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SNAIL and miR-34a feed-forward regulation of ZNF281/ZBP99 promotes epithelial-mesenchymal transition.
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- المؤلفون: Hahn S;Hahn S; Jackstadt R; Siemens H; Hünten S; Hermeking H
- المصدر:
The EMBO journal [EMBO J] 2013 Nov 27; Vol. 32 (23), pp. 3079-95. Date of Electronic Publication: 2013 Nov 01.
- نوع النشر :
Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
- اللغة:
English
- معلومة اضافية
- المصدر:
Publisher: Wiley Blackwell Country of Publication: England NLM ID: 8208664 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1460-2075 (Electronic) Linking ISSN: 02614189 NLM ISO Abbreviation: EMBO J Subsets: MEDLINE
- بيانات النشر:
Publication: 2014- : London : Wiley Blackwell
Original Publication: Eynsham, Oxford, England : Published for the European Molecular Biology Organization by IRL Press, [c1982-
- الموضوع:
- نبذة مختصرة :
Here, we show that expression of ZNF281/ZBP-99 is controlled by SNAIL and miR-34a/b/c in a coherent feed-forward loop: the epithelial-mesenchymal transition (EMT) inducing factor SNAIL directly induces ZNF281 transcription and represses miR-34a/b/c, thereby alleviating ZNF281 mRNA from direct down-regulation by miR-34. Furthermore, p53 activation resulted in a miR-34a-dependent repression of ZNF281. Ectopic ZNF281 expression in colorectal cancer (CRC) cells induced EMT by directly activating SNAIL, and was associated with increased migration/invasion and enhanced β-catenin activity. Furthermore, ZNF281 induced the stemness markers LGR5 and CD133, and increased sphere formation. Conversely, experimental down-regulation of ZNF281 resulted in mesenchymal-epithelial transition (MET) and inhibition of migration/invasion, sphere formation and lung metastases in mice. Ectopic c-MYC induced ZNF281 protein expression in a SNAIL-dependent manner. Experimental inactivation of ZNF281 prevented EMT induced by c-MYC or SNAIL. In primary CRC samples, expression of ZNF281 increased during tumour progression and correlated with recurrence. Taken together, these results identify ZNF281 as a component of EMT-regulating networks, which contribute to metastasis formation in CRC.
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- الرقم المعرف:
0 (DNA-Binding Proteins)
0 (MIRN34 microRNA, human)
0 (MicroRNAs)
0 (Repressor Proteins)
0 (Snail Family Transcription Factors)
0 (TP53 protein, human)
0 (Trans-Activators)
0 (Transcription Factors)
0 (Tumor Suppressor Protein p53)
0 (ZNF148 protein, human)
0 (ZNF281 protein, human)
- الموضوع:
Date Created: 20131105 Date Completed: 20140128 Latest Revision: 20220321
- الموضوع:
20240829
- الرقم المعرف:
PMC3844956
- الرقم المعرف:
10.1038/emboj.2013.236
- الرقم المعرف:
24185900
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