Study on the effect of EGCG-induced apoptosis in squamous cell carcinoma of the head and neck
Xu Ting
Abstract
Xu Ting
Abstract
OBJECTIVE To investigate the effect of epigallocatechin-3-gallate(EGCG)on the induction of apoptosis and its possible molecular mechanism in head and neck cancer cells. METHODS Head and neck cancer cells Tu177 and Tu212 were treated with EGCG at different concentration for 72 hours. Flow cytometry analysis was employed for apoptosis, and Western blot was used to detect the expression of apoptosis-related proteins. Meanwhile, Tu177 and Tu212 were treated with EGCG, AKT activity was detected at different time points. RESULTS EGCG induced apoptosis of head and neck cancer cells in a dose dependent manner, the expression levels of cleaved-caspase 9, -caspase 3, and PARP were obviously up-regulated in EGCG treated cells. At the same time, the expression of p-AKT was down-regulated in a time-dependent manner by EGCG. CONCLUSION EGCG could induce apoptosis in head and neck cancer cells possibly through AKT and mitochondrial mediated pathways.
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
OBJECTIVE To investigate the effect of epigallocatechin-3-gallate(EGCG)on the induction of apoptosis and its possible molecular mechanism in head and neck cancer cells. METHODS Head and neck cancer cells Tu177 and Tu212 were treated with EGCG at different concentration for 72 hours. Flow cytometry analysis was employed for apoptosis, and Western blot was used to detect the expression of apoptosis-related proteins. Meanwhile, Tu177 and Tu212 were treated with EGCG, AKT activity was detected at different time points. RESULTS EGCG induced apoptosis of head and neck cancer cells in a dose dependent manner, the expression levels of cleaved-caspase 9, -caspase 3, and PARP were obviously up-regulated in EGCG treated cells. At the same time, the expression of p-AKT was down-regulated in a time-dependent manner by EGCG. CONCLUSION EGCG could induce apoptosis in head and neck cancer cells possibly through AKT and mitochondrial mediated pathways.
Key concepts: Apoptosis, Flow cytometry, Head and neck squamous-cell carcinoma, Western blot, Protein kinase B, Cancer research, Cancer cell, Poly ADP ribose polymerase