Human telomerase catalytic subunit (hTERT) suppresses p53-mediated anti-apoptotic response via induction of basic fibroblast growth factor
- Authors
- Jin, Xun; Beck, Samuel; Sohn, Young-Woo; Kim, Jun-Kyum; Kim, Sung-Hak; Yin, Jinlong; Pian, Xumin; Kim, Sung-Chan; Choi, Yun-Jaie; Kim, Hyunggee
- Issue Date
- 31-8월-2010
- Publisher
- NATURE PUBLISHING GROUP
- Keywords
- bFGF; basic fibroblast growth factor; EGFR; epidermal growth factor receptor; HFFS; human fetal fibroblast
- Citation
- EXPERIMENTAL AND MOLECULAR MEDICINE, v.42, no.8, pp.574 - 582
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- EXPERIMENTAL AND MOLECULAR MEDICINE
- Volume
- 42
- Number
- 8
- Start Page
- 574
- End Page
- 582
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/115853
- DOI
- 10.3858/emm.2010.42.8.058
- ISSN
- 1226-3613
- Abstract
- Although human telomerase catalytic subunit (TERT) has several cellular functions including telomere homeostasis, genomic stability, cell proliferation, and tumorigenesis, the molecular mechanism underlying anti-apoptosis regulated by TERT remains to be elucidated. Here, we show that ectopic expression of TEAT in spontaneously immortalized human fetal fibroblast (HFFS) cells, which are a telomerase- and p53-positive, leads to increases of cell proliferation and transformation, as well as a resistance to DNA damage response and inactivation of p53 function. We found that TEAT and a mutant TEAT (no telomerase activity) induce expression of basic fibroblast growth factor (bFGF), and ectopic expression of bFGF also allows cells to be resistant to DNA-damaging response and to suppress activation of p53 function under DNA-damaging induction. Furthermore, loss of TEAT or bFGF markedly increases a p53 activity and DNA-damage sensitivity in HFFS, HeLa and U87MG cells. Therefore, our findings indicate that a novel TERT-bFGF axis accelerates the inactivation of p53 and consequent increase of resistance to DNA-damage response.
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- Appears in
Collections - College of Life Sciences and Biotechnology > Division of Biotechnology > 1. Journal Articles
- Graduate School > Department of Biotechnology > 1. Journal Articles
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