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MG624, an α7-nAChR antagonist, inhibits angiogenesis via the Egr-1/FGF2 pathway

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An Erratum to this article was published on 03 March 2012

Abstract

Small cell lung cancer (SCLC) demonstrates a strong etiological association with smoking. Although cigarette smoke is a mixture of about 4,000 compounds, nicotine is the addictive component of cigarette smoke. Several convergent studies have shown that nicotine promotes angiogenesis in lung cancers via the α7-nicotinic acetylcholine receptor (α7-nAChR) on endothelial cells. Therefore, we conjectured that α7-nAChR antagonists may attenuate nicotine-induced angiogenesis and be useful for the treatment of human SCLC. For the first time, our study explores the anti-angiogenic activity of MG624, a small-molecule α7-nAChR antagonist, in several experimental models of angiogenesis. We observed that MG624 potently suppressed the proliferation of primary human microvascular endothelial cells of the lung (HMEC-Ls). Furthermore, MG624 displayed robust anti-angiogenic activity in the Matrigel, rat aortic ring and rat retinal explant assays. The anti-angiogenic activity of MG624 was assessed by two in vivo models, namely the chicken chorioallantoic membrane model and the nude mice model. In both of these experimental models, MG624 inhibited angiogenesis of human SCLC tumors. Most importantly, the administration of MG624 was not associated with any toxic side effects, lethargy or discomfort in the mice. The anti-angiogenic activity of MG624 was mediated via the suppression of nicotine-induced FGF2 levels in HMEC-Ls. MG624 decreased nicotine-induced early growth response gene 1 (Egr-1) levels in HMEC-Ls, and reduced the levels of Egr-1 on the FGF2 promoter. Consequently, this process decreased FGF2 levels and angiogenesis. Our findings suggest that the anti-angiogenic effects of MG624 could be useful in anti-angiogenic therapy of human SCLCs.

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Acknowledgments

We thank Dr. Srikumar Chellappan and his laboratory for continuous support. We are grateful to Carla Cook, Dr. Travis Salisbury and Dr. Nalini Santanam for their help in the real-time PCR experiments. We also acknowledge Dr. Cattini and Dr. Nilson for providing us the constructs used in this study. This work was supported by the grants Young Clinical Scientist Award (#82115) from the Flight Attendant Medical Association, Miami, FL, Research Starter Grant from the PhRMA Foundation, Washington D.C., ASPET-Astellas Award, NIH-ROI-NIDDK65003 (to RDE). AMD and KCB are recipients of graduate fellowships from the WVSGC.

Conflict of interest

None of the authors have any conflict of interest.

Ethics statement

All experiments were performed in the United States of America and they comply with the laws of the USA.

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Authors and Affiliations

  1. Department of Pharmacology, Physiology, and Toxicology, Joan C. Edwards School of Medicine, Marshall University, 1700 3rd Avenue, Huntington, WV, 25755, USA

    Kathleen C. Brown, Jamie K. Lau, Aaron M. Dom, Clayton M. Crabtree, Brandon S. Shiflett, Aileen J. Marcelo, Nancy A. Proper, Richard D. Egleton, Elsa I. Mangiarua & Piyali Dasgupta

  2. Department of Biochemistry and Microbiology, Joan C. Edwards School of Medicine, Marshall University, Huntington, WV, 25755, USA

    Theodore R. Witte & W. Elaine Hardman

  3. Department of Biology, Alderson-Broaddus College, Philippi, WV, 26416, USA

    Haitao Luo & Yi Charlie Chen

  4. Department of Biology, West Virginia University, Morgantown, WV, 26506, USA

    Yashoni H. Shah

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  1. Kathleen C. Brown
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  2. Jamie K. Lau
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Correspondence to Piyali Dasgupta.

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Kathleen C. Brown, Jamie K. Lau and Aaron M. Dom contributed equally to the work presented here and should therefore be regarded as equivalent authors.

An erratum to this article can be found at http://dx.doi.org/10.1007/s10456-012-9258-0.

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Brown, K.C., Lau, J.K., Dom, A.M. et al. MG624, an α7-nAChR antagonist, inhibits angiogenesis via the Egr-1/FGF2 pathway. Angiogenesis 15, 99–114 (2012). https://doi.org/10.1007/s10456-011-9246-9

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