Ahnak functions as a tumor suppressor via modulation of TGF beta/Smad signaling pathway
- Authors
- Lee, I. H.; Sohn, M.; Lim, H. J.; Yoon, S.; Oh, H.; Shin, S.; Shin, J. H.; Oh, S-H; Kim, J.; Lee, D. K.; Noh, D. Y.; Bae, D. S.; Seong, J. K.; Bae, Y. S.
- Issue Date
- 18-Sep-2014
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- ONCOGENE, v.33, no.38, pp.4675 - 4684
- Journal Title
- ONCOGENE
- Volume
- 33
- Number
- 38
- Start Page
- 4675
- End Page
- 4684
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/12297
- DOI
- 10.1038/onc.2014.69
- ISSN
- 0950-9232
- Abstract
- We provide detailed mechanisms of Ahnak-mediated potentiation of transforming growth factor beta (TGF beta) signaling, which leads to a negative regulation of cell growth. We show that Smad3 interacts with Ahnak through MH2 domain and that Ahnak stimulates Smad3 localization into nucleus leading to potentiating TGF beta-induced transcriptional activity of R-Smad. Moreover, overexpression of Ahnak resulted in growth retardation and cell cycle arrest through downregulation of c-Myc and cyclin D1/D2. We describe results from analyses of Ahnak(-/-) mouse model expressing middle T antigen in a mammary gland-specific manner (MMTVTg/+ Ahnak(-/-)), which showed significantly progressed hyperplasia of mammary glands compared with MMTVTg/+ Ahnak(+/+). Finally, we screened multiple human breast cancer tissues and showed that the expression of Ahnak in cancer tissues is lower than that in control tissues by 50%. Taken together, these data indicate that Ahnak mediates a negative regulation of cell growth and acts as novel tumor suppressor through potentiation of TGF beta signaling.
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