scholarly journals Long Noncoding RNAs Hepatocyte Nuclear Factor 4A Antisense RNA 1 and Hepatocyte Nuclear Factor 1A Antisense RNA 1 are Involved in Ritonavir-induced Cytotoxicity in Hepatoma Cells

2021 ◽  
pp. DMD-AR-2021-000693
Author(s):  
Xiaofei Wang ◽  
Yihang Yu ◽  
Pei Wang ◽  
Kun Yang ◽  
Yiting Wang ◽  
...  
Keyword(s):  
Antisense Rna ◽  
Noncoding Rnas ◽  
Hepatoma Cells ◽  
Long Noncoding Rnas ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor

scholarly journals Functional Activity of Human Hepatoma Cells Transfected with Adenovirus-Mediated Hepatocyte Nuclear Factor (HNF)-4 Gene

2004 ◽  
Vol 13 (4) ◽  
pp. 393-404 ◽  
Author(s):  
Takafumi Naiki ◽  
Masahito Nagaki ◽  
Yoshihiro Shidoji ◽  
Hisanori Kojima ◽  
Hisataka Moriwaki
Keyword(s):  
Functional Activity ◽  
Hepatoma Cells ◽  
Nuclear Factor ◽  
Human Hepatoma ◽  
Hepatocyte Nuclear Factor ◽  
Human Hepatoma Cells

scholarly journals Overproduction of a truncated hepatocyte nuclear factor 3 protein inhibits expression of liver-specific genes in hepatoma cells.

1995 ◽  
Vol 15 (10) ◽  
pp. 5453-5460 ◽  
Author(s):  
V Vallet ◽  
B Antoine ◽  
P Chafey ◽  
A Vandewalle ◽  
A Kahn
Keyword(s):  
Transcription Factors ◽  
Dna Binding ◽  
Binding Sites ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Hepatoma Cells ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Regulatory Regions ◽  
Truncated Protein ◽  
Fork Head

Transcription of hepatocyte-specific genes requires the interaction of their regulatory regions with several nuclear factors. Among them is the hepatocyte nuclear factor 3 (HNF3) family, composed of the HNF3 alpha, HNF3 beta, and HNF3 gamma proteins, which are expressed in the liver and have very similar fork head DNA binding domains. The regulatory regions of numerous hepatocyte-specific genes contain HNF3 binding sites. We examined the role of HNF3 proteins in the liver-specific phenotype by turning off the HNF3 activity in well-differentiated mhAT3F hepatoma cells. Cells were stably transfected with a vector allowing the synthesis of an HNF3 beta fragment consisting of the fork head DNA binding domain without the transactivating amino- and carboxy-terminal domains. The truncated protein was located in the nuclei of cultured hepatoma cells and competed with endogenous HNF3 proteins for binding to cognate DNA sites. Overproduction of this truncated protein, lacking any transactivating activity, induced a dramatic decrease in the expression of liver-specific genes, including those for albumin, transthyretin, transferrin, phosphoenolpyruvate carboxykinase, and aldolase B, whereas the expression of the L-type pyruvate kinase gene, containing no HNF3 binding sites, was unaltered. Neither were the concentrations of various liver-specific transcription factors (HNF3, HNF1, HNF4, and C/EBP alpha) affected. In partial revertants, with a lower ratio of truncated to full-length endogenous HNF3 proteins, previously extinguished genes were re-expressed. Thus, the transactivating domains of HNF3 proteins are needed for the proper expression of a set of liver-specific genes but not for expression of the genes encoding transcription factors found in differentiated hepatocytes.

scholarly journals Liver-enriched transcription factors uncoupled from expression of hepatic functions in hepatoma cell lines.

1997 ◽  
Vol 17 (11) ◽  
pp. 6311-6320 ◽  
Author(s):  
D Chaya ◽  
C Fougère-Deschatrette ◽  
M C Weiss
Keyword(s):  
Transcription Factors ◽  
Hepatoma Cell ◽  
Hepatoma Cells ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
Hepatic Differentiation ◽  
Hepatoma Cell Lines ◽  
Differentiated Cells ◽  
Heritable Phenotype ◽  
Nuclear Factor 1

Among the liver-enriched transcription factors identified to date, only expression of hepatocyte nuclear factor 4 (HNF4) and hepatocyte nuclear factor 1 (HNF1) is in strict correlation with hepatic differentiation in cultured rat hepatoma cells. Indeed, differentiated hepatoma cells that stably express an extensive set of adult hepatic functions express liver-enriched transcription factors, while dedifferentiated cells that have lost expression of all these hepatic functions no longer express HNF4 and HNF1. We describe a new heritable phenotype, designated as uncoupled, in which there is a spontaneous dissociation between the expression of these transcription factors and that of the hepatic functions. Cells presenting this phenotype, isolated from differentiated hepatoma cells, cease to accumulate all transcripts coding for hepatic functions but nevertheless maintain expression of HNF4 and HNF1. Transitory transfection experiments indicate that these two factors present in these cells have transcriptional activity similar to that of differentiated hepatoma cells. Characterization of the appropriate intertypic cell hybrids demonstrates that this new phenotype is recessive to the dedifferentiated state and fails to be complemented by differentiated cells. These results indicate the existence of mechanisms that inhibit transcription of genes coding for hepatocyte functions in spite of the presence of functional HNF4 and HNF1. Cells of the uncoupled phenotype present certain properties of oval cells described for pathological states of the liver.

scholarly journals E2F1-Induced lncRNA BAIAP2-AS1 Overexpression Contributes to the Malignant Progression of Hepatocellular Carcinoma via miR-361-3p/SOX4 Axis

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Yan Yang ◽  
Hong Ge ◽  
De-qing Li ◽  
Ai-xia Xu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Therapeutic Target ◽  
Antisense Rna ◽  
Noncoding Rnas ◽  
Malignant Progression ◽  
Long Noncoding Rnas ◽  
Positive Interaction ◽  
Potential Therapeutic Target ◽  
Proliferation And Metastasis ◽  
Hcc Cells

Currently, plenty of researches have revealed that long noncoding RNAs (lncRNAs) can act as crucial roles during the progression of various tumors, including hepatocellular carcinoma (HCC). Here, we measured the expression of lncRNA BAIAP2 antisense RNA 1(BAIAP2-AS1) as well as its contribution to the developments of HCC. In this study, the expressions of BAIAP2-AS1 and SOX4 were distinctly upregulated in HCC cells and tissues, and high BAIAP2-AS1 may be a novel biomarker for HCC. E2F1 activated BAIAP2-AS1 expression. The silence of BAIAP2-AS1 inhibited the proliferation and metastasis of HepG2 and PLC5 cells. Assays for relationship verification showed that BAIAP2-AS1 regulated the expression of SOX4 and miR-361-3p. Rescue experiments further confirmed the positive interaction between miR-361-3p and BAIAP2-AS1 as well as between miR-361-3p and SOX4. Overall, BAIAP2-AS1 modulated the miR-361-3p/SOX4 axis to promote the development of HCC. Thus, our study offers a potential therapeutic target for treating HCC.

scholarly journals Hepatocyte Nuclear Factor 4 Provokes Expression of Epithelial Marker Genes, Acting As a Morphogen in Dedifferentiated Hepatoma Cells

1998 ◽  
Vol 140 (4) ◽  
pp. 935-946 ◽  
Author(s):  
Gerald F. Späth ◽  
Mary C. Weiss
Keyword(s):  
Epithelial Cell ◽  
Hepatoma Cells ◽  
Stable Expression ◽  
Junctional Complex ◽  
Cell Phenotype ◽  
Marker Genes ◽  
Specific Gene ◽  
Nuclear Factor ◽  
Hepatocyte Nuclear Factor ◽  
E Cadherin

Abstract. We have recently shown that stable expression of an epitope-tagged cDNA of the hepatocyte- enriched transcription factor, hepatocyte nuclear factor (HNF)4, in dedifferentiated rat hepatoma H5 cells is sufficient to provoke reexpression of a set of hepatocyte marker genes. Here, we demonstrate that the effects of HNF4 expression extend to the reestablishment of differentiated epithelial cell morphology and simple epithelial polarity. The acquisition of epithelial morphology occurs in two steps. First, expression of HNF4 results in reexpression of cytokeratin proteins and partial reestablishment of E-cadherin production. Only the transfectants are competent to respond to the synthetic glucocorticoid dexamethasone, which induces the second step of morphogenesis, including formation of the junctional complex and expression of a polarized cell phenotype. Cell fusion experiments revealed that the transfectant cells, which show only partial restoration of E-cadherin expression, produce an extinguisher that is capable of acting in trans to downregulate the E-cadherin gene of well-differentiated hepatoma cells. Bypass of this repression by stable expression of E-cadherin in H5 cells is sufficient to establish some epithelial cell characteristics, implying that the morphogenic potential of HNF4 in hepatic cells acts via activation of the E-cadherin gene. Thus, HNF4 seems to integrate the genetic programs of liver-specific gene expression and epithelial morphogenesis.

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