory was reached up to(15.70±0.75)% in the group treated by 10-4 mol/L 5-aza-CdR after 96 hours.An apoptosis peak appeared before diploid peak.The proportion of Go/G1 phase cells Was significantly increased(F=6479.46, P=0.000),especially up to(89.70±0.91)% in the group treated by 10-4 mo/L 5-aza-CdR after 96 h. However,the proportion of S phase cells Was obviously decreased(F=4222.26,P=0.000),especially down to(9.10±0.48)% in the group treated bv 10-4mol/L 5-aza-CdR after 96 h.Conclusions The proliferation of Eca109 cells is inhibited bv 5-aza-CdR in a time-and-concentration-dependent manner.Moreover,the 5-aza-CdR can inhibit cell growth by regulation of DNA cycle and apoptosis. Key words: Esophageal neoplasms; Tumor cells,caltured; Azacitidine DNA methylation

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Objective To explore the effect of the DNA methyltransferase 5-aza-2'-deoxycytidine (5-aza-CdR)on human esophageal squamous cancer Ecal09 cells.nethods Human esophageal squamous cell cancer(ESCC)Eca109 cells were treated by 5-aza-CdR with 10-7,10-6,1O-5,10-4,0 mol/L. Respectively.Consequently,the growth rate of the cells was detected by MTT assay and morphological structure Was observed.Meanwhile,cell apoptosis and cell cycle were analyzed by flow cytometry method. (FCM).ResulIs The proliferation of Eea109 cells Was inhibited by 5-aza-CdR from 10-7 to 10-4 mol/L Moreover,the inhibition rate showed time-and-concentration-dependent manner(24~96 h,F=160.06,P=0.000,10-7~10-4 mol/L,F:60.95,P:0.000).The maximum rate of inhibitory was reached up to(15.70±0.75)% in the group treated by 10-4 mol/L 5-aza-CdR after 96 hours.An apoptosis peak appeared before diploid peak.The proportion of Go/G1 phase cells Was significantly increased(F=6479.46, P=0.000),especially up to(89.70±0.91)% in the group treated by 10-4 mo/L 5-aza-CdR after 96 h. However,the proportion of S phase cells Was obviously decreased(F=4222.26,P=0.000),especially down to(9.10±0.48)% in the group treated bv 10-4mol/L 5-aza-CdR after 96 h.Conclusions The proliferation of Eca109 cells is inhibited bv 5-aza-CdR in a time-and-concentration-dependent manner.Moreover,the 5-aza-CdR can inhibit cell growth by regulation of DNA cycle and apoptosis. Key words: Esophageal neoplasms; Tumor cells,caltured; Azacitidine DNA methylation

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Available abstract

Objective To explore the effect of the DNA methyltransferase 5-aza-2'-deoxycytidine (5-aza-CdR)on human esophageal squamous cancer Ecal09 cells.nethods Human esophageal squamous cell cancer(ESCC)Eca109 cells were treated by 5-aza-CdR with 10-7,10-6,1O-5,10-4,0 mol/L. Respectively.Consequently,the growth rate of the cells was detected by MTT assay and morphological structure Was observed.Meanwhile,cell apoptosis and cell cycle were analyzed by flow cytometry method. (FCM).ResulIs The proliferation of Eea109 cells Was inhibited by 5-aza-CdR from 10-7 to 10-4 mol/L Moreover,the inhibition rate showed time-and-concentration-dependent manner(24~96 h,F=160.06,P=0.000,10-7~10-4 mol/L,F:60.95,P:0.000).The maximum rate of inhibitory was reached up to(15.70±0.75)% in the group treated by 10-4 mol/L 5-aza-CdR after 96 hours.An apoptosis peak appeared before diploid peak.The proportion of Go/G1 phase cells Was significantly increased(F=6479.46, P=0.000),especially up to(89.70±0.91)% in the group treated by 10-4 mo/L 5-aza-CdR after 96 h. However,the proportion of S phase cells Was obviously decreased(F=4222.26,P=0.000),especially down to(9.10±0.48)% in the group treated bv 10-4mol/L 5-aza-CdR after 96 h.Conclusions The proliferation of Eca109 cells is inhibited bv 5-aza-CdR in a time-and-concentration-dependent manner.Moreover,the 5-aza-CdR can inhibit cell growth by regulation of DNA cycle and apoptosis. Key words: Esophageal neoplasms; Tumor cells,caltured; Azacitidine DNA methylation

Key concepts: Flow cytometry, Molecular biology, Apoptosis, Deoxycytidine, Methyltransferase, Cell cycle, Cell growth, Cell culture

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Effect of DNA methyltransferase 5-aza-2'-deoxycytidine on proliferation of human esophageal squamous cancer cell line Eca109 in vitro — Research Paper | ScholarLens