Ataxin-1 regulates epithelial–mesenchymal transition of cervical cancer cells
Metrics: PDF 1202 views | HTML 1476 views | ?
A-Ram Kang1, Hyoung-Tae An1, Jesang Ko1, Seongman Kang1
1Division of Life Sciences, College of Life Sciences and Biotechnology, Korea University, Seoul 02841, Korea
Seongman Kang, email: firstname.lastname@example.org
Keywords: ATXN1, cervical cancer, epithelial–mesenchymal transition, notch intracellular domain
Received: October 31, 2016 Accepted: December 21, 2016 Published: February 14, 2017
The mutant form of the protein ataxin-1 (ATXN1) causes the neurodegenerative disease spinocerebellar ataxia type-1. Recently, ATXN1 was reported to enhance E-cadherin expression in the breast cancer cell line MCF-7, suggesting a potential association between ATXN1 and cancer development. In the present study, we discovered a novel mechanism through which ATXN1 regulates the epithelial–mesenchymal transition (EMT) of cancer cells. Hypoxia-induced upregulation of the Notch intracellular domain expression decreased ATXN1 expression via MDM2-associated ubiquitination and degradation. In cervical cancer cells, ATXN1 knockdown induced EMT by directly regulating Snail expression, leading to matrix metalloproteinase activation and the promotion of cell migration and invasion. These findings provide insights into a novel mechanism of tumorigenesis and will facilitate the development of new and more effective therapies for cancer.
All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.