The Effects of Artesunate on the Expression of EGFR and ABCG2 in A549 Human Lung Cancer Cells and a Xenograft Model

Ma, Hu; Yao, Qing; Zhang, Anmei; Lin, Sheng; Wang, Xinxin; Wu, Lei; Sun, Jianping; Chen, Zhengtang

doi:10.3390/molecules161210556

Cited by 54 publications

(27 citation statements)

References 35 publications

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“…Langroudi et al [119] Implanted mouse spontaneous mammary ductal carcinoma, started when tumors reached 500 mm 3 Ma et al [199] A549 human non-small cell lung carcinoma mouse xenograft; started when tumors reached 100 mm 3 , artesunate (60 or 120 mg/kg/day, p.o., 2 weeks).…”

Section: Lai Andmentioning

confidence: 99%

Development of artemisinin compounds for cancer treatment

2012

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Artemisinin contains an endoperoxide moiety that can react with iron to form cytotoxic free radicals. Cancer cells contain significantly more intracellular free iron than normal cells and it has been shown that artemisinin and its analogs selectively cause apoptosis in many cancer cell lines. In addition, artemisinin compounds have been shown to have anti-angiogenic, anti-inflammatory, anti-metastasis, and growth inhibition effects. These properties make artemisinin compounds attractive cancer chemotherapeutic drug candidates. However, simple artemisinin analogs are less potent than traditional cancer chemotherapeutic agents and have short plasma half-lives, and would require high dosage and frequent administration to be effective for cancer treatment. More potent and target-selective artemisinin-compounds are being developed. These include artemisinin dimers and trimers, artemisinin hybrid compounds, and tagging of artemisinin compounds to molecules that are involved in the intracellular iron-delivery mechanism. These compounds are promising potent anticancer compounds that produce significantly less side effect than traditional chemotherapeutic agents.

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Section: Lai Andmentioning

confidence: 99%

Development of artemisinin compounds for cancer treatment

2012

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“…Studies have identified that artemisinin has inhibitory effect on A549 human lung adenocarcinoma cells, and that its mechanism of action may be to inhibit cell proliferation, induce apoptosis and cell cycle arrest (54,55). Thus, the co-administration of artemisinin derivatives with other anti-cancer agents may increase the concentration of those anti-cancer drugs in the cell (56). In the present study, it was identified that artesunate can inhibit the proliferation, apoptosis and invasion of EOMA cells in vitro by reducing the expression of HIF-1α, VEGF-A and VEGFR-2.…”

Section: Discussionmentioning

confidence: 99%

Artesunate inhibits proliferation and invasion of mouse hemangioendothelioma cells in?vitro and of tumor growth in?vivo

et al. 2017

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Abstract. Artesunate has been demonstrated to be a novel potential antitumor agent in numerous studies. However, its efficacy in infantile hemangioma is unknown. The aim of the present study was to investigate the role of artesunate in the control of vascular tumor biological behavior and molecular mechanism using mouse hemangioendothelioma endothelial (EOMA) cells and a nude mouse model. Cell viability, apoptosis and invasion were determined by an MTT assay, flow cytometric analysis and Transwell invasion assay, respectively. Reverse transcription-quantitative polymerase chain reaction and western blotting were utilized to examine the expression of genes and proteins. Inoculated EOMA cells were injected into the subcutaneous tissues of nude mice to observe the effect of artesunate therapy on the vascular tumor, an effect that was similar to that of pingyangmycin (PYM). It was identified that artesunate treatment (0-600 µg/ml) inhibited cell growth in a time-and dose-dependent manner. Artesunate at 300 µg/ml significantly reduced the proliferation and invasion of EOMA cells, and significantly decreased the expression of vascular endothelial growth factor (VEGF)-A, VEGFR-1, VEGFR-2 and hypoxia inducible factor-1α over time; caspase-3 was simultaneously upregulated in vitro. Artesunate significantly inhibited tumor growth, and the curative effect was similar to that observed with PYM in vivo. It was concluded that artesunate could effectively inhibit the growth of vascular tumors, and thus could be a novel drug candidate for the treatment of infantile hemangioma.

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“…In recent years, there is increasing evidence that ART has anti-cancer capability [16]; ART has been shown to have a profound cytotoxic action against several tumors, such as Kaposi’s sarcoma, hepatocellular carcinoma, non-small cell lung cancer and cervical cancer [17,18,19,20]. However, whether ART can inhibit the growth of bladder cancer has not yet been reported.…”

Section: Introductionmentioning

confidence: 99%

Artesunate Induces Apoptosis of Bladder Cancer Cells by miR-16 Regulation of COX-2 Expression

Zuo

Wang

Xue

2014

IJMS

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Bladder cancer is the most common malignant tumor of the urinary tract and remains one of the major causes of cancer death worldwide. In this study, we investigated the effect and mechanism of Artesunate (ART), a traditional Chinese medicine, on inducing apoptosis of human bladder cancer cells. In vivo antitumor activity was investigated in bladder cancer in rat by subcutaneous injection of different concentration of ART. The effect of ART on growth inhibition and apoptosis of bladder cancer cells was evaluated using dimethylthiazoly-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis, respectively. Cyclooxygenase-2 (COX-2) and miR-16 expression levels were determined with real-time PCR. The concentrations of prostaglandin E2 (PGE2) in the supernatants of bladder cancer cells were measured with an ELISA kit. The miR-16 inhibitor or mimic were transfected into cells to up- or down-regulate miR-16 expression. ART efficiently inhibited orthotopic tumor growth in the bladder cancer rat, which is accompanied with an increase of miR-16 expression and a decrease of COX-2 expression. In vitro, ART could induce cytotoxicity and apoptosis in bladder cancer cells, but presented a much lighter toxicity effect against normal human urothelial cells. ART significantly increased miR-16 expression and decreased the expression of COX-2 and the production of PGE2. More importantly, down-regulation of miR-16 expression could reverse the effect of ART on apoptosis and COX-2 expression in bladder cells. Moreover, exogenous PGE2 could inhibit apoptosis of bladder cancer cells treated with ART. In conclusion, ART can elicit an anti-tumor effect against bladder cancer by up-regulation of miR-16 expression, which resulted in the decrease of COX-2 expression and PGE2 production. Hence, ART might be an effective drug for the treatment of bladder cancer.

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The Effects of Artesunate on the Expression of EGFR and ABCG2 in A549 Human Lung Cancer Cells and a Xenograft Model

Cited by 54 publications

References 35 publications

Development of artemisinin compounds for cancer treatment

Development of artemisinin compounds for cancer treatment

Artesunate inhibits proliferation and invasion of mouse hemangioendothelioma cells in?vitro and of tumor growth in?vivo

Artesunate Induces Apoptosis of Bladder Cancer Cells by miR-16 Regulation of COX-2 Expression

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