Methylseleninic acid restricts tumor growth in nude mice model of metastatic breast cancer probably via inhibiting angiopoietin-2Reportar como inadecuado

Methylseleninic acid restricts tumor growth in nude mice model of metastatic breast cancer probably via inhibiting angiopoietin-2 - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

BMC Cancer

, 12:192

First Online: 28 May 2012Received: 19 January 2012Accepted: 28 May 2012DOI: 10.1186-1471-2407-12-192

Cite this article as: Wu, X., Zhang, Y., Pei, Z. et al. BMC Cancer 2012 12: 192. doi:10.1186-1471-2407-12-192


BackgroundAngiopoietin-2 Ang-2 plays critical roles in vascular morphogenesis and its upregulation is frequently associated with various tumors. Previous studies showed that certain selenium compounds possess anti-tumor effects. However, the underlining mechanism has not been elucidated in detail. Plus, results of research on the anti-tumor effects of selenium compounds remain controversial.

MethodsWe investigated levels of Ang-2 and vascular endothelial growth factor VEGF on the estrogen-independent bone metastatic mammary cancer MDA-MB-231 cells in response to treatment by methylseleninic acid MSeA, and further examined the effects of MSeA oral administration on xenograft mammary tumors of athymic nude mice by RT-PCR, Western, radioimmuno assay, and Immunohistochemistry.

ResultsTreatment of MDA-MB-231 cells with MSeA caused significant reduction of Ang-2 mRNA transcripts and secretion of Ang-2 proteins by the cells. Level of VEGF protein was accordingly decreased following the treatment. Compared with the controls, oral administration of MSeA 3 mg-kg-day for 18 days to the nude mice carrying MDA-MB-231 induced tumors resulted in significant reduction in xenograft tumor volume and weights, significant decrease in microvascular density, and promotion of vascular normalization by increasing pericytes coverage. As expected, level of VEGF was also decreased in MSeA treated tumors.

ConclusionsOur results point out that MSeA exerts its anti-tumor effects, at least in part, by inhibiting the Ang-2-Tie2 pathway, probably via inhibiting VEGF.

KeywordsSelenium MSeA Ang-2 VEGF MDA-MB-231 cells Xenograft tumor Electronic supplementary materialThe online version of this article doi:10.1186-1471-2407-12-192 contains supplementary material, which is available to authorized users.

Xiaojing Wu, Yidi Zhang contributed equally to this work.

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Autor: Xiaojing Wu - Yidi Zhang - Zengyang Pei - Si Chen - Xu Yang - Yin Chen - Degui Lin - Runlin Z Ma


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