MiR-204/ZEB2 axis functions as key mediator for MALAT1-induced epithelial–mesenchymal transition in breast cancer. Issue 7 (July 2017)
- Record Type:
- Journal Article
- Title:
- MiR-204/ZEB2 axis functions as key mediator for MALAT1-induced epithelial–mesenchymal transition in breast cancer. Issue 7 (July 2017)
- Main Title:
- MiR-204/ZEB2 axis functions as key mediator for MALAT1-induced epithelial–mesenchymal transition in breast cancer
- Authors:
- Wang, Yuzhou
Zhou, Yijin
Yang, Zhicheng
Chen, Baoying
Huang, Wennan
Liu, Yongyuan
Zhang, Ying - Abstract:
- Long non-coding RNAs recently were identified as key mediators of cancer metastasis. This study provided evidence that long non-coding RNA MALAT1 was up-regulated in breast cancer tissues and cell lines. MALAT1 promoted cancer cell invasion through inducing epithelial–mesenchymal transition. Interestingly, we revealed there was a reciprocal repression between MALAT1 and miR-204. ZEB2 was identified as a downstream target of miR-204 and MALAT1 exerted its function mainly through the miR-204/ZEB2 axis. Our findings suggested that MALAT1 may serve as a new diagnostic biomarker and therapy target for breast cancer.
- Is Part Of:
- Tumor biology. Volume 39:Issue 7(2017)
- Journal:
- Tumor biology
- Issue:
- Volume 39:Issue 7(2017)
- Issue Display:
- Volume 39, Issue 7 (2017)
- Year:
- 2017
- Volume:
- 39
- Issue:
- 7
- Issue Sort Value:
- 2017-0039-0007-0000
- Page Start:
- Page End:
- Publication Date:
- 2017-07
- Subjects:
- MALAT1 -- miR-204 -- ZEB2 -- epithelial–mesenchymal transition
Cancer -- Periodicals
Oncology -- Periodicals
Tumors -- Periodicals
616.994 - Journal URLs:
- https://www.iospress.nl/journal/tumor-biology/ ↗
https://uk.sagepub.com/en-gb/eur/tumor-biology/journal202707 ↗
http://www.springer.com/gb/ ↗ - DOI:
- 10.1177/1010428317690998 ↗
- Languages:
- English
- ISSNs:
- 1010-4283
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 9070.645500
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- 8655.xml