Role of Specific CCAAT/Enhancer-binding Protein Isoforms in Intestinal Epithelial Cells

Gheorghiu, Ionela; Deschênes, Claude; Blais, Mylène; Boudreau, François; Rivard, Nathalie; Asselin, Claude

doi:10.1074/jbc.m107591200

Cited by 30 publications

(34 citation statements)

References 50 publications

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“…We also found that cyclin E protein levels were reduced in the C/EBPd-overexpressing cells. A previous study showed that C/EBPs bind to E2F4 in intestinal cells and suggested that this led to decreased expression of E2F target genes such as cyclin E (Gheorghiu et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies suggested that the interactions between C/EBPs and E2F transcription factors results in down-regulation of c-Myc (Johansen et al, 2001;Gery et al, 2004) and possibly cyclin E (Gheorghiu et al, 2001). We consequently tested the possibility that C/EBPd regulates c-Myc and cyclin E expression in KCL22 and K562 CML cells.…”

Section: C/ebpd Represses Expression Of C-myc and Cyclin Ementioning

confidence: 99%

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C/EBPδ expression in a BCR-ABL-positive cell line induces growth arrest and myeloid differentiation

et al. 2005

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CCAAT/enhancer-binding proteins (C/EBPs) are a family of highly conserved transcription factors that have important roles in normal myelopoiesis as well as associated with myeloid disorders. The chronic myelogenous leukemia (CML) cell lines, KCL22 and K562, express exceptionally low levels of endogenous C/EBPs and provide a good model to test the effects of C/EBPs on myeloid differentiation. To explore the possibility that C/ EBPd can promote differentiation in BCR-ABL-positive cells, we generated stable KCL22 and K562 clones that expressed an inducible C/EBPd gene. C/EBPd expression resulted in G0/G1 proliferative arrest and a moderate increase in apoptosis of the KCL22 and the K562 cells. Within 4 days of inducing expression of C/EBPd, myeloid differentiation of the CML blast cells occurred as shown by morphologic changes and induction of secondary granule-specific genes. We also showed that during granulocytic differentiation of KCL22 cells, the C/EBPd protein was detected in immunocomplexes with both Rb and E2F1. Furthermore, expression of C/EBPd was associated with downregulation of c-Myc and cyclin E and upregulation of the cyclin-dependent kinase inhibitor p27Kip1 in both the KCL22 and K562 cell lines. These results show that expression of C/EBPd in BCR-ABLpositive leukemic cells in blast crisis is sufficient for neutrophil differentiation and point to the therapeutic potential of ectopic induction of C/EBPd in the acute phase of CML.

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Section: Discussionmentioning

confidence: 99%

Section: C/ebpd Represses Expression Of C-myc and Cyclin Ementioning

confidence: 99%

C/EBPδ expression in a BCR-ABL-positive cell line induces growth arrest and myeloid differentiation

et al. 2005

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“…Therefore, toxic effects of the DNA/lipo- It is now known that, by translational regulation, C/ EBPβ gene gives at least two different protein products: a 38 kDa full length protein, LAP and a 20 kDa truncated protein, LIP. Most studies have shown that LAP is related to maintenance of normal cellular phenotype or tumor suppression, whereas the LIP is a functional LAP antagonist and may promote transformed phenotype [27][28][29][30][31][32][33]. In our work, the pCN plasmid harbors the full-length C/EBP coding sequence, and the full-length C/EBP was transcribed (data not shown); however, which was the main expressed protein remains to be determined.…”

Section: The C/ebpβ/ and Vector/liposome Complexes Did Not Appear Toxmentioning

confidence: 91%

Systemic delivery of full-length C/EBPβ/liposome complex suppresses growth of human colon cancer in nude mice

Sun

Liu

2005

Cell Res

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C/EBPβ (CCAAT/enhancer-binding protein β) is an important transcription factor involved in cellular proliferation and differentiation. Overexpression of the full-length C/EBPβ protein results in cellular growth arrest and apoptosis. Using a nonviral liposome as carrier, we delivered the full-length C/EBPβ expression plasmid, pCN, into nude mice bearing CW-2 human colon cancer tumors via tail vein. Southern blots revealed that the major organs and tumors were transfected. Experimental gene therapy showed that a strong suppression of tumor growth was observed in the pCNtreated mice, and such suppression was due to the overexpression of C/EBPβ, leading to the increased apoptosis in tumors of pCN-treated mice. No apparent toxic effects of pCN/liposome complex were observed in the animals. Thus, C/EBPβ has tumor suppression effect in vivo and may be used in gene therapy for cancers.

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“…8D). We then analyzed the potential involvement of the C/EBP␤ site, which has been described to participate to the glucocorticoid response (43). For this purpose, we used the mut C/EBP␤, the ⌬-1836 (deleted C/EBP␤ site), and the ⌬-1805 (deleted GRE and C/EBP␤ sites) promoter constructs.…”

Section: Transcription Factors Belonging To the Sp And Klf Family Indmentioning

confidence: 99%

Krüppel-like Factors Regulate the Lama1 Gene Encoding the Laminin α1 Chain

Piccinni¹,

Bolcato-Bellemin²,

Klein³

et al. 2004

Journal of Biological Chemistry

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Laminin-1 (␣1␤1␥1), a basement membrane (BM) constituent, has been associated with differentiation processes and also with malignant progression. In the intestinal tissue, the ␣1 chain is expressed and secreted in the subepithelial BM during the developmental period; in the adult rodent tissue, it is restricted to the BM of the dividing cells. To understand how laminin ␣1 chain expression is regulated, we cloned and characterized a 2-kb promoter region of the Lama1 mouse gene. Analysis of the promoter was conducted in the Caco2-TC7 intestinal epithelial cells by transient transfection of serially deleted and site-directed mutated promoter constructs, by electrophoretic mobility shift assays, and expression of selected transcription factors. We determined that a proximal region, which includes an Sp1-binding GC box and a Krü ppel-like element, was important for the promoter activity. This region is conserved between the human and mouse genes. Interestingly, two Krü ppellike factors KLF4 and KLF5 exhibit opposing effects on the Lama1 promoter activity that are decreased and increased, respectively, in the intestinal epithelial cells. These data corroborate the complementary expression of KLF4 and KLF5 along the intestinal crypt-villus axis and the parallel expression of KLF5 and laminin ␣1 chain in the crypt region. Finally, we showed that glucocorticoids stimulate the promoter activity. This study is the first characterization of the Lama1 promoter; we identified regulatory elements that may account for the expression pattern of the endogenous protein in the mouse intestine.

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Role of Specific CCAAT/Enhancer-binding Protein Isoforms in Intestinal Epithelial Cells

Cited by 30 publications

References 50 publications

C/EBPδ expression in a BCR-ABL-positive cell line induces growth arrest and myeloid differentiation

C/EBPδ expression in a BCR-ABL-positive cell line induces growth arrest and myeloid differentiation

Systemic delivery of full-length C/EBPβ/liposome complex suppresses growth of human colon cancer in nude mice

Krüppel-like Factors Regulate the Lama1 Gene Encoding the Laminin α1 Chain

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