CYR61 controls p53 and NF-kappa B expression through PI3K/Akt/mTOR pathways in carboplatin-induced ovarian cancer cells
- Authors
- Lee, Kwang-Beom; Byun, Hyun-Jung; Park, Sung Ho; Park, Chan-Yong; Lee, Seung-Hoon; Rho, Seung Bae
- Issue Date
- 1-Feb-2012
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- CCN1 (CYR61); Apoptosis; Carboplatin; NF-kappa B; PI3K/Akt; Ovarian carcinoma cells
- Citation
- CANCER LETTERS, v.315, no.1, pp.86 - 95
- Journal Title
- CANCER LETTERS
- Volume
- 315
- Number
- 1
- Start Page
- 86
- End Page
- 95
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/16582
- DOI
- 10.1016/j.canlet.2011.10.016
- ISSN
- 0304-3835
- Abstract
- CYR61 over-expression promotes cell proliferation by inhibiting carboplatin-induced apoptosis, decreasing Bax expression, and increasing Bcl-xL, Mcl-1, and Bcl-2. At the same time, down-regulating p53 expression, while up-regulated NF-kappa B expression. Additionally, p21 and p53 promoter activities were reduced, while NF-kappa B and Bcl-2 activities increased. In parallel, CYR61-expressing cells, during carboplatin-induced apoptosis, resulted in an increase of Akt phosphorylation, while rapamycin-treated cells were not affected. Carboplatin effectively inhibited the activation of mTOR signaling cascade, which includes mTOR, 4E-BP1, p70S6K, HIF-1 alpha, and VEGF. These results provide evidence that CYR61 promotes cell proliferation and inhibits apoptosis. (C) 2011 Elsevier Ireland Ltd. All rights reserved.
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