ArticleOncogene2004
Overexpression of CEACAM6 promotes insulin-like growth factor I-induced pancreatic adenocarcinoma cellular invasiveness.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 22 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- The Role of Biliary Carcinoembryonic Antigen-Related Cellular Adhesion Molecule 6 (CEACAM6) as a Biomarker in Cholangiocarcinoma.PloS one · 2016Trial
- Targeted Suppression of CEACAM6 via pHLIP-Delivered RNAs in Pancreatic Ductal Adenocarcinoma.Medicina (Kaunas, Lithuania) · 2025Article
- CEACAM6 expression and function in tumor biology: a comprehensive review.Discover oncology · 2024Review
- The emerging roles of CEACAM6 in human cancer (Review).International journal of oncology · 2024Review
- CEACAM6's Role as a Chemoresistance and Prognostic Biomarker for Pancreatic Cancer: A Comparison of CEACAM6's Diagnostic and Prognostic Capabilities with Those of CA19-9 and CEA.Life (Basel, Switzerland) · 2021Article
- Synergistic Anti-Cancer Effects of AKT and SRC Inhibition in Human Pancreatic Cancer Cells.Yonsei medical journal · 2018Article
- Article
- Oncolytic Viruses-Interaction of Virus and Tumor Cells in the Battle to Eliminate Cancer.Frontiers in oncology · 2017Review
- Diverse oligomeric states of CEACAM IgV domains.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Structure of the N-terminal dimerization domain of CEACAM7.Acta crystallographica. Section F, Structural biology communications · 2015Article
- Emerging Role and Targeting of Carcinoembryonic Antigen-related Cell Adhesion Molecule 6 (CEACAM6) in Human Malignancies.Clinical cancer drugs · 2015Article
- CD66+ cells in cervical precancers are partially differentiated progenitors with neoplastic traits.Cancer research · 2014Article
- Carcinoembryonic antigen-related cell adhesion molecules (CEACAM) 1, 5 and 6 as biomarkers in pancreatic cancer.PloS one · 2014Article
- Focal overexpression of CEACAM6 contributes to enhanced tumourigenesis in head and neck cancer via suppression of apoptosis.Molecular cancer · 2012Article
- Influenza A virus neuraminidase protein enhances cell survival through interaction with carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) protein.The Journal of biological chemistry · 2012Article
- Establishment and characterization of a new human pancreatic adenocarcinoma cell line with high metastatic potential to the lung.BMC cancer · 2010Article
- The role of Src in solid tumors.The oncologist · 2009Review
- CEACAM6 attenuates adenovirus infection by antagonizing viral trafficking in cancer cells.The Journal of clinical investigation · 2009Article
- Anti-metastatic effects of liposomal gemcitabine in a human orthotopic LNCaP prostate cancer xenograft model.Clinical & experimental metastasis · 2009Article
- Article
Corrections and comments
- Expression of concern
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carcinoembryonic antigen-related cell adhesion molecule 6 (CEACAM6) is a glycosylphosphatidylinositol-linked immunoglobulin superfamily member that is overexpressed in a variety of human cancers. We have recently reported that suppression of CEACAM6 expression impairs pancreatic adenocarcinoma progression in vivo. In order to characterize the mechanisms through which CEACAM6 influences the malignant phenotype, CEACAM6-overexpressing Capan2 pancreatic adenocarcinoma cells were established by stable transfection. We determined the effect of CEACAM6 overexpression on cellular invasiveness towards insulin-like growth factor I (IGF-I), a peptide of critical importance in pancreatic cancer malignant cellular behavior and tumor progression. IGF-I-induced cellular invasiveness and IGF-IR expression were significantly increased in clones overexpressing CEACAM6. Using inhibitory anti-IGF-IR antibody, a requirement for IGF-IR signaling in the enhanced invasiveness towards IGF-I induced by CEACAM6 overexpression was confirmed. CEACAM6-overexpressing clones exhibited increased Akt and c-Src kinase activities, as well as higher levels of matrix metalloproteinase-2 (MMP-2) expression and activity in the presence of IGF-I. While Akt kinase is both necessary and sufficient to induce IGF-IR upregulation, c-Src kinase activity is necessary, but alone is insufficient to upregulate IGF-IR expression. CEACAM6 is an important determinant of pancreatic adenocarcinoma malignant cellular behavior and, together with its downstream targets, warrants further investigation as a therapeutic target in this disease.
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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.