Casticin, a flavonoid, potentiates TRAIL-induced apoptosis through modulation of anti-apoptotic proteins and death receptor 5 in colon cancer cells

Tang, Sanyuan; Zhong, Meizuo; Yuan, Guang-Jin; Suping, Hou; Yin, Leilan; Jiang, Hao; Yu, Zheng-Υang

doi:10.3892/or.2012.2127

Cited by 42 publications

(36 citation statements)

References 32 publications

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“…Oxidative stress by chemopreventive agents, including curcumin and casticin, has been implicated in DR5 upregulation and apoptosis (35)(36)(37). Furthermore, numerous natural antitumor compounds have been reported to induce ROS production (35,37).…”

Section: Ros Is Involved In Andrographolide-induced Sensitization To mentioning

confidence: 99%

Andrographolide induces apoptotic and non-apoptotic death and enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in gastric cancer cells

et al. 2017

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Abstract. Andrographolide, a natural compound isolated from Andrographis paniculata, has been reported to possess antitumor activity. In the present study, the effect of andrographolide in human gastric cancer (GC) cells was investigated. Andrographolide induced cell death with apoptotic and non-apoptotic features. At a low concentration, andrographolide potentiated apoptosis and reduction of clonogenicity triggered by recombinant human tumor necrosis factor-related apoptosis-inducing ligand (rhTRAIL). Exposure of GC cells to andrographolide altered the expression level of several growth-inhibiting and apoptosis-regulating proteins, including death receptors. It was demonstrated that activity of the TRAIL-R2 (DR5) pathway was critical in the development of andrographolide-mediated rhTRAIL sensitization, since its inhibition significantly reduced the extent of apoptosis induced by the combination of rhTRAIL and andrographolide. In addition, andrographolide increased reactive oxygen species (ROS) generation in a dose-dependent manner. N-acetyl cysteine prevented andrographolide-mediated DR5 induction and the apoptotic effect induced by the combination of rhTRAIL and andrographolide. Collectively, the present study demonstrated that andrographolide enhances TRAIL-induced apoptosis through induction of DR5 expression. This effect appears to involve ROS generation in GCs.

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Section: Ros Is Involved In Andrographolide-induced Sensitization To mentioning

confidence: 99%

Andrographolide induces apoptotic and non-apoptotic death and enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in gastric cancer cells

et al. 2017

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“…It has been identified that the C-3 and C-4' methoxy and C-3' and C-5 hydroxy functional groups provide the strong anti-proliferative activity of this flavonoid (18). Casticin exhibits weaker cytotoxicity but greater selectivity than taxol, (the IC 50 of taxol for tumor cells is at the nmol/l level, while the IC 50 of casticin is at the µmol/l level) (19).…”

Section: Introductionmentioning

confidence: 99%

Casticin inhibits the activity of transcription factor Sp1 and the methylation of RECK in MGC803 gastric cancer cells

Yang

Huang

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. The present study investigated the effect of casticin on reversion-inducing-cysteine-rich protein with kazal motifs (RECK) gene expression and intracellular methylation levels in MGC803 gastric cancer cells. Cells were treated with 1, 10 and 30 µmol/l casticin. Western blotting and reverse transcription-quantitative polymerase chain reaction assays were performed to determine the protein expression and mRNA levels of RECK and DNA methyltransferase 1 (DNMT1), respectively. High-performance liquid chromatography coupled to electrospray ionization tandem mass spectrometry was used to detect RECK methylation. In addition, MGC803 cell proliferation was measured by an MTT assay and the DNA-binding activity of transcription factor Sp1 was determined using an enzyme-linked immunosorbent assay. The results demonstrated that treatment with 1, 10 and 30 µmol/l casticin significantly increased RECK protein expression and mRNA levels. In addition, casticin (30 µmol/l) decreased RECK promoter methylation levels by 31%, global DNA methylation levels by 39% and nuclear methylation activity by 71.6%. Furthermore, casticin downregulated the mRNA levels and protein expression of DNMT1. The MTT assay demonstrated that MGC803 cell proliferation was inhibited by casticin treatment and DNA binding assays indicated that casticin reduced the DNA-binding activity of Sp1. The present study therefore indicated that casticin inhibits the proliferation of gastric cancer MGC803 cells by upregulating RECK gene expression and reducing intracellular methylation levels.

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“…They are derived from plants and were also found in insect tea. The flavones from different plants all showed strong apoptotic effects in cancer cells (Liu et al, 2014;Tang et al, 2013). In this study, insect tea had a strong apoptotic-inducing effect in HepG2 cancer cells.…”

Section: Chemical Constituents Of Insect Teamentioning

confidence: 77%

Apoptotic effects of insect tea in HepG2 human hepatoma cells

Suo

Péng

Wang

et al. 2015

CyTA - Journal of Food

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Insect tea is a traditional and special tea in China. After the HepG2 cancer cells were treated with insect tea ethanol extracts (ITEE) for 48 h, HepG2 cell proliferation was inhibited, with 40, 80 and 160 μg/mL of ITEE showing inhibitory rates of 35.1%, 59.7% and 86.3%, respectively. Compared to the lower concentration, 160 μg/mL ITEE significantly induced apoptosis as determined by flow cytometry analysis, which showed the content of sub-G1 cancer cells was 38.8%. By RT-PCR, ITEE induced apoptosis in HepG2 cancer cells by increasing caspase-3, caspase-8, caspase-9, Bax, p53, p21, E2F1, p73 and decreasing Bcl-2, Bcl-xL, HIAP-1 and HIAP-2 mRNA expression levels. Insect tea is rich in polyphenols, caffeine, flavones, vitamin C and amino acids. There were 17 kinds of amino acids in insect tea. The functional components of insect tea induce apoptosis in HepG2 cancer cells. Insect tea is a good functional food by its anticancer effects.Keywords: insect tea; apoptosis; HepG2 cells; cancer; mRNA expression El té de insecto es un té tradicional y especial en China. Después que se trataran las células cancerígenas HepG2 con extractos de etanol del té de insecto (ITEE) durante 48 h, se inhibió la proliferación de las células HepG2 con 40, 80 y 160 μg/mL de ITEE mostrando unos niveles de inhibición de 35,1%, 59,7% y 86.3%, respectivamente. En comparación con una menor concentración, 160 μg/mL de ITEE indujo apoptosis de forma significativa como fue determinado mediante la citometría de flujo, la cual mostró que el contenido de células cancerígenas sub-G1 era de 38,8%. Mediante RT-PCR, el ITEE indujo apoptosis en las células cancerígenas HepG2 a través del aumento de caspasa-3, caspasa-8, caspasa-9, Bax, p53, p21, E2F1, p73 y disminuyendo los niveles de expresión de Bcl-2, Bcl-xL, HIAP-1 y HIAP-2 mRNA. El té de insecto es rico en polifenoles, cafeína, flavonas, vitamina C y aminoácidos. Se obtuvieron 17 tipos de aminoácidos en el té de insecto. Los componentes funcionales del té de insecto indujeron apoptosis en las células cancerígenas HepG2. El té de insecto se trata de una bebida funcional gracias a sus efectos anti cáncer.

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Casticin, a flavonoid, potentiates TRAIL-induced apoptosis through modulation of anti-apoptotic proteins and death receptor 5 in colon cancer cells

Cited by 42 publications

References 32 publications

Andrographolide induces apoptotic and non-apoptotic death and enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in gastric cancer cells

Andrographolide induces apoptotic and non-apoptotic death and enhances tumor necrosis factor-related apoptosis-inducing ligand-mediated apoptosis in gastric cancer cells

Casticin inhibits the activity of transcription factor Sp1 and the methylation of RECK in MGC803 gastric cancer cells

Apoptotic effects of insect tea in HepG2 human hepatoma cells

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