Advanced glycation end products promote triple negative breast cancer cells via ERK and NF-kappa B pathway
- Authors
- Lee, Kyung Jin; Yoo, Ji Won; Kim, Yun Kyu; Choi, Jae Ho; Ha, Tae-Yong; Gil, Minchan
- Issue Date
- Jan-2018
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- Advanced glycosylation end product; Breast cancer; Invasion; Migration; MMP-9; NK-kappa B
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.495, no.3, pp 2195 - 2201
- Pages
- 7
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 495
- Number
- 3
- Start Page
- 2195
- End Page
- 2201
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/4772
- DOI
- 10.1016/j.bbrc.2017.11.182
- ISSN
- 0006-291X
1090-2104
- Abstract
- Advanced glycation end products (AGEs) are harmful compounds generated by nonspecific glycation of proteins and lipids. The accumulation of AGEs is associated with various diseases, including breast cancer. AGEs have been shown to promote a breast cancer cell line by enhancing proliferation, invasion and migration. In this study, we investigated the effect and associated mechanism of AGEs on triple negative breast cancer cells. AGEs enhanced the proliferation, tumorigenicity, invasion and migration of primary breast cancer cells. AGEs also enhanced the RNA and protein expression of matrix metalloproteinase (MMP)-9 and its gelatinase activity. Enhanced MMP-9 expression was mediated by extracellular-signal regulated kinase (ERK) and nuclear factor kappa B (NF-kappa B) pathways. Moreover, inhibitors of ERK and NF-kappa B signaling attenuated the effect of AGEs on tumorigenicity, invasion and migration of primary breast cancer cells. Taken together, we suggest that AGEs directly promote primary breast cancer cells via the ERK and NF-kappa B pathway, which may lead to advanced therapeutic modalities of breast cancer. (C) 2017 Elsevier Inc. All rights reserved.
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