ArticleLiver international : official journal of the International Association for the Study of the Liver2013
Loss of exon 4 in a human T-cell factor-4 isoform promotes hepatic tumourigenicity.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Evolutionary diversification of the canonical Wnt signaling effector TCF/LEF in chordates.Development, growth & differentiation · 2022Article
- Aberrant expression of alternative isoforms of transcription factors in hepatocellular carcinoma.World journal of hepatology · 2018Review
- Associations between serum HBX quasispecies and their integration in hepatocellular carcinoma.International journal of clinical and experimental pathology · 2017Article
- Chronic Ethanol-Induced Impairment of Wnt/β-Catenin Signaling is Attenuated by PPAR-δ Agonist.Alcoholism, clinical and experimental research · 2015Article
- Immortalized Human Hepatic Cell Lines for In Vitro Testing and Research Purposes.Methods in molecular biology (Clifton, N.J.) · 2015Article
- TCF7L2 is a master regulator of insulin production and processing.Human molecular genetics · 2014Article
- Strategies for immortalization of primary hepatocytes.Journal of hepatology · 2014Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundT-cell factor (TCF) proteins represent key transcription factors that activate Wnt/β-catenin signalling. We have reported that a pair of TCF-4 isoforms (TCF-4C and TCF-4D) exhibit differential TCF transcriptional activity in hepatocellular carcinoma (HCC) cells, although their structure differs by only the presence (TCF-4D) or absence (TCF-4C) of exon 4.
aimTo demonstrate a regulatory role of exon 4 in HCC development.
methodsTCF-4C and TCF-4D expression profiles were examined in 27 pairs of human HCC and adjacent liver tissues. The functional role of the TCF-4 isoforms was evaluated in OUMS-29 (an immortalized hepatocyte-derived) and HAK-1A (a well-differentiated HCC) cell lines using stable clones overexpressing the TCF-4 isoforms.
resultsTCF-4C was significantly upregulated in HCC tissues compared with corresponding peritumour and normal liver tissues; in contrast, there was no difference in TCF-4D expression. TCF-4C clones derived from both cell lines exhibited increased TCF activity, Wnt-responsive target genes, cell proliferation, cell cycle progression and resistance to chemotherapeutic drugs compared with TCF-4D clones. Capability of cell migration and colony formation was significantly higher in TCF-4C than TCF-4D clones. In a nude mice xenograft model, the HAK-1A-derived TCF-4C clone rapidly developed tumours compared with the TCF-4D clone. TCF-4C clone-derived tumours exhibited upregulation of Wnt-responsive target genes compared with the slow developing and small TCF-4D-derived tumours.
conclusionThese results demonstrate that the TCF-4C isoform lacking exon 4 is associated with a malignant phenotype compared with the exon 4-harbouring TCF-4D isoform, indicating that exon 4 of TCF-4 plays a prominent role in HCC development.
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