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Dual targeting of ANGPT1 and TGFBR2 genes by miR-204 controls angiogenesis in breast cancer
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Dual targeting of ANGPT1 and TGFBR2 genes by miR-204 controls angiogenesis in breast cancer
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Journal Article
Dual targeting of ANGPT1 and TGFBR2 genes by miR-204 controls angiogenesis in breast cancer
2016
Overview
Deregulated expression of microRNAs has been associated with angiogenesis. Studying the miRNome of locally advanced breast tumors we unsuspectedly found a dramatically repression of miR-204, a small non-coding RNA with no previous involvement in tumor angiogenesis. Downregulation of miR-204 was confirmed in an independent cohort of patients and breast cancer cell lines. Gain-of-function analysis indicates that ectopic expression of miR-204 impairs cell proliferation, anchorage-independent growth, migration, invasion, and the formation of 3D capillary networks
in vitro
. Likewise,
in vivo
vascularization and angiogenesis were suppressed by miR-204 in a nu/nu mice model. Genome-wide profiling of MDA-MB-231 cells expressing miR-204 revealed changes in the expression of hundred cancer-related genes. Of these, we focused on the study of pro-angiogenic ANGPT1 and TGFβR2. Functional analysis using luciferase reporter and rescue assays confirmed that ANGPT1 and TGFβR2 are novel effectors downstream of miR-204. Accordingly, an inverse correlation between miR-204 and ANGPT1/TGFβR2 expression was found in breast tumors. Knockdown of TGFβR2, but not ANGPT1, impairs cell proliferation and migration whereas inhibition of both genes inhibits angiogenesis. Taken altogether, our findings reveal a novel role for miR-204/ANGPT1/TGFβR2 axis in tumor angiogenesis. We propose that therapeutic manipulation of miR-204 levels may represent a promising approach in breast cancer.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/89
/ 38/109
/ 38/61
/ 631/67
/ 692/4028
/ 82
/ 82/1
/ 82/80
/ Angiopoietin-1 - biosynthesis
/ Breast Neoplasms - blood supply
/ Breast Neoplasms - metabolism
/ Female
/ Genomes
/ Humanities and Social Sciences
/ Humans
/ miRNA
/ Neoplasm Proteins - biosynthesis
/ Neoplasm Proteins - genetics
/ Neovascularization, Pathologic - genetics
/ Neovascularization, Pathologic - metabolism
/ Neovascularization, Pathologic - pathology
/ Neovascularization, Pathologic - therapy
/ Protein-Serine-Threonine Kinases - biosynthesis
/ Protein-Serine-Threonine Kinases - genetics
/ Receptors, Transforming Growth Factor beta - biosynthesis
/ Receptors, Transforming Growth Factor beta - genetics
/ RNA, Neoplasm - biosynthesis
/ Science
/ Tumors
