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Cell Death Dis. 2018 Jul 26;9(8):821. doi: 10.1038/s41419-018-0854-9.

MiR-205-5p inhibition by locked nucleic acids impairs metastatic potential of breast cancer cells.

Author information

1
Department of Medical, Oral and Biotechnological Sciences, Center of Excellence on Aging and Translational Medicine (CeSi-Met), G. D'Annunzio University, Chieti-Pescara, Italy. antonelladecola@hotmail.it.
2
Department of Medicine and Aging Science, Center of Excellence on Aging and Translational Medicine (CeSi-Met), G. D'Annunzio University, Chieti-Pescara, Italy.
3
Department of DiBiMIS, University of Palermo, Palermo, Italy.
4
Department of Medical, Oral and Biotechnological Sciences, Center of Excellence on Aging and Translational Medicine (CeSi-Met), G. D'Annunzio University, Chieti-Pescara, Italy. delaurenzi@unich.it.

Abstract

Mir-205 plays an important role in epithelial biogenesis and in mammary gland development but its role in cancer still remains controversial depending on the specific cellular context and target genes. We have previously reported that miR-205-5p is upregulated in breast cancer stem cells targeting ERBB pathway and leading to targeted therapy resistance. Here we show that miR-205-5p regulates tumorigenic properties of breast cancer cells, as well as epithelial to mesenchymal transition. Silencing this miRNA in breast cancer results in reduced tumor growth and metastatic spreading in mouse models. Moreover, we show that miR-205-5p knock-down can be obtained with the use of specific locked nucleic acids oligonucleotides in vivo suggesting a future potential use of this approach in therapy.

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