Glaucocalyxin A Activates FasL and Induces Apoptosis Through Activation of the JNK Pathway in Human Breast Cancer Cells
| Autor: | Xiao-Gang Jiang, Zu-Bin Zhang, Zhen-Lun Gu, Mei Li |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
Cancer Research
Programmed cell death Fas Ligand Protein Cell cycle checkpoint Cell Survival Epidemiology Apoptosis Breast Neoplasms Cell Line Tumor Humans Viability assay Phosphorylation skin and connective tissue diseases Cell Proliferation Cell Death Chemistry Cell growth Kinase JNK Mitogen-Activated Protein Kinases Public Health Environmental and Occupational Health Cell biology Enzyme Activation G2 Phase Cell Cycle Checkpoints Oncology Cancer cell MCF-7 Cells Female Mitogen-Activated Protein Kinases Signal transduction Diterpenes Kaurane Signal Transduction |
| Zdroj: | Asian Pacific Journal of Cancer Prevention. 14:5805-5810 |
| ISSN: | 1513-7368 |
| DOI: | 10.7314/apjcp.2013.14.10.5805 |
| Popis: | THis study was conducted to analyze the molecular mechanisms responsible for anti-proliferation effects of glaucocalyxin A in cultured MCF-7 and Hs578T breast cancer cells. The concentration that reduced cell viability to 50% (IC50) after 72 h treatment was derived and potential molecular mechanisms of anti-proliferation using the IC50 were investigated as changes in cell cycle arrest and apoptosis. Gene and protein expression changes related to apoptosis were investigated by semi-quantitative RT-PCR and western blotting, respectively. Involvement of phosphorylated mitogen-activated protein kinases and JNK signaling in regulation of these molecules was characterized by western blotting. Cell viability decreased in a concentration-dependent manner and the IC50 was determined as 1 μM in MCF-7 and 4 μM in Hs578T cell. Subsequently, we demonstrated that the GLA-induced MCF-7 and Hst578T cell death was due to cell cycle arrest at the G2/M transition and was associated with activation of the c-jun N-terminal kinase (JNK) pathway. We conclude that GLA has the potential to inhibit the proliferation of human breast cancer cells through the JNK pathway and suggest its application forthe effective therapy for patients with breast cancer. |
| Databáze: | OpenAIRE |
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