Brain cancer stem-like cell genesis from p53-deficient mouse astrocytes by oncogenic Ras
- Authors
- Lee, Joong-Seob; Gil, Jung-Eun; Kim, Jong-Hoon; Kim, Tae-Kyung; Jin, Xun; Oh, Se-Yeong; Sohn, Young-Woo; Jeon, Hye-Min; Park, Hyo-Jung; Park, Jong-Whi; Shin, Yong-Jae; Chung, Yong Gu; Lee, Jang-Bo; You, Seungkwon; Kim, Hyunggee
- Issue Date
- 18-Jan-2008
- Publisher
- ACADEMIC PRESS INC ELSEVIER SCIENCE
- Keywords
- astrocyte; brain cancer stem-like cells; cell differentiation fate; glioma; H-ras; p53
- Citation
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.365, no.3, pp.496 - 502
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Volume
- 365
- Number
- 3
- Start Page
- 496
- End Page
- 502
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/124222
- DOI
- 10.1016/j.bbrc.2007.11.005
- ISSN
- 0006-291X
- Abstract
- Here, we show that H-ras(v12) causes the p53-knockout mouse astrocytes (p53-/- astrocytes) to be transformed into brain cancer stem-like cells. H-ras(v12) triggers the p53-/- astrocytes to express a Nestin and a Cd133, which are expressed in normal and cancer neural stem cells. H-ras(V12) also induces the formation of a single cell-derived neurosphere under neural stem cell culture conditions. Furthermore, H-ras(_)(V12)overexpressing p53-/- astrocytes (p53-/-ast-H-ras(v12)) possess an in vitro self-renewal capacity, and are aberrantly differentiated into Tuj 1-positve neurons both in vitro and in vivo. Amongst a variety of Ras-mediated canonical signaling pathways, we demonstrated that the MEK/ERK signaling pathway is responsible for neurosphere formation in P53-deficient astrocytes, whereas the PI3K/AKT signaling pathway is involved in oncogenic transformation in these cells. These findings suggest that the activation of Ras signaling pathways promotes the generation of brain cancer stem-like cells from p53-deficient mouse astrocytes by changing cell fate and transforming cell properties. (c) 2007 Elsevier Inc. All rights reserved.
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Collections - Graduate School > Department of Biotechnology > 1. Journal Articles
- College of Medicine > Department of Medical Science > 1. Journal Articles
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