The effects of epigallocatechin gallate on nasopharyngeal carcinoma cells and expression of STAT3
HE Xiao-son
Abstract
HE Xiao-son
Abstract
Objective To study the effects of epigallocatechin gallate( EGCG) on nasopharyngeal carcinoma cells and expression of STAT3,and thus to further investigate the mechanism of EGCG in antinasopharyngeal carcinoma. Methods CNE2 cells were treated by EGCG of different concentrations. MTT,Hoechst33258 staining and RT- PCR were introduced for assessment of the growth,apoptosis and STAT3 mRNA of CNE2 cells,respectively. Results Significant inhibition on CNE2 cell proliferation by EGCG was observed in concentration- and time- dependent manners( P 0. 05).The typical apoptosis bodies in CNE2 cells were observed. As the increase of EGCG concentration,the number of apoptotic cells was significantly increased( P 0. 05). The expression of STAT3 mRNA was also significantly down- regulated by EGCG in concentration- and time- dependent manners( P 0. 05). Conclusion EGCG inhibits the proliferation and in induces the apoptosis of CNE2 cells,probably via the induced down- regulation in STAT3 mRNA.
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Objective To study the effects of epigallocatechin gallate( EGCG) on nasopharyngeal carcinoma cells and expression of STAT3,and thus to further investigate the mechanism of EGCG in antinasopharyngeal carcinoma. Methods CNE2 cells were treated by EGCG of different concentrations. MTT,Hoechst33258 staining and RT- PCR were introduced for assessment of the growth,apoptosis and STAT3 mRNA of CNE2 cells,respectively. Results Significant inhibition on CNE2 cell proliferation by EGCG was observed in concentration- and time- dependent manners( P 0. 05).The typical apoptosis bodies in CNE2 cells were observed. As the increase of EGCG concentration,the number of apoptotic cells was significantly increased( P 0. 05). The expression of STAT3 mRNA was also significantly down- regulated by EGCG in concentration- and time- dependent manners( P 0. 05). Conclusion EGCG inhibits the proliferation and in induces the apoptosis of CNE2 cells,probably via the induced down- regulation in STAT3 mRNA.
Key concepts: Nasopharyngeal carcinoma, Apoptosis, STAT3, Epigallocatechin gallate, Messenger RNA, Staining, Chemistry, Gallate