Oncosuppressive role of p53-induced miR-205 in triple negative breast cancer
| Autor: | Luca Braccioli, Gianpiero Di Leva, Carlo M. Croce, Ilaria Plantamura, Gerard J. Nuovo, Dario Palmieri, Marianna Sasso, Claudia Piovan, Monica Tortoreto, Marilena V. Iorio, Tiziana Triulzi, Cristian Taccioli, Patrizia Casalini, Elda Tagliabue |
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| Jazyk: | angličtina |
| Rok vydání: | 2012 |
| Předmět: |
Cancer Research
Transcription Genetic medicine.medical_treatment Molecular Sequence Data Down-Regulation Breast Neoplasms Mice SCID Cell fate determination Biology Response Elements Q1 Targeted therapy Mice Cell Line Tumor microRNA Genetics medicine E2F1 Animals Humans Triple-negative breast cancer Cellular Senescence Cell Proliferation Base Sequence Cell growth Cell Cycle General Medicine Cell cycle Molecular biology Xenograft Model Antitumor Assays R1 Gene Expression Regulation Neoplastic MicroRNAs Oncology Papers Cancer research Molecular Medicine Female Laminin Tumor Suppressor Protein p53 Cell aging E2F1 Transcription Factor Protein Binding |
| ISSN: | 1574-7891 |
| Popis: | An increasing body of evidence highlights an intriguing interaction between microRNAs and transcriptional factors involved in determining cell fate, including the well known “genome guardian” p53. Here we show that miR-205, oncosuppressive microRNA lost in breast cancer, is directly transactivated by oncosuppressor p53. Moreover, evaluating miR-205 expression in a panel of cell lines belonging to the highly aggressive triple negative breast cancer (TNBC) subtype, which still lacks an effective targeted therapy and characterized by an extremely undifferentiated and mesenchymal phenotype, we demonstrated that this microRNA is critically down-expressed compared to a normal-like cell line. Re-expression of miR-205 where absent strongly reduces cell proliferation, cell cycle progression and clonogenic potential in vitro, and inhibits tumor growth in vivo, and this tumor suppressor activity is at least partially exerted through targeting of E2F1, master regulator of cell cycle progression, and LAMC1, component of extracellular matrix involved in cell adhesion, proliferation and migration. |
| Databáze: | OpenAIRE |
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