Research Papers:
A contrasting function for miR-137 in embryonic mammogenesis and adult breast carcinogenesis
PDF | HTML | Supplementary Files | How to cite
Metrics: PDF 1932 views | HTML 14956 views | ?
Abstract
Jong-Min Lee1,*, Kyoung-Won Cho2,*, Eun-Jung Kim1, Qinghuang Tang1, Kye-Seong Kim3, Cheryll Tickle4 and Han-Sung Jung1,5
1 Division in Anatomy and Developmental Biology, Department of Oral Biology, Oral Science Research Center, BK21 PLUS Project, Yonsei University College of Dentistry, Seoul, Korea
2 Department of Radiology, Seoul National University Hospital, Seoul, Korea
3 Graduate School of Biomedical Science and Engineering, College of Medicine, Hanyang University, Seoul, Korea
4 Department of Biology and Biochemistry, University of Bath, Bath, UK
5 Oral Biosciences, Faculty of Dentistry, The University of Hong Kong, Hong Kong SAR
* These authors have contributed equally to this work
Correspondence to:
Han-Sung Jung, email:
Keywords: mammary gland development, breast cancer, miR-137, tumour suppressor, tachykinin-1
Received: March 13, 2015 Accepted: May 02, 2015 Published: May 20, 2015
Abstract
MicroRNAs are differentially expressed in breast cancer cells and have been implicated in cancer formation, tumour invasion and metastasis. We investigated the miRNA expression profiles in the developing mammary gland. MiR-137 was expressed prominently in the developing mammary gland. When the miR-137 was over-expressed in the embryo, the mammary epithelium became thickened. Moreover, genes associated with mammary gland formation such as Tbx3 and Lef1 were not expressed. This suggests that miR-137 induces gland formation and invasion. When miR-137 was over-expressed in MDA-MB-231 cells, their ability to form tumours in adult mice was significantly reduced. These data support miR-137 decides epithelial cell behavior in the human breast cancer. It also suggests that miR-137 is a potential therapeutic target for amelioration of breast cancer progression.
![Creative Commons License](/images/80x15.png)
PII: 4218