Triptolide induced DNA damage in A375.S2 human malignant melanoma cells is mediated via reduction of DNA repair genes

Chueh, Fu Shin; Chen, Yung Liang; Hsu, Shu Chun; Yang, Jai Sing; Hsueh, Shu Ching; Ji, Bin; Lu, Hsu Feng; Chung, Jing Gung

doi:10.3892/or.2012.2170

Cited by 36 publications

(32 citation statements)

References 52 publications

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“…Statistical analyses of the data were performed using Student's t-test and one-way analysis of variance (ANOVA). Statistical significance was set at P<0.05 (43).…”

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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“…Statistical analyses of the data were performed using Student's t-test and one-way analysis of variance (ANOVA). Statistical significance was set at P<0.05 (43).…”

Section: Methodsmentioning

confidence: 99%

“…Incubation with primary antibodies was done overnight at 4˚C. Immunoreactive proteins were visualised with the ECL chemiluminescent detection system (Perkin Elmer Life Sciences, MA, USA) and BioMax LightFilm (Eastman Kodak, New Heaven, CT, USA) according to the manufacturer's instructions (43).…”

Section: Methodsmentioning

confidence: 99%

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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“…Recently, triptolide was shown to induce extracellular signal-regulated kinase activation and affect the generation of reactive oxygen species and the induction of endoplasmic reticulum stress via the PERK-eIF2α pathway (20). In addition, a previous study has demonstrated that triptolide induces cell cycle arrest and apoptosis in human tumor cells by inducing DNA damage and the expression of repair-associated genes (21). Therefore, the observations of the present study indicate that triptolide induces apoptosis in breast cancer cells by a mechanism associated with the Wnt/β-catenin signaling pathway, further improving the understanding of the role of triptolide as a potential treatment for breast cancer.…”

Section: Discussionmentioning

confidence: 99%

Triptolide induces apoptosis of breast cancer cells via a mechanism associated with the Wnt/β-catenin signaling pathway

Shao

Guo

et al. 2014

Experimental and Therapeutic Medicine

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Triptolide is a diterpene triepoxide compound extracted from the medicinal plant, Tripterygium wilfordii Hook F. The aim of the present study was to determine whether triptolide inhibits the proliferation of breast cancer cells and to further investigate the associated molecular mechanisms. The effects of triptolide on the cell viability of three breast cancer cell lines, specifically, highly metastatic MDA-MB-231, human epidermal growth factor receptor 2-positive BT-474 and estrogen receptor-positive MCF7 cells, were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and apoptosis assays. Western blot analysis was performed to investigate the expression levels of β-catenin in the control and triptolide-treated cells. The results demonstrated that triptolide treatment caused cell death in the three types of malignant cell lines. Treatment with 25 nM triptolide for 48 h exhibited marked inhibitory effects on the cell viability of the three types of cells, with greater effects observed in BT-474 cells compared with the other two cell types. When compared with the cells not treated with triptolide, 50 nM triptolide treatment resulted in apoptosis of MDA-MB-231, BT-474 and MCF7 cells with apoptotic rates of ~80%. Western blot analysis indicated that triptolide treatment of MDA-MB-231, BT-474 and MCF7 cells decreased the expression levels of β-catenin to 5–10% of the levels observed in the cells treated with dimethyl sulfoxide only. Therefore, the results of the present study indicate that triptolide induces the apoptosis of breast cancer cells via a mechanism associated with the Wnt/β-catenin signaling pathway.

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“…NCI‐H460 cells (2 × 10 5 cells/well) were maintained on the 12‐well cell culture cluster overnight then treated with 0, 15, 20, 25, 30, and 35 μM BDMC for 48 h. Cells were harvested with trypsin, rinsed three times in phosphate‐buffered saline (PBS), and stained with PI (5 μg/mL) in PBS and measured percentage of viable cells by flow cytometry (Becton‐Dickinson, San Jose, CA) as described previously (Chueh et al, ).…”

Section: Methodsmentioning

confidence: 99%

Bisdemethoxycurcumin induces DNA damage and inhibits DNA repair associated protein expressions in NCI-H460 human lung cancer cells

Sai

Huang

et al. 2015

Environ. Toxicol.

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Nonsmall cell lung carcinoma (NSCLC) is a devastating primary lung tumor resistant to conventional therapies. Bisdemethoxycurcumin (BDMC) is one of curcumin derivate from Turmeric and has been shown to induce NSCLC cell death. Although there is one report to show BDMC induced DNA double strand breaks, however, no available information to show BDMC induced DNA damage action with inhibited DNA repair protein in lung cancer cells in detail. In this study, we tested BDMC-induced DNA damage and condensation in NCI-H460 cells by using Comet assay and DAPI staining examinations, respectively and we found BDMC induced DNA damage and condension. Western blotting was used to examine the effects of BDMC on protein expression associated with DNA damage and repair and results indicated that BDMC suppressed the protein levels associated with DNA damage and repair, such as 14-3-3σ (an important checkpoint keeper of DDR), O6-methylguanine-DNA methyltransferase, DNA repair proteins breast cancer 1, early onset, mediator of DNA damage checkpoint 1 but activate phosphorylated p53 and p-H2A.X (phospho Ser140) in NCI-H460 cells. Confocal laser systems microscopy was used for examining the protein translocation and results show that BDMC increased the translocation of p-p53 and p-H2A.X (phospho Ser140) from cytosol to nuclei in NCI-H460 cells. In conclusion, BDMC induced DNA damage and condension and affect DNA repair proteins in NCI-H460 cells in vitro. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1859-1868, 2016.

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Triptolide induced DNA damage in A375.S2 human malignant melanoma cells is mediated via reduction of DNA repair genes

Cited by 36 publications

References 52 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

Triptolide induces apoptosis of breast cancer cells via a mechanism associated with the Wnt/β-catenin signaling pathway

Bisdemethoxycurcumin induces DNA damage and inhibits DNA repair associated protein expressions in NCI-H460 human lung cancer cells

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