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Yin Yang-1 suppresses differentiation of hepatocellular carcinoma cells through the downregulation of CCAAT/enhancer-binding protein alpha
- Source :
- Journal of molecular medicine (Berlin, Germany). 90(9)
- Publication Year :
- 2011
-
Abstract
- As a member of the GLI-Kruppel family of transcriptional factors, Yin Yang-1 (YY1) functions as an oncogene in various types of cancers. However, the role of YY1 in hepatocellular carcinogenesis remains unknown. In this report, we investigated the relevance of YY1 to hepatocellular carcinoma (HCC) development. We found that YY1 was upregulated in HCC cell lines. Ectopic YY1 expression promoted the growth of non-tumor liver cells that expressed low level of YY1. In contrast, YY1 depletion inhibited the growth of HCC cells which was accompanied with distinct morphological changes. Moreover, the phenotypic changes induced by YY1 depletion were attributed to cellular differentiation rather than cellular senescence. CCAAT/enhancer-binding protein alpha (CEBPA) which was important to regulate differentiation of hepatocytes was found as the direct target downregulated by YY1. Restoration of CEBPA in YY1-expressing HCC cells induced cellular differentiation and growth inhibition while knockdown of CEBPA expression in non-tumor liver cells promoted cell growth. In summary, our study demonstrated that YY1 could promote hepatocellular carcinogenesis and inhibit cellular differentiation through the downregulation of CEBPA expression.
- Subjects :
- Carcinoma, Hepatocellular
Liver cytology
Cellular differentiation
Down-Regulation
Biology
medicine.disease_cause
Cell Line
Downregulation and upregulation
Cell Line, Tumor
Drug Discovery
CEBPA
medicine
Humans
Genetics (clinical)
YY1 Transcription Factor
Regulation of gene expression
Oncogene
Cell growth
Liver Neoplasms
Cell Differentiation
DNA Methylation
digestive system diseases
Gene Expression Regulation, Neoplastic
Liver
embryonic structures
Cancer research
CCAAT-Enhancer-Binding Proteins
Molecular Medicine
Carcinogenesis
Gene Deletion
Subjects
Details
- ISSN :
- 14321440
- Volume :
- 90
- Issue :
- 9
- Database :
- OpenAIRE
- Journal :
- Journal of molecular medicine (Berlin, Germany)
- Accession number :
- edsair.doi.dedup.....93d99f15e035fec6aeab76f5e866585a