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Jing Yu,Qi Li,Qing Xu,Lingzhi Liu,Binghua Jiang.Journal of Biomedical Research,2011,25(3):170-177
MiR-148a inhibits angiogenesis by targeting ERBB3
  
DOI10.1016/S1674-8301(11)60022-5
Keywordsbreast cancer, microRNA-148a, angiogenesis, ERBB3
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Jing Yu Lab of Reproductive Medicine, Department of Pathology, Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing Medical University, Nanjing ,Jiangsu , China
Qi Li Lab of Reproductive Medicine, Department of Pathology, Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing Medical University, Nanjing ,Jiangsu , China
Qing Xu Lab of Reproductive Medicine, Department of Pathology, Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing Medical University, Nanjing ,Jiangsu , China
Lingzhi Liu Lab of Reproductive Medicine, Department of Pathology, Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing Medical University, Nanjing ,Jiangsu , China
Binghua Jiang Lab of Reproductive Medicine, Department of Pathology, Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Cancer Center, Nanjing Medical University, Nanjing ,Jiangsu , China/Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, USA
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Abstract
      MicroRNAs (miRNAs) play an important role in carcinogenesis in various solid cancers including breast can-cer. Down-regulation of microRNA-148a (miR-148a) has been reported in certain cancer types. However, the biological role of miR-148a and its related targets in breast cancer are unknown yet. In this study, we showed that the level of miR-148a was lower in MCF7 cells than that in MCF10A cells. V-erb-b2 erythroblastic leukemia viral oncogene homolog 3 (ERBB3) is a direct target of miR-148a in human breast cancer cells through direct binding of miR-148a to ERBB3 3¨-UTR region. Overexpression of miR-148a in MCF7 cells inhibited ERBB3 expression, blocked the downstream pathway activation including activation of AKT, ERK1/2, and p70S6K1, and decreased HIF-1α expression. Furthermore, forced expression of miR-148a attenuated tumor angiogenesis in vivo. Our re-sults identify ERBB3 as a direct target of miR-148a, and provide direct evidence that miR-148a inhibits tumor an-giogenesis through ERBB3 and its downstream signaling molecules. This information would be helpful for target-ing the miR-148a/ERBB3 pathway for breast cancer prevention and treatment in the future.
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