Abstract P4-07-18: PDGFRbeta-induced miR-9 is up-regulated in triple negative breast cancer
Autor: | Rosaria Orlandi, Marilena V. Iorio, Angela Moliterni, Maria Luisa Carcangiu, Elvira D'Ippolito, Ilaria Plantamura, Stefania Cresta, Elda Tagliabue, F. de Braud, Anna Tessari |
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Rok vydání: | 2013 |
Předmět: |
Oncology
CA15-3 Cancer Research medicine.medical_specialty business.industry medicine.medical_treatment Cancer medicine.disease Fold change Targeted therapy Breast cancer Downregulation and upregulation Internal medicine microRNA medicine skin and connective tissue diseases business Triple-negative breast cancer |
Zdroj: | Cancer Research. 73:P4-07 |
ISSN: | 1538-7445 0008-5472 |
DOI: | 10.1158/0008-5472.sabcs13-p4-07-18 |
Popis: | miR-9 has been described as an oncogenic microRNA associated to a metastatic phenotype and able to induce EMT (epithelial-to-mesenchymal transition) through direct targeting of E-cadherin. However, data available concerning the expression and the role of this microRNA in different subgroups of breast cancer are still not exhaustive. Evaluating miR-9 expression by Real-Time PCR in a series of 92 breast cancer specimens (35 luminal, 36 HER2, 21 triple negative), we found that this microRNA is increasingly higher in HER2 and Triple Negative versus ER positive patients (fold change 3 and 8 respectively). Moreover, preliminary analysis of miR-9 expression in correlation with bio-pathological features and clinical data also indicates a trend in association with disease progression. Triple Negative Breast Cancers represent a very aggressive breast cancer subgroup, still lacking specific markers for an effective targeted therapy; we investigated whether miR-9 might play a role in the biology of this tumor subtype. Preliminary data indicate that miR-9 is activated downstream PDGFRbeta, which represents a crucial player in the aggressive phenotype of Triple Negative Breast Cancer. In summary, here we show that miR-9 is significantly upregulated in triple negative breast cancer in comparison with other breast cancer subgroups and is activated downstream PDGFRbeta. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P4-07-18. |
Databáze: | OpenAIRE |
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