Bufalin induces autophagy-mediated cell death in human colon cancer cells through reactive oxygen species generation and JNK activation

Xie, Chuan‐Ming; Chan, Wood Yee; Yu, Sidney; Zhao, Jun; Chen, Cheng

doi:10.1016/j.freeradbiomed.2011.06.016

Cited by 224 publications

(185 citation statements)

References 44 publications

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“…SAS cells were treated with or without (0 and 25 µM) tetrandrine for 24 h then were fixed with a solution containing 2.5% glutaraldehyde and 2% paraformaldehyde (in 0.1 M cacodylate buffer, pH 7.3) for 1 h. After fixation, the samples were postfixed for 30 min in the same buffer containing 1% OsO 4 . Ultra-thin sections were observed under a transmission electron microscope (JEM-1200EX, JEOL Ltd., Tokyo, Japan) at 100 kV (41).…”

Section: Methodsmentioning

confidence: 99%

“…SAS cells were treated with 25 µM tetrandrine for 0, 2, 4 and 6 h and then cells were harvested and stained with 1 mg/ml acridine orange for a period of 20 min and analysed by a fluorescence microscope (41).…”

Section: Methodsmentioning

confidence: 99%

“…SAS cells were transfected with pEGFP-LC3 for 16 h and then were treated with 0, 10, 20 and 30 µM tetrandrine for 6 h. The cells were harvested, fixed with 4% paraformaldehyde for 10 min at room temperature. Cells were stained with LC-3-FITC for a period of 20 min and analysed by a fluorescence microscope (41).…”

Section: Methodsmentioning

confidence: 99%

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Tetrandrine induces cell death in SAS human oral cancer cells through caspase activation-dependent apoptosis and LC3-I and LC3-II activation-dependent autophagy

Huang¹,

Lien

Meng

et al. 2013

International Journal of Oncology

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Abstract. Numerous studies have demonstrated that autophagy is associated with cancer development. Thus, agents to induce autophagy could be employed in some cases for the treatment of cancer. Our results showed that tetrandrine significantly decreased the viability of SAS cells in a concentration-and time-dependent manner. Tetrandrine induced nuclear condensation, demonstrated by DAPI staining. The early events in apoptosis analysed by Annexin V/PI staining indicated that the percentage of cells staining positive for Annexin V was slightly increased in SAS cells with tetrandrine treatment but was much lower following bafilomycin A1 pre-treatment. Tetrandrine caused AVO and MDC induction in SAS cells in a concentration-dependent manner by fluorescence microscopy. Tetrandrine also caused LC-3 expression in SAS cells in a time-dependent manner. Our results show that tetrandrine treatment induced the levels of cleaved caspase-3 in a concentration-and time-dependent manner. Tetrandrine treatment induced the levels of LC-3 II, Atg-5, beclin-1, p-S6, p-ULK, p-mTOR, p-Akt (S473) and raptor. Tetrandrine decreased cell viability, but bafilomycin A1, 3-MA, chloroquine and NAC protected tetrandrine-treated SAS cells against decrease of cell viability. Atg-5, beclin-1 siRNA decreased tetrandrineinduced cleaved caspase-3 and cleaved PARP in SAS cells and protected tetrandrine-treated SAS cells against decrease in cell viability. Chloroquine, NAC and bafilomycin A1 also decreased tetrandrine-induced cleaved caspase-3 and cleaved PARP in SAS cells. Our results indicate the tetrandrine induces apoptosis and autophagy of SAS human cancer cells via caspase-dependent and LC3-I and LC3-II-dependent pathways.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Tetrandrine induces cell death in SAS human oral cancer cells through caspase activation-dependent apoptosis and LC3-I and LC3-II activation-dependent autophagy

Huang¹,

Lien

Meng

et al. 2013

International Journal of Oncology

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“…JNK activation increased expression of ATG5 and Beclin-1. ROS antioxidants (N-acetylcysteine and vitamin C), the JNK-specific inhibitor SP600125, and JNK2 siRNA attenuated bufalin-induced autophagy (Xie et al, 2011).…”

Section: Colon Cancermentioning

confidence: 99%

Bufalin, a Traditional Oriental Medicine, Induces Apoptosis in Human Cancer Cells

Takai

Kira²,

Ishii³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…Da-Wei Ding 1 , Yong-Hong Zhang 1 *, Xin-En Huang 2 ,Qing An 3 , Xun Zhang 4 (Yin et al, 2012), such as human gastric (Li et al, 2009), hepatocellular (Qi et al, 2011), endometrial and ovarian (Takai et al, 2008), leukemia (Chen et al, 2009) and other malignant cells (Xie et al, 2011). However, whether or not do bufalin inhibit the proliferation of human lung cancer cells and its molecular mechanisms are seldom reported.…”

Section: Bufalin Induces Mitochondrial Pathway-mediated Apoptosis In mentioning

confidence: 99%

Bufalin Induces Mitochondrial Pathway-Mediated Apoptosis in Lung Adenocarcinoma Cells

Ding

Zhang²,

Huang³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Background: To evaluate the effects of bufalin in A549 human lung adenocarcinoma epithelial cells in vitro and assess the underlying mechanisms. Materials and Methods: Human A549 non-small cell lung cancer (NSCLC) cells were treated with various concentrations of bufalin. Cell proliferation was measured by CCK-8 assay, apoptotic cell percentage was calculated by flow cytometry and morphological change was observed by inverted phase contrast microscopy/transmission electron microscopy. In addition, the membrane potential of mitochondria was detected by JC-1 fluorescence microscopy assay, and the related protein expression of cytochrome C and caspase-3 was analyzed by Western blotting. Results: Bufalin could inhibit the proliferation of A549 cells via induction of apoptosis, with the evidence of characteristic morphological changes in the nucleus and mitochondria. Furthermore, bufalin decreased the mitochondrial membrane potential with up-regulation of cytochrome C in the cytosol, and activation of caspase-3. Conclusions: Bufalin inhibits the proliferation of A549 cells and triggers mitochondria-dependent apoptosis, pointing to therapeutic application for NSCLC.

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Bufalin induces autophagy-mediated cell death in human colon cancer cells through reactive oxygen species generation and JNK activation

Cited by 224 publications

References 44 publications

Tetrandrine induces cell death in SAS human oral cancer cells through caspase activation-dependent apoptosis and LC3-I and LC3-II activation-dependent autophagy

Tetrandrine induces cell death in SAS human oral cancer cells through caspase activation-dependent apoptosis and LC3-I and LC3-II activation-dependent autophagy

Bufalin, a Traditional Oriental Medicine, Induces Apoptosis in Human Cancer Cells

Bufalin Induces Mitochondrial Pathway-Mediated Apoptosis in Lung Adenocarcinoma Cells

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