OBJECTIVETo investigate the effect of emodin on proliferation and cell cycle distribution of human oral squamous carcinoma cells in vitro.

METHODSCultured human oral squamous carcinoma Tca8113 cells were treated with 2.5, 5, 10, 20, 40, 60 and 80 µmol/L emodin for 24, 48 or 72 h, with the cells treated with 0.1% DMSO as control. MTT assay and flow cytometry were used to evaluate the changes in cell proliferation and cell cycle distribution, respectively. Western blotting was employed to analyze the changes in the expression levels of the cell cycle-related proteins CDK2, cyclin E and P21 after emodin treatment.

RESULTSEmodin significantly inhibited the growth and proliferation of Tca8113 cells within 72 h in a time- and dose-dependent manner, and caused cell cycle arrest in G0-G1 phase. Western blotting revealed that emodin treatment significantly lowered the expression levels of CDK2, cyclin E and P21 proteins in Tca8113 cells (P<0.05).

CONCLUSIONEmodin can inhibit the proliferation of Tca8113 cells and affect their cell cycle distribution possibly by inhibiting the signaling pathways of cell cycle regulation.

Carcinoma, Squamous Cell ; pathology ; Cell Cycle ; drug effects ; Cell Line, Tumor ; drug effects ; Cell Proliferation ; drug effects ; Cyclin E ; metabolism ; Cyclin-Dependent Kinase 2 ; metabolism ; Cyclin-Dependent Kinase Inhibitor p21 ; metabolism ; Emodin ; pharmacology ; Humans ; Mouth Neoplasms ; pathology ; Oncogene Proteins ; metabolism ; Signal Transduction

Objective To investigate the effect of emodin on proliferation and cell cycle distribution of human oral squamous carcinoma cells in vitro. Methods Cultured human oral squamous carcinoma Tca8113 cells were treated with 2.5, 5, 10, 20, 40, 60 and 80μmol/L emodin for 24, 48 or 72 h, with the cells treated with 0.1%DMSO as control. MTT assay and flow cytometry were used to evaluate the changes in cell proliferation and cell cycle distribution, respectively. Western blotting was employed to analyze the changes in the expression levels of the cell cycle-related proteins CDK2, cyclin E and P21 after emodin treatment. Results Emodin significantly inhibited the growth and proliferation of Tca8113 cells within 72 h in a time-and dose-dependent manner, and caused cell cycle arrest in G0-G1 phase. Western blotting revealed that emodin treatment significantly lowered the expression levels of CDK2, cyclin E and P21 proteins in Tca8113 cells (P<0.05). Conclusion Emodin can inhibit the proliferation of Tca8113 cells and affect their cell cycle distribution possibly by inhibiting the signaling pathways of cell cycle regulation.

Objective To investigate the effect of emodin on proliferation and cell cycle distribution of human oral squamous carcinoma cells in vitro. Methods Cultured human oral squamous carcinoma Tca8113 cells were treated with 2.5, 5, 10, 20, 40, 60 and 80μmol/L emodin for 24, 48 or 72 h, with the cells treated with 0.1%DMSO as control. MTT assay and flow cytometry were used to evaluate the changes in cell proliferation and cell cycle distribution, respectively. Western blotting was employed to analyze the changes in the expression levels of the cell cycle-related proteins CDK2, cyclin E and P21 after emodin treatment. Results Emodin significantly inhibited the growth and proliferation of Tca8113 cells within 72 h in a time-and dose-dependent manner, and caused cell cycle arrest in G0-G1 phase. Western blotting revealed that emodin treatment significantly lowered the expression levels of CDK2, cyclin E and P21 proteins in Tca8113 cells (P<0.05). Conclusion Emodin can inhibit the proliferation of Tca8113 cells and affect their cell cycle distribution possibly by inhibiting the signaling pathways of cell cycle regulation.