Pharmacological Actions of Multi-Target-Directed Evodiamine

Yu, Hui; Jin, Hongwei; Gong, Wuzhuang; Wang, Zhanli; Liang, Huaping

doi:10.3390/molecules18021826

Cited by 148 publications

(111 citation statements)

References 131 publications

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“…In addition, another study showed that EVO promoted translocation of apoptosis-inducing factor (AIF) into the nucleus of human leukemia u937 cells (46). Collectively, EVO was found to induce the apoptosis of many tumor cell lines via caspase-dependent and caspase-independent signaling pathways (47). Moreover, Liu et al proved that EVO-mediated autophagy leading to increased apoptosis and reduction in cell viability was via a calcium-JNK signaling pathway (48).…”

Section: Discussionmentioning

confidence: 99%

Evodiamine inhibits the proliferation of human osteosarcoma cells by blocking PI3K/Akt signaling

Meng

Shu

et al. 2015

Oncology Reports

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Abstract. Osteosarcoma (OS) is the most common non-hematologic primary malignancy of bone, and multiple chemotherapeutic agents have been applied in the treatment of OS for over 40 years. Nevertheless, due to the poor prognosis of OS, it is essential to develop a novel treatment strategy. Evodiamine (EVO), a quinolone alkaloid extracted from the fruit of Evodia rutaecarpa, has been demonstrated to inhibit tumor cell proliferation. Thus, the main aim of the present study was to investigate the anti-proliferative and apoptosis-inducing effects of evodiamine (EVO) on human OS 143B cells, but also the possible mechanisms underlying these effects. The results of crystal violet staining, flow cytometry, western blot analysis and an in vivo experiment demonstrated that EVO exhibits significant inhibitory effects on cell proliferation, exhibits apoptosis-inducing effects and arrests the cell cycle in 143B cells. According to our findings of polymerase chain reaction (PCR), western blot analysis and recombinant adenoviral transfection, we confirmed that EVO upregulates both the protein and gene levels of phosphatase and tensin homolog (PTEN) in a concentration-dependent manner in 143B cells. Overexpression of PTEN reinforced the anti-proliferative effect of EVO in the 143B cells, while knockdown of PTEN upregulated PI3K/Akt signaling transduction and reversed the inhibitory effect of EVO on 143B cell proliferation. Further analysis indicated that EVO upregulated the expression of PTEN by inactivating PI3K/Akt signaling by decreasing phosphorylated Akt1/2. Based on the above results, we conclude that PTEN/PI3K/Akt signaling is involved in the inhibitory effect on human OS 143B cell proliferation by EVO.

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Section: Discussionmentioning

confidence: 99%

Evodiamine inhibits the proliferation of human osteosarcoma cells by blocking PI3K/Akt signaling

Meng

Shu

et al. 2015

Oncology Reports

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“…Evodiamine (1, Figure 1) is a quinolone alkaloid isolated from the fruit of Evodia rutaecarpa (Chinese name: Wu-Chu-Yu), which is one of the most popular and multi-purpose Traditional Chinese Medicines widely used for treating diverse human disorders [1] and is also very attractive as a component of healthy foods [2,3]. It was demonstrated by Hu [4] and Linag [1] that evodiamine possesses a wide range of biological activities related to anti-inflammatory, anti-obesity and antitumor properties.…”

Section: Introductionmentioning

confidence: 99%

Design, Synthesis and Evaluation of N13-Substituted Evodiamine Derivatives against Human Cancer Cell Lines

Song

Chen

et al. 2013

Molecules

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Abstract:Attempting to improve the anticancer activity and solubility of evodiamine in simulated gastric fluid (SGF) and simulated intestinal fluid (SIF) solutions, thirty-eight N13-substituted evodiamine derivatives were designed, synthesized and tested for antitumor activities against six kinds of human cancer cell lines, namely prostate cancer (DU-145 and PC-3), lung cancer (H460), breast cancer (MCF-7), colon cancer (HCT-5) and glioblastoma (SF-268). The solubility of these compounds in SGF and SIF solutions was evaluated, and apoptosis induced by 2-2, 2-3, 2-16 and 3-2 was determined. The results showed: (1) among all compounds examined, 2-16 showed the highest antitumor activity and a broader spectrum of activity, with IC 50 values ranging from 1-2 µM; (2) their solubility was obviously improved; (3) 2-3, 2-16 and 3-2 had a significant impact inducing apoptosis in some cancer cell lines. The preliminary structure-activity relationships of these derivatives were discussed.

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“…It has been demonstrated that EVO possessed a plenty of pharmacologic activities, such as anti-obesity, anti-inflammatory , and anti-infectious effect (Li-Weber, 2013;Yu et al, 2013). Furthermore, many studies declared that EVO was a promising anti-tumor agent (Jiang & Hu, 2009), which could suppress proliferation (Chen et al, 2010), induce apoptosis (Rasul et al, 2012), and inhibit metastasis (Takada et al, 2005) of cancer cells.…”

Section: Introductionmentioning

confidence: 99%

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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Pharmacological Actions of Multi-Target-Directed Evodiamine

Cited by 148 publications

References 131 publications

Evodiamine inhibits the proliferation of human osteosarcoma cells by blocking PI3K/Akt signaling

Evodiamine inhibits the proliferation of human osteosarcoma cells by blocking PI3K/Akt signaling

Design, Synthesis and Evaluation of N13-Substituted Evodiamine Derivatives against Human Cancer Cell Lines

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

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