ArticleMolecular medicine reports2018
The transcription factor 7 like 2‑binding protein TIP5 activates β‑catenin/transcription factor signaling in hepatocellular carcinoma.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- The alternative splicing landscape of hepatocellular carcinoma and its potential for HCC detection.Hepatology communications · 2026Article
- Pan-cancer and multi-omics analyses revealed the diagnostic and prognostic value of BAZ2A in liver cancer.Scientific reports · 2024Article
- BAZ2A-RNA mediated association with TOP2A and KDM1A represses genes implicated in prostate cancer.Life science alliance · 2023Article
- Bromodomain (BrD) Family Members as Regulators of Cancer Stemness-A Comprehensive Review.International journal of molecular sciences · 2023Review
- Article
- LINC00885 promotes cervical cancer progression through sponging miR-3150b-3p and upregulating BAZ2A.Biology direct · 2022Article
- The emerging role of ISWI chromatin remodeling complexes in cancer.Journal of experimental & clinical cancer research : CR · 2021Review
- PDLIM2 prevents the malignant phenotype of hepatocellular carcinoma cells by negatively regulating β-catenin.Cancer gene therapy · 2021Article
- GSK2801, a BAZ2/BRD9 Bromodomain Inhibitor, Synergizes with BET Inhibitors to Induce Apoptosis in Triple-Negative Breast Cancer.Molecular cancer research : MCR · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant activation of β‑catenin/transcription factor 7 like 2 (TCF7L2) signaling is frequently observed during the progression of hepatocellular carcinoma (HCC). However, regulation of the nuclear β‑catenin/TCF7L2 complex remains largely unknown. In the present study, immunoprecipitation and glutathione S‑transferase pull‑down assays identified transcription termination factor‑1 interacting protein 5 (TIP5) as a binding partner of TCF7L2. TIP5 activated β‑catenin/TCF7L2 signaling by enhancing the interaction between β‑catenin and TCF7L2. The results from quantitative polymerase chain reaction and western blot analysis indicated that TIP5 was upregulated in clinical HCC samples. In addition, TIP5 positively regulated the proliferation of HCC cells in the MTT assay, colony formation in the soft agar assay, migration in the Boyden chamber assay and epithelial‑mesenchymal transition of HCC cells by activating β‑catenin/TCF7L2 signaling. Therefore, the results of the present study demonstrate that TIP5 serves an oncogenic role in HCC by activating β‑catenin/TCF7L2 signaling, suggesting that TIP5 may be a promising therapeutic target for HCC.
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