ArticleCancer research2009
Role of cyclin D1 as a mediator of c-Met- and beta-catenin-induced hepatocarcinogenesis.
Article in Cancer research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 88 citations in OpenAlex.
- Targeting ferroptosis induction via nanomaterials in hepatocellular carcinoma: an insight into mechanism and therapeutic potential.Journal of nanobiotechnology · 2026Review
- WNT-β-catenin signalling in hepatocellular carcinoma: from bench to clinical trials.Nature reviews. Gastroenterology & hepatology · 2026Review
- Targeting CAFs-Mediated Stromal Signaling in a Patient-Derived Organotypic Colorectal Tumor Model.Molecular cancer therapeutics · 2025Article
- Cell Function Experiments and Bioinformatics Analysis Jointly Revealed the Antineoplastic Effect of Lumican on Hepatocellular Carcinoma.Phenomics (Cham, Switzerland) · 2025Article
- Precision targeting of β-catenin induces tumor reprogramming and immunity in hepatocellular cancers.Nature communications · 2025Article
- Hepatocellular carcinoma: signaling pathways and therapeutic advances.Signal transduction and targeted therapy · 2025Review
- A Saffron-based Polyherbal Formulation DuK Prevents Hepatocellular Carcinoma in Male Wistar Rats.Current cancer drug targets · 2025Article
- Wnt/β-Catenin Signaling in Liver Pathobiology.Annual review of pathology · 2025Review
- Role of the Wnt/β-catenin signaling pathway in the development of HCC.Frontiers in immunology · 2025Review
- Suppression of Hepatocellular Carcinoma by Deletion of SIRT2 in Hepatocytes via Elevated C/EBPβ/GADD45γ.Cellular and molecular gastroenterology and hepatology · 2025Article
- Preclinical Models of Hepatocellular Carcinoma: Current Utility, Limitations, and Challenges.Biomedicines · 2024Review
- Unraveling the relationship between histone methylation and nonalcoholic fatty liver disease.World journal of hepatology · 2024Review
- Wnt/β-catenin signaling pathway in liver biology and tumorigenesis.In vitro cellular & developmental biology. Animal · 2024Review
- Hydrodynamic Transfection of Hepatocytes for the Study of Hepatocellular Carcinogenesis.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Pathogenesis of Hepatocellular Carcinoma: The Interplay of Apoptosis and Autophagy.Biomedicines · 2023Review
- Wnt/β-Catenin Signaling as a Driver of Stemness and Metabolic Reprogramming in Hepatocellular Carcinoma.Cancers · 2022Review
- Alleviation of cisplatin-induced hepatotoxicity and nephrotoxicity by L-carnitine.Iranian journal of basic medical sciences · 2022Article
- Targeting Wnt/β-Catenin Pathways in Primary Liver Tumours: From Microenvironment Signaling to Therapeutic Agents.Cancers · 2022Review
- β-Catenin signaling in hepatocellular carcinoma.The Journal of clinical investigation · 2022Review
- The Relationship between MACC1/c-Met/Cyclin D1 Axis Expression and Prognosis in ESCC.Analytical cellular pathology (Amsterdam) · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Activation of c-Met signaling and beta-catenin mutations are frequent genetic events observed in liver cancer development. Recently, we demonstrated that activated beta-catenin can cooperate with c-Met to induce liver cancer formation in a mouse model. Cyclin D1 (CCND1) is an important cell cycle regulator that is considered to be a downstream target of beta-catenin. To determine the importance of CCND1 as a mediator of c-Met- and beta-catenin-induced hepatocarcinogenesis, we investigated the genetic interactions between CCND1, beta-catenin, and c-Met in liver cancer development using mouse models. We coexpressed CCND1 with c-Met in mice and found CCND1 to cooperate with c-Met to promote liver cancer formation. Tumors induced by CCND1/c-Met had a longer latency period, formed at a lower frequency, and seemed to be more benign compared with those induced by beta-catenin/c-Met. In addition, when activated beta-catenin and c-Met were coinjected into CCND1-null mice, liver tumors developed despite the absence of CCND1. Intriguingly, we observed a moderate accelerated tumor growth and increased tumor malignancy in these CCND1-null mice. Molecular analysis showed an up-regulation of cyclin D2 (CCND2) expression in CCND1-null tumor samples, indicating that CCND2 may replace CCND1 in hepatic tumorigenesis. Together, our results suggest that CCND1 functions as a mediator of beta-catenin during HCC pathogenesis, although other molecules may be required to fully propagate beta-catenin signaling. Moreover, our data suggest that CCND1 expression is not essential for liver tumor development induced by c-Met and beta-catenin.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.