Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Molecular Biology of the Cell |
| Vol/bind | 18 |
| Udgave nummer | 11 |
| Sider (fra-til) | 4615-24 |
| Antal sider | 9 |
| ISSN | 1059-1524 |
| DOI | |
| Status | Udgivet - 2007 |
| Udgivet eksternt | Ja |
Bibliografisk note
Keywords: Cadherins; Cell Cycle; Cell Line, Tumor; Cyclin D1; Down-Regulation; Epithelial Cells; Humans; Mesoderm; Mutation; Nerve Tissue Proteins; Promoter Regions (Genetics); RNA-Binding Proteins; Transcription, GeneticAdgang til dokumentet
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I: Molecular Biology of the Cell, Bind 18, Nr. 11, 2007, s. 4615-24.
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Direct repression of cyclin D1 by SIP1 attenuates cell cycle progression in cells undergoing an epithelial mesenchymal transition.
AU - Mejlvang, Jakob
AU - Kriajevska, Marina
AU - Vandewalle, Cindy
AU - Chernova, Tatyana
AU - Sayan, A Emre
AU - Berx, Geert
AU - Mellon, J Kilian
AU - Tulchinsky, Eugene
N1 - Keywords: Cadherins; Cell Cycle; Cell Line, Tumor; Cyclin D1; Down-Regulation; Epithelial Cells; Humans; Mesoderm; Mutation; Nerve Tissue Proteins; Promoter Regions (Genetics); RNA-Binding Proteins; Transcription, Genetic
PY - 2007
Y1 - 2007
N2 - Zinc finger transcription factors of the Snail/Slug and ZEB-1/SIP1 families control epithelial-mesenchymal transitions in development in cancer. Here, we studied SIP1-regulated mesenchymal conversion of epidermoid A431 cells. We found that concomitant with inducing invasive phenotype, SIP1 inhibited expression of cyclin D1 and induced hypophosphorylation of the Rb tumor suppressor protein. Repression of cyclin D1 was caused by direct binding of SIP1 to three sequence elements in the cyclin D1 gene promoter. By expressing exogenous cyclin D1 in A431/SIP1 cells and using RNA interference, we demonstrated that the repression of cyclin D1 gene by SIP1 was necessary and sufficient for Rb hypophosphorylation and accumulation of cells in G1 phase. A431 cells expressing SIP1 along with exogenous cyclin D1 were highly invasive, indicating that SIP1-regulated invasion is independent of attenuation of G1/S progression. However, in another epithelial-mesenchymal transition model, gradual mesenchymal conversion of A431 cells induced by a dominant negative mutant of E-cadherin produced no effect on the cell cycle. We suggest that impaired G1/S phase progression is a general feature of cells that have undergone EMT induced by transcription factors of the Snail/Slug and ZEB-1/SIP1 families.
AB - Zinc finger transcription factors of the Snail/Slug and ZEB-1/SIP1 families control epithelial-mesenchymal transitions in development in cancer. Here, we studied SIP1-regulated mesenchymal conversion of epidermoid A431 cells. We found that concomitant with inducing invasive phenotype, SIP1 inhibited expression of cyclin D1 and induced hypophosphorylation of the Rb tumor suppressor protein. Repression of cyclin D1 was caused by direct binding of SIP1 to three sequence elements in the cyclin D1 gene promoter. By expressing exogenous cyclin D1 in A431/SIP1 cells and using RNA interference, we demonstrated that the repression of cyclin D1 gene by SIP1 was necessary and sufficient for Rb hypophosphorylation and accumulation of cells in G1 phase. A431 cells expressing SIP1 along with exogenous cyclin D1 were highly invasive, indicating that SIP1-regulated invasion is independent of attenuation of G1/S progression. However, in another epithelial-mesenchymal transition model, gradual mesenchymal conversion of A431 cells induced by a dominant negative mutant of E-cadherin produced no effect on the cell cycle. We suggest that impaired G1/S phase progression is a general feature of cells that have undergone EMT induced by transcription factors of the Snail/Slug and ZEB-1/SIP1 families.
U2 - 10.1091/mbc.E07-05-0406
DO - 10.1091/mbc.E07-05-0406
M3 - Journal article
C2 - 17855508
SN - 1059-1524
VL - 18
SP - 4615
EP - 4624
JO - Molecular Biology of the Cell
JF - Molecular Biology of the Cell
IS - 11
ER -