[Cell cycle arrest and apoptosis induced by arsenic trioxide in human lung cancer cell line].
J. Dong, Yong Wu, Xiaoxv Dong, Liyun Xu, L Liu
Abstract
J. Dong, Yong Wu, Xiaoxv Dong, Liyun Xu, L Liu
Abstract
BACKGROUND: To explore the potential therapeutic effect of arsenic trioxide(As₂O₃ ) on human lung cancer. METHODS: Cell growth curves, cell proliferation, cell cycle and apoptosis of human lung cancer cell line GLC-82 were detected by theMTT method and flowcytometry (FCM) . RESULTS: The data showed that As₂O₃ significantly inhibited proliferation of GLC-82 cells and the inhibiting effects had a dose-and time-dependence. The cell proliferation inhibition rate was 81. 05% when treated with 4. 0 Lmol/L As₂O₃ for 96 hours. The change of DNA content of GLC-82 cells indicated that As₂O₃ was able to block cell cycle progress in G2/M phase, with appearance of sub-G1 peak in a dose-dependent manner. CONCLUSIONS: As₂O₃ can effectively inhibit the proliferation of human lung cancer cell line GLC-82 and the possible mechanisms may be related to G2/M phase arrest and apoptosis induced by As₂O₃.
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BACKGROUND: To explore the potential therapeutic effect of arsenic trioxide(As₂O₃ ) on human lung cancer. METHODS: Cell growth curves, cell proliferation, cell cycle and apoptosis of human lung cancer cell line GLC-82 were detected by theMTT method and flowcytometry (FCM) . RESULTS: The data showed that As₂O₃ significantly inhibited proliferation of GLC-82 cells and the inhibiting effects had a dose-and time-dependence. The cell proliferation inhibition rate was 81. 05% when treated with 4. 0 Lmol/L As₂O₃ for 96 hours. The change of DNA content of GLC-82 cells indicated that As₂O₃ was able to block cell cycle progress in G2/M phase, with appearance of sub-G1 peak in a dose-dependent manner. CONCLUSIONS: As₂O₃ can effectively inhibit the proliferation of human lung cancer cell line GLC-82 and the possible mechanisms may be related to G2/M phase arrest and apoptosis induced by As₂O₃.
Key concepts: Arsenic trioxide, Apoptosis, Lung cancer, Cell cycle, Cell growth, Cell cycle checkpoint, Cell culture, Cancer research