Emodin azide methyl anthraquinone derivative triggers mitochondrial-dependent cell apoptosis involving in caspase-8-mediated Bid cleavage

Yan, Yanyan; Liang, Yong-ju; Zhang, Jianye; Shi, Chengjun; Lü, Yu; Gu, Lanlan; Fu, Liwu

doi:10.1158/1535-7163.mct-07-2362

Cited by 80 publications

(74 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…recent data indicate that the mitochondrial pathway is controlled and regulated by Bcl-2 family protein (5,(22)(23)(24)(25). Bcl-2 family proteins such as Bcl-2 and Bax have been identified as major regulators in controlling the release of mitochondrial cytochrome c (26). Moreover, p53-mediated apoptosis is associated with Bcl-2 and Bax (27,28).…”

Section: (S)-rg3 Induced Apoptosis By Activating Ampkmentioning

confidence: 99%

20(S)-Ginsenoside Rg3-induced apoptosis in HT-29 colon cancer cells is associated with AMPK signaling pathway

Chung¹

2010

Mol Med Rep

View full text Add to dashboard Cite

Abstract. 20(S)-ginsenoside rg3 [20(S)-rg3)], one of the main constituents isolated from Panax ginseng, has been shown to have an anti-cancer effect and to induce apoptosis by interfering with several signaling pathways. However, the molecular mechanisms of aMP-activated protein kinase (aMPK) associated with apoptosis in HT-29 colon cancer cells remain unclear. in the present study, we investigated whether 20(S)-rg3 exerts an anti-proliferative effect and induces apoptosis by modulating the aMPK signaling pathway in HT-29 cells. 20(S)-rg3-treated cells displayed several apoptotic features, including dna fragmentation, proteolytic cleavage of poly (adP-ribose) polymerase (ParP) and morphological changes. 20(S)-rg3 downregulated the expression of anti-apoptotic protein B-cell cll/lymphoma 2 (Bcl2), up-regulated the expression of pro-apoptotic protein of p53 and Bcl-2-associated X protein (Bax), and caused the release of mitochondrial cytochrome c, ParP, caspase-9 and caspase-3. However, 20(S)-rg3-induced apoptosis was completely abolished in the presence of compound c (aMPK inhibitor) or small interfering rna for aMPK (siaMPK). in addition, STo-609 (caMKKβ inhibitor) attenuated 20(S)-rg3-induced aMPK activation and apoptosis. These results suggest that 20(S)-rg3-induced apoptosis in HT-29 cells is mediated via the aMPK signaling pathway, and that 20(S)-rg3 is capable of inducing apoptosis in colon cancer.

show abstract

Section: (S)-rg3 Induced Apoptosis By Activating Ampkmentioning

confidence: 99%

20(S)-Ginsenoside Rg3-induced apoptosis in HT-29 colon cancer cells is associated with AMPK signaling pathway

Chung¹

2010

Mol Med Rep

View full text Add to dashboard Cite

show abstract

“…1A), an active monomer extracted from Rheum, Polygonum, Buckthorn and Senna, has been shown to be active against pancreatic (5,6), lung (7,8), breast (9,10), liver (11), prostate (12,13), ovarian (14), cervical (15), colon (16), gallbladder (17) and human tongue cancer SCC-4 cells (18,19). Moreover, it has been reported that emodin induces apoptosis of human breast cancer MCF-7 (20) and MDA-MB-453 cells (21). However, there are no reports on the effect of emodin on breast cancer MDA-MB-231 cells.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effect of emodin on migration, invasion and metastasis of human breast cancer MDA-MB-231 cells in vitro and in vivo

et al. 2014

View full text Add to dashboard Cite

Abstract. In breast cancer, metastasis is the main reason for patient mortality. In the present study, we used breast cancer MDA-MB-231 cells and a mouse xenograft model to demonstrate the effect of emodin on the migration, invasion and metastasis of human breast cancer MDA-MB-231 cells and the related mechanisms. In vitro, wound healing and Transwell assays showed that emodin dose-dependently inhibited the migration and invasion of MDA-MB-231 cells. Enzyme-linked immunosorbent assay (ELISA) showed that emodin decreased the secretion of MMP-2 and MMP-9. Western blot analysis showed that emodin downregulated the expression levels of MMP-2, MMP-9, uPA and uPAR as well as p38 inhibitor SB203580 and ERK inhibitor PD980559, even though TIMP-1 and TIMP-2 were not obviously changed in the MDA-MB-231 cells. Furthermore, emodin inhibited the activity of p38 and ERK1/2 in the MDA-MB-231 cells. In vivo, emodin inhibited lung metastasis in mice bearing the breast cancer MDA-MB-231 xenografts with no obvious changes in body weight, liver and kidney functions. These results indicated that emodin inhibited the lung metastasis of human breast cancer in a mouse xenograft model, and inhibited the invasion of MDA-MB-231 cells associated with the downregulation of MMP-2, MMP-9, uPA and uPAR expression as well as decreased activity of p38 and ERK.

show abstract

“…Apoptosis plays an important role in the maintenance of cellular homeostasis by regulating cell division and cell death (Yan et al, 2008). Cancer cells are characterized by uncontrolled proliferation and reduced apoptosis.…”

Section: Resultsmentioning

confidence: 99%

Evaluation on Anticancer Effect Against HL-60 Cells and Toxicity in vitro and in vivo of the Phenethyl Acetate Isolated from a Marine Bacterium Streptomyces griseus

Lee¹,

Zhang²,

Ko³

et al. 2015

Fisheries and aquatic sciences

View full text Add to dashboard Cite

We previously identified Streptomyces griseus as an anti-cancer agent . In this study, we isolated compounds from S. griseus and evaluated their anticancer effect and toxicity in vitro and in vivo. Preparative centrifugal partition chromatography (CPC) was used to obtain three compounds, cyclo, cyclo( L -Phe-trans-4-hydroxy-L -Pro) and phenethyl acetate (PA). We chose PA, which had the highest anticancer activity, as a target compound for further experiments. PA induced the formation of apoptotic bodies, DNA fragmentation, DNA accumulation in G 0 /G 1 phase, and reactive oxygen species (ROS) formation. Furthermore, PA treatment increased Bax/Bcl-xL expression, activated caspase-3, and cleaved poly-ADP-ribose polymerase (PARP) in HL-60 cells. Simultaneous evaluation in vitro and in vivo, revealed that PA exhibited no toxicity in Vero cells and zebrafish embryos. We revealed, for the first time, that PA generates ROS, and that this ROS accumulation induced the Bcl signaling pathway.

show abstract

Emodin azide methyl anthraquinone derivative triggers mitochondrial-dependent cell apoptosis involving in caspase-8-mediated Bid cleavage

Cited by 80 publications

References 46 publications

20(S)-Ginsenoside Rg3-induced apoptosis in HT-29 colon cancer cells is associated with AMPK signaling pathway

20(S)-Ginsenoside Rg3-induced apoptosis in HT-29 colon cancer cells is associated with AMPK signaling pathway

Inhibitory effect of emodin on migration, invasion and metastasis of human breast cancer MDA-MB-231 cells in vitro and in vivo

Evaluation on Anticancer Effect Against HL-60 Cells and Toxicity in vitro and in vivo of the Phenethyl Acetate Isolated from a Marine Bacterium Streptomyces griseus

Contact Info

Product

Resources

About