ArticleMolecular cancer2012
Cooperative interaction of MUC1 with the HGF/c-Met pathway during hepatocarcinogenesis.
Article in Molecular cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 84 citations in OpenAlex.
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- Evolution of the MUC1 gene in eutherian mammals as an adaptation responsible for the increasing incidence of cancer in humans.Biochimica et biophysica acta. Reviews on cancer · 2026Review
- Multi-omics profiling identifies ectopic olfactory receptors as putative drivers of tumor progression and prognostic indicators in clear cell renal cell carcinoma.Clinical and experimental medicine · 2026Article
- Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice.Nature communications · 2025Article
- The tumor distance to the main hepatic vessels is a predictor of recurrence-free survival and overall survival in hepatocellular cancer.Langenbeck's archives of surgery · 2025Article
- Reprogramming tumor-associated macrophages and inhibiting tumor neovascularization by targeting MANF-HSF1-HSP70-1 pathway: An effective treatment for hepatocellular carcinoma.Acta pharmaceutica Sinica. B · 2024Article
- Mucin 1 expression is regulated by hsa_circ_0055054/microRNA‑122‑5p and promotes hepatocellular carcinoma development.Oncology letters · 2024Article
- MUC1 promotes cervical squamous cell carcinoma through ERK phosphorylation-mediated regulation of ITGA2/ITGA3.BMC cancer · 2024Article
- Review
- CAR-T cell therapy for hepatocellular carcinoma: current trends and challenges.Frontiers in immunology · 2024Review
- scRNA-Seq and Bulk-Seq Analysis Identifies S100A9 Plasma Cells as a Potentially Effective Immunotherapeutic Agent for Multiple Myeloma.Journal of inflammation research · 2024Article
- Whole-exome sequencing identifies a set of genes as markers of hepatocellular carcinoma early recurrence.Hepatology international · 2023Article
- Review
- Cross-talk between cancer and Pseudomonas aeruginosa mediates tumor suppression.Communications biology · 2023Article
- Targeting Wnt/β-Catenin Pathways in Primary Liver Tumours: From Microenvironment Signaling to Therapeutic Agents.Cancers · 2022Review
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- The tumor microenvironment of hepatocellular carcinoma and its targeting strategy by CAR-T cell immunotherapy.Frontiers in endocrinology · 2022Review
- MUC1 is responsible for the pro-metastatic potential of calycosin in pancreatic ductal adenocarcinoma.American journal of cancer research · 2022Article
- Early Feasibility Assessment: A Method for Accurately Predicting Biotherapeutic Dosing to Inform Early Drug Discovery Decisions.Frontiers in pharmacology · 2022Article
- Analysis ofJournal of Cancer · 2022Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundHepatocyte growth factor (HGF) induced c-Met activation is known as the main stimulus for hepatocyte proliferation and is essential for liver development and regeneration. Activation of HGF/c-Met signaling has been correlated with aggressive phenotype and poor prognosis in hepatocellular carcinoma (HCC). MUC1 is a transmembrane mucin, whose over-expression is reported in most cancers. Many of the oncogenic effects of MUC1 are believed to occur through the interaction of MUC1 with signaling molecules. To clarify the role of MUC1 in HGF/c-Met signaling, we determined whether MUC1 and c-Met interact cooperatively and what their role(s) is in hepatocarcinogenesis.
resultsMUC1 and c-Met over-expression levels were determined in highly motile and invasive, mesenchymal-like HCC cell lines, and in serial sections of cirrhotic and HCC tissues, and these levels were compared to those in normal liver tissues. Co-expression of both c-Met and MUC1 was found to be associated with the differentiation status of HCC. We further demonstrated an interaction between c-Met and MUC1 in HCC cells. HGF-induced c-Met phosphorylation decreased this interaction, and down-regulated MUC1 expression. Inhibition of c-Met activation restored HGF-mediated MUC1 down-regulation, and decreased the migratory and invasive abilities of HCC cells via inhibition of β-catenin activation and c-Myc expression. In contrast, siRNA silencing of MUC1 increased HGF-induced c-Met activation and HGF-induced cell motility and invasion.
conclusionsThese findings indicate that the crosstalk between MUC1 and c-Met in HCC could provide an advantage for invasion to HCC cells through the β-catenin/c-Myc pathway. Thus, MUC1 and c-Met could serve as potential therapeutic targets in HCC.
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