ArticleCell death & disease2024
Proteomic profiling reveals CEACAM6 function in driving gallbladder cancer aggressiveness through integrin receptor, PRKCD and AKT/ERK signaling.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- The B7 family subgroup reflects tumor cell heterogeneity and patient post-operative prognosis in gallbladder cancer.Biology direct · 2026Article
- Targeting sialic acid metabolism: a therapeutic strategy against gastric cancer driven by WZ35.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Emergence of Liquid Biopsy in Precision Oncology: A Review of its diagnostic, Predictive and Therapeutic Applications in Gallbladder Cancer.Journal of gastrointestinal cancer · 2026Review
- Integrative Omics Analysis Reveals the Potential Value of CEACAM6 in Pan-Gastrointestinal Cancers.Immunity, inflammation and disease · 2026Article
- Integrative multi-omics and machine learning reveals the spatial niche distribution and role of CYP27A1Frontiers in immunology · 2026Article
- Molecular Mechanisms of Lymph Node Metastasis in Gallbladder Cancer: Insights into the Tumor Microenvironment.Biomedicines · 2025Review
- Cytokine and epigenetic regulation of CEACAM6 mediates EGFR-driven signaling and drug response in lung adenocarcinoma.NPJ precision oncology · 2025Article
- CD151 Promotes Cancer Progression in Triple-Negative Breast Cancer by Inducing EMT through the MAPK Signaling Pathway.Breast cancer (Dove Medical Press) · 2025Article
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Authors and funding
20 authors.
Funding
Abstract
Gallbladder cancer (GBC) presents as an aggressive malignancy with poor patient outcome. Like other epithelial cancers, the mechanisms of GBC cancer progression remain vague and efforts in finding targeted therapies fall below expectations. This study combined proteomic analysis of formalin-fixed paraffin-embedded (FFPE) GBC samples, functional and molecular characterization of potential oncogenes and identification of potential therapeutic strategies for GBC. We identified Carcinoembryonic Antigen-related Cell Adhesion Molecule 6 (CEACAM6) as one of the significantly most upregulated proteins in GBC. CEACAM6 overexpression has been observed in other cancer entities but the molecular function remains unclear. Our functional analyses in vitro and in vivo mouse models revealed that CEACAM6 supported the initial steps of cancer progression and metastasis by decreasing cell adhesion and promoting migration and invasion of GBC cells. Conversely, CEACAM6 knockdown abolished GBC aggressiveness by increasing cell adhesion while reducing cell migration, cell proliferation, and colony formation. BirA-BioID followed by mass-spectrometry revealed Integrin Beta-1 (ITGB1) and Protein Kinase C Delta (PRKCD) as direct molecular and functional partners of CEACAM6 supporting GBC cell migration. ERK and AKT signaling and their downstream target genes were regulated by CEACAM6 and thus the treatment with AKT inhibitor capivasertib or ERK inhibitor ulixertinib mitigated the CEACAM6-induced migration. These findings demonstrate that CEACAM6 is crucially involved in gallbladder cancer progression by promoting migration and inhibiting cell adhesion through ERK and AKT signaling providing specific options for treatment of CEACAM6-positive cancers.
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