Egr-1 is required for neu/HER2-induced mammary tumors
- Authors
- Oh, Sunhwa; Kim, Hyungjoo; Nam, Keesoo; Shin, Incheol
- Issue Date
- May-2018
- Publisher
- ELSEVIER SCIENCE INC
- Keywords
- Egr-1; Neu; HER2; Mammary tumors
- Citation
- CELLULAR SIGNALLING, v.45, pp.102 - 109
- Indexed
- SCIE
SCOPUS
- Journal Title
- CELLULAR SIGNALLING
- Volume
- 45
- Start Page
- 102
- End Page
- 109
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/17001
- DOI
- 10.1016/j.cellsig.2018.02.003
- ISSN
- 0898-6568
- Abstract
- Egr-1 is known to function mainly as a tumor suppressor through direct regulation of multiple tumor suppressor genes. To determine the role of Egr-1 in breast tumors in vivo, we used mouse models of breast cancer induced by HER2/neu. We compared neu-overexpressing Egr-1 knockout mice (neu/Egr-1 KO) to neu-overexpressing Egr-1 wild type or heterozygote mice (neu/Egr-1 WT or neu/Egr-1 het) with regard to onset of tumor appearance and number of tumors per mouse. In addition, to examine the role of Egr-1 in vitro, we established neu/Egr-1 WT and KO tumor cell lines derived from breast tumors developed in each mouse. Egr-1 deletion delayed tumor development in vivo and decreased the rate of cell growth in vitro. These results suggest that Egr-1 plays an oncogenic role in HER2/neu-driven mammary tumorigenesis.
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