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Sasanquasaponin Triggers Tumor Cell Apoptosis via Distinct Pathways that Involve the Cell surface, Mitochondria, and Endoplasmic Reticulum
Author(s) -
Tang Ling,
Ma Liyuan,
Fu Xueyan,
Jiang Yu,
Wang Yongqi,
Medeiros Denis,
Lin Dingbo
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.780.9
Objective Sasanquasaponin (SQS) is a bioactive ingredient from seeds of the Chinese oil plant Camellia oleifera Abel. It has been reported that SQS has significant antioxidant activities. The objective of this study is to characterize the property of SQS in cancer prevention. Methods SQS was extracted in acetone:water and purified to achieve the purity at 96.6 %, as fingerprinted by HPLC. Human cancer cell lines including lung cancer A549, breast cancer MCF‐7, leukemia HL‐60 and Jurkat cells were treated with SQS for 24 hours. Cell proliferation and apoptosis was tested by MTT assay and flow cytometry. Alteration of protein expression and caspase activation were monitored by Western blot. Results SQS at 20–40 μg/mL significantly inhibited proliferation of A549, MCF‐7 and HL‐60 cells. SQS at 2 μg/mL induced Jurkat cell cycle arrest at the phases of both S and G2/M, increased protein expression of Fas ligand, and activated caspase‐8, caspase‐9, PARP, and caspase‐3, in a dose‐dependent manner. In contrast, SQS declined protein expression of endoplasmic reticulum (ER) stress biomarkers BiP, IRE1, ATF6, PERK, and CHOP. eIF2α and NFκB were not altered. Conclusions SQS‐induced cancer cell apoptosis may be through distinct pathways which involve the cell surface death receptor, mitochondria dysfunction, and alteration of cellular ER stress status in cancer cells in culture. Grant Funding Source : China Natural Science Foundation(NSFC) N0.30801509

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