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Overexpression of miR‐20b inhibits the expression of HIF‐1α and STAT‐3 in invasive ductal carcinoma of the breast (1138.2)
Author(s) -
Zanetti Juliana,
Darin Patrícia,
Lucca Fernando,
RibeiroSilva Alfredo
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1138.2
Subject(s) - stat , microrna , stat protein , cancer research , immunohistochemistry , ductal carcinoma , breast carcinoma , breast cancer , carcinoma , angiogenesis , transcription factor , hypoxia inducible factors , downregulation and upregulation , medicine , biology , pathology , stat3 , cancer , apoptosis , gene , biochemistry
It is known that the hypoxia inducible factor‐1α (HIF‐1α) and the signal transducer and activator of transcription 3 (STAT‐3) are targets of miR‐20b. The role played by microRNAs (miRNAs) in breast cancer has been mainly studied using tumor cells. In this study, we investigated the expression of miR‐20b in formalin‐fixed paraffin embedded (FFPE) samples, as also as HIF‐1α and STAT‐3, in samples of invasive ductal carcinoma (IDC). The expression of miR‐20b and the proteins HIF‐1α and STAT‐3 was evaluated by real time PCR and immunohistochemistry, respectively. We found that the overexpression of miR‐20b (3‐fold; p<0.05) is accompanied by the downregulation of STAT‐3 (70%; p<0.001) in FFPE samples of IDC. We also observed that HIF‐1α expression in IDC and control samples was not statistically significant. Our results suggest that miR‐20b regulates the expression of HIF‐1α and its transcription factor STAT‐3 in IDC. These findings are relevant since HIF‐1α expression has been correlated with increased intratumoral angiogenesis, cancer progression and poor prognosis in breast cancer. Grant Funding Source : Supported by FAPESP 2012/05235‐3