Induction of mitotic arrest and apoptosis by evodiamine in human leukemic T-lymphocytes

Huang, Yu‐Chun; Guh, Jih‐Hwa; Teng, Che-Ming

doi:10.1016/j.lfs.2003.11.025

Cited by 62 publications

(56 citation statements)

References 28 publications

(30 reference statements)

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“…That evodiamine down-regulates Cyclin D1 expression may explain the results from earlier reports indicating that this agent induces G 2 /M arrest rather than G 1 /S arrest (4,5). It also may explain the antiproliferative effects of evodiamine through TNF-induced NF-B-mediated down-regulation of Cyclin D1 by evodiamine.…”

Section: Figmentioning

confidence: 73%

Evodiamine Abolishes Constitutive and Inducible NF-κB Activation by Inhibiting IκBα Kinase Activation, Thereby Suppressing NF-κB-regulated Antiapoptotic and Metastatic Gene Expression, Up-regulating Apoptosis, and Inhibiting Invasion

Takada

Kobayashi

Aggarwal

2005

Journal of Biological Chemistry

171

102

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Evodiamine, an alkaloidal component extracted from the fruit of Evodiae fructus (Evodia rutaecarpa Benth., Rutaceae), exhibits antiproliferative, antimetastatic, and apoptotic activities through a poorly defined mechanism. Because several genes that regulate cellular proliferation, carcinogenesis, metastasis, and survival are regulated by nuclear factor-B (NF-B), we postulated that evodiamine mediates its activity by modulating NF-B activation. In the present study, we investigated the effect of evodiamine on NF-B and NF-B-regulated gene expression activated by various carcinogens. We demonstrate that evodiamine was a highly potent inhibitor of NF-B activation, and it abrogated both inducible and constitutive NF-B activation. The inhibition corresponded with the sequential suppression of IB␣ kinase activity, IB␣ phosphorylation, IB␣ degradation, p65 phosphorylation, p65 nuclear translocation, and p65 acetylation. Evodiamine also inhibited tumor necrosis factor (TNF)-induced Akt activation and its association with IKK. Suppression of Akt activation was specific, because it had no effect on JNK or p38 MAPK activation.

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Section: Figmentioning

confidence: 73%

Evodiamine Abolishes Constitutive and Inducible NF-κB Activation by Inhibiting IκBα Kinase Activation, Thereby Suppressing NF-κB-regulated Antiapoptotic and Metastatic Gene Expression, Up-regulating Apoptosis, and Inhibiting Invasion

Takada

Kobayashi

Aggarwal

2005

Journal of Biological Chemistry

171

102

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“…Previous studies had been demonstrated that EVO inhibits the proliferation of cancer cells by blocking cell cycle progression (Huang et al, 2004(Huang et al, , 2005Rasul et al, 2012;Du et al, 2013). An analysis of DNA content in the samples treated with PLGA and EVO-PLGA NPs has been respectively performed to test whether the reduced proliferation observed was due to cell cycle arrest.…”

Section: Cell Cycle Analysismentioning

confidence: 97%

Preparation, characterization, and anticancer efficacy of evodiamine-loaded PLGA nanoparticles

et al. 2014

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Evodiamine (EVO) is a plant-derived indolequinazoline alkaloid with potential anticancer activity. However, low bioavailability caused by its poor water solubility limits it anticancer efficacy in clinic. To enhance the solubility and improve the bioavailability of EVO, a delivery system based on poly (lactic-co-glycolic acid) (PLGA) nanoparticles loaded with EVO (EVO-PLGA NPs) for treating breast cancer was prepared in this study. The physicochemical characterization and in vitro antitumor evaluation of EVO-PLGA NPs were determined. EVO-PLGA NPs could persistently control the release of EVO for 180 h. 3-[4,5-Dimethyl-2-thiazolyl]-2,5-diphenyl tetrazolium bromide (MTT) assessment and colony formation assay showed that EVO-PLGA NPs could enhance the toxicity and the proliferation inhibition effect of EVO on MCF-7 breast cancer cells. EVO-PLGA NPs did not strengthen G2/M arrest effect of EVO-treated cells after 24h incubation. Meanwhile, EVO-PLGA NPs could increase the expression of cyclin B1 and decrease the expression of b-actin. Taken together, these results suggested that -PLGA NPs is promising for improving anticancer efficacy of EVO in breast cancer therapy.

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“…However, it is known that some pro-apoptotic phenotype inducers including vincristine, b-catenin, nocodazole, paclitaxel, evodiamine, etc. render increased proportions of G 2 /M-stage cells [38][39][40][41][42][43][44][45]. Thus, our findings in RK13 cells require confirmation using cultured nerve cells, in which apoptosis is known to be a feature of prion diseases.…”

Section: Rk13mentioning

confidence: 98%

Cell expression of a four extra octarepeat mutated PrP^C modifies cell structure and cell cycle regulation

Martín¹,

Herva²,

Espinosa³

et al. 2006

FEBS Letters

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RK13 cell lines generated to express bovine PrP C with a four extra octarepeat insertional mutation (Bo10ORPrP C ) show partially insoluble PrP C and lower rates of cell growth when compared to either the same cells expressing wild type C or the original RK13 cell line. The expression of C in cell cultures was also associated with changes in cell size and reorganization of the actin cytoskeleton. This last process was reversed by Clostridium difficile toxin-B, a specific inhibitor of small GTPase proteins. Further, in clones expressing Bo-10ORPrP C , increased proportions of cells at cell cycle stage G2/M were observed. Proteasome inhibitors caused a further expansion of G2/M-stage cells that was more marked in cell lines expressing Bo-10ORPrP C than those expressing Bo-6ORPrP C , while this effect was minimal or null in the original RK13 cell line. Hence, the presence of Bo10ORPrP C in RK13 cells promotes cell cycle arrest at G2/M, and the effect is amplified by proteasome inhibition. These findings suggest a role for PrP C in cell morphology and cell cycle regulation, and open new avenues for understanding the mechanisms underlying PrP mutation-associated diseases.

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Induction of mitotic arrest and apoptosis by evodiamine in human leukemic T-lymphocytes

Cited by 62 publications

References 28 publications

Evodiamine Abolishes Constitutive and Inducible NF-κB Activation by Inhibiting IκBα Kinase Activation, Thereby Suppressing NF-κB-regulated Antiapoptotic and Metastatic Gene Expression, Up-regulating Apoptosis, and Inhibiting Invasion

Evodiamine Abolishes Constitutive and Inducible NF-κB Activation by Inhibiting IκBα Kinase Activation, Thereby Suppressing NF-κB-regulated Antiapoptotic and Metastatic Gene Expression, Up-regulating Apoptosis, and Inhibiting Invasion

Preparation, characterization, and anticancer efficacy of evodiamine-loaded PLGA nanoparticles

Cell expression of a four extra octarepeat mutated PrP^C modifies cell structure and cell cycle regulation

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Induction of mitotic arrest and apoptosis by evodiamine in human leukemic T-lymphocytes

Cited by 62 publications

References 28 publications

Evodiamine Abolishes Constitutive and Inducible NF-κB Activation by Inhibiting IκBα Kinase Activation, Thereby Suppressing NF-κB-regulated Antiapoptotic and Metastatic Gene Expression, Up-regulating Apoptosis, and Inhibiting Invasion

Evodiamine Abolishes Constitutive and Inducible NF-κB Activation by Inhibiting IκBα Kinase Activation, Thereby Suppressing NF-κB-regulated Antiapoptotic and Metastatic Gene Expression, Up-regulating Apoptosis, and Inhibiting Invasion

Preparation, characterization, and anticancer efficacy of evodiamine-loaded PLGA nanoparticles

Cell expression of a four extra octarepeat mutated PrPC modifies cell structure and cell cycle regulation

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Cell expression of a four extra octarepeat mutated PrP^C modifies cell structure and cell cycle regulation