Zhonghua zhong liu za zhi [Chinese journal of oncology] · 2010
[Down-regulation of mTOR activity and survivin expression during tamoxifen-induced apoptosis in hepatoblastoma cells].
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Guo Ren-Hua, Wang Tong-Shan, Chen Xiao-Feng, Huang Zu-Hu, Shu Yong-Qian
Аннотация
OBJECTIVE: The aim of this study was to investigate the changes in mTOR activity and survivin expression in liver cancer cell line HepG2 cells treated with tamoxifen.
METHODS: Survivin transcription level and p70S6K was demonstrated by PCR, dual-luciferase reporter assay and Western blot analysis, respectively, and the apoptosis in the HepG2 cells was detected by flow cytometry.
RESULTS: Tamoxifen leads to apoptosis of the cells and reduction in survivin expression, as well as a dramatic reduction in the activated form of p70S6K. Treating HepG2 cells with rapamycin, a specific mTOR inhibitor, significantly reduced the survivin protein level but not affected the survivin transcription, indicating that tamoxifen and rapamycin were synergistic in regards to down-regulation of survivin expression in hepatocellular carcinoma cells.
CONCLUSIONS: Our results suggest that tamoxifen down-regulates survivin expression in HepG2 cells and it is mediated by transcriptional and post-transcriptional level via PI3K/Akt/mTOR pathway to induce apoptosis.
METHODS: Survivin transcription level and p70S6K was demonstrated by PCR, dual-luciferase reporter assay and Western blot analysis, respectively, and the apoptosis in the HepG2 cells was detected by flow cytometry.
RESULTS: Tamoxifen leads to apoptosis of the cells and reduction in survivin expression, as well as a dramatic reduction in the activated form of p70S6K. Treating HepG2 cells with rapamycin, a specific mTOR inhibitor, significantly reduced the survivin protein level but not affected the survivin transcription, indicating that tamoxifen and rapamycin were synergistic in regards to down-regulation of survivin expression in hepatocellular carcinoma cells.
CONCLUSIONS: Our results suggest that tamoxifen down-regulates survivin expression in HepG2 cells and it is mediated by transcriptional and post-transcriptional level via PI3K/Akt/mTOR pathway to induce apoptosis.
Предметные рубрики MeSH
Antibiotics, AntineoplasticAntineoplastic Agents, HormonalApoptosisCell ProliferationDown-RegulationDrug SynergismHep G2 CellsHumansInhibitor of Apoptosis ProteinsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, MessengerRibosomal Protein S6 Kinases, 70-kDaSignal TransductionSirolimusSurvivinTOR Serine-Threonine KinasesTamoxifen