A miR-192-EGR1-HOXB9 regulatory network controls the angiogenic switch in cancer

Sherry Y. Wu, Rajesha Rupaimoole, Fangrong Shen, Sunila Pradeep, Chad V. Pecot, Cristina Ivan, Archana S. Nagaraja, Kshipra M. Gharpure, Elizabeth Pham, Hiroto Hatakeyama, Michael H. McGuire, Monika Haemmerle, Viviana Vidal-Anaya, Courtney Olsen, Cristian Rodriguez-Aguayo, Justyna Filant, Ehsan A. Ehsanipour, Shelley M. Herbrich, Sourindra N. Maiti, Li Huang, Ji Hoon Kim, Xinna Zhang, Hee-Dong Han, Guillermo N. Armaiz-Pena, Elena G. Seviour, Sue Tucker, Min Zhang, Da Yang, Laurence J. N. Cooper, Rouba Ali-Fehmi, Menashe Bar-Eli, Ju-Seog Lee, Prahlad T. Ram, Keith A. Baggerly, Gabriel Lopez-Berestein, Mien-Chie Hung and Anil K. Sood ()
Additional contact information
Sherry Y. Wu: The University of Texas MD Anderson Cancer Center
Rajesha Rupaimoole: The University of Texas MD Anderson Cancer Center
Fangrong Shen: The University of Texas MD Anderson Cancer Center
Sunila Pradeep: The University of Texas MD Anderson Cancer Center
Chad V. Pecot: The University of Texas MD Anderson Cancer Center
Cristina Ivan: The University of Texas MD Anderson Cancer Center
Archana S. Nagaraja: The University of Texas MD Anderson Cancer Center
Kshipra M. Gharpure: The University of Texas MD Anderson Cancer Center
Elizabeth Pham: The University of Texas MD Anderson Cancer Center
Hiroto Hatakeyama: The University of Texas MD Anderson Cancer Center
Michael H. McGuire: The University of Texas MD Anderson Cancer Center
Monika Haemmerle: The University of Texas MD Anderson Cancer Center
Viviana Vidal-Anaya: The University of Texas MD Anderson Cancer Center
Courtney Olsen: The University of Texas MD Anderson Cancer Center
Cristian Rodriguez-Aguayo: The University of Texas MD Anderson Cancer Center
Justyna Filant: The University of Texas MD Anderson Cancer Center
Ehsan A. Ehsanipour: The University of Texas MD Anderson Cancer Center
Shelley M. Herbrich: The University of Texas MD Anderson Cancer Center
Sourindra N. Maiti: The University of Texas MD Anderson Cancer Center
Li Huang: The University of Texas MD Anderson Cancer Center
Ji Hoon Kim: The University of Texas MD Anderson Cancer Center
Xinna Zhang: Center for RNA Interference and Non-Coding RNA, The University of Texas MD Anderson Cancer Center
Hee-Dong Han: The University of Texas MD Anderson Cancer Center
Guillermo N. Armaiz-Pena: The University of Texas MD Anderson Cancer Center
Elena G. Seviour: The University of Texas MD Anderson Cancer Center
Sue Tucker: The University of Texas MD Anderson Cancer Center
Min Zhang: University of Pittsburgh
Da Yang: University of Pittsburgh
Laurence J. N. Cooper: The University of Texas MD Anderson Cancer Center
Rouba Ali-Fehmi: Wayne State University School of Medicine, Karmanos Cancer Institute
Menashe Bar-Eli: The University of Texas MD Anderson Cancer Center
Ju-Seog Lee: The University of Texas MD Anderson Cancer Center
Prahlad T. Ram: The University of Texas MD Anderson Cancer Center
Keith A. Baggerly: The University of Texas MD Anderson Cancer Center
Gabriel Lopez-Berestein: The University of North Carolina
Mien-Chie Hung: The University of Texas MD Anderson Cancer Center
Anil K. Sood: The University of Texas MD Anderson Cancer Center

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract A deeper mechanistic understanding of tumour angiogenesis regulation is needed to improve current anti-angiogenic therapies. Here we present evidence from systems-based miRNA analyses of large-scale patient data sets along with in vitro and in vivo experiments that miR-192 is a key regulator of angiogenesis. The potent anti-angiogenic effect of miR-192 stems from its ability to globally downregulate angiogenic pathways in cancer cells through regulation of EGR1 and HOXB9. Low miR-192 expression in human tumours is predictive of poor clinical outcome in several cancer types. Using 1,2-dioleoyl-sn-glycero-3-phosphatidylcholine (DOPC) nanoliposomes, we show that miR-192 delivery leads to inhibition of tumour angiogenesis in multiple ovarian and renal tumour models, resulting in tumour regression and growth inhibition. This anti-angiogenic and anti-tumour effect is more robust than that observed with an anti-VEGF antibody. Collectively, these data identify miR-192 as a central node in tumour angiogenesis and support the use of miR-192 in an anti-angiogenesis therapy.

Date: 2016
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DOI: 10.1038/ncomms11169

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