Volume 7 Supplement 2

São Paulo Advanced School of Comparative Oncology: Abstracts

Open Access

miR-18a as a potential regulator of estrogen-related genes in human breast carcinomas

  • Renata C Bueno1Email author,
  • Fabíola E Rosa2,
  • Francisco A Moraes-Neto3,
  • José Roberto F Caldeira4,
  • Sandra A Drigo5 and
  • Silvia R Rogatto5
BMC Proceedings20137(Suppl 2):P59

DOI: 10.1186/1753-6561-7-S2-P59

Published: 4 April 2013


Estrogen receptor (ER) status has been used as a biomarker in breast carcinomas (BC), allowing the identification of tumors that may respond to ER antagonists or aromatase inhibitors. Two previous studies by our group evaluating gene and miRNA expression profiles in BC samples from Brazilian patients revealed 15 genes and 3 microRNAs as significantly associated with BC, according to ER status. The aim of this study was to evaluate the correlation between these 3 microRNAs and ER-related genes in BC.

Materials and methods

miRDIP algorithm was applied to select candidates among 15 ER-related genes for transcriptional regulation by hsa-miR-26a, hsa-miR-26b and miR-18a. Correlation analyses were performed between transcript levels ofERRB4, TMEM205, SUSD3, DNAJC12, RERG, SCN7A, TBC1D9, TCEA3, THSD4, TIGD6 and miRNAs (miR-26a, miR-26b, and miR-18a) in BC compared with normal breast samples. miRNA expression was assessed in 63 BC and 5 normal breast samples by quantitative RT-PCR using as internal reference RNU48, RNU44 and U47.


Down-expression of miR-18a was significantly associated with ER-positive tumors (P=0.005), while down-expression of miR-26a and miR-26b were significantly associated with ER-negative tumors (P=0.006 and P=0.003, respectively). Additionally, a significant negative correlation was detected between overexpression of ERBB4 and TMEM205 and underexpression of miR-18a(P<0.001; r=-0.703 and P<0.001; r=-0.746, respectively).


Our preliminary results suggest thatin ER-positive tumors, over-expression of ERBB4 (receptor tyrosine kinase) and TMEM205 (encoding a hypothetical protein associated with cisplatin resistance) genes could be explained by miR-18a down-expression. Functional studies are being conducted to confirm these findings. This study may contribute for the identification of potential therapeutic agents in BC.

Financial support


Authors’ Affiliations

Department of Genetics, São Paulo State University
Department of Pathology, São Paulo State University
Department of Pathology, Amaral Carvalho Hospital
Department of Senology, Amaral Carvalho Hospital
NeoGene Laboratory, Department of Urology, São Paulo State University, Botucatu, SP, Brazil, A. C. Camargo Cancer Treatment and Research Center


© Bueno et al; licensee BioMed Central Ltd. 2013

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.