ArticleOncogenesis2012
The CEACAM1 tumor suppressor is an ATM and p53-regulated gene required for the induction of cellular senescence by DNA damage.
Article in Oncogenesis, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
The trial behind it
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
19 citing papers in PubMed, 26 citations in OpenAlex.
- CEACAM1 participation in breast cancer progression.Molecular oncology · 2026Article
- CEACAM1 Is Associated With an Immune-Activated Tumor Microenvironment and Therapeutic Stratification in Sarcoma.International journal of genomics · 2026Article
- ATM and p53 in aging and cancer: a double-edged sword in genomic integrity.Biogerontology · 2025Review
- Transcriptional activation of genes associated with the matrisome is a common feature of senescent endothelial cells.Biogerontology · 2025Article
- Inhibitory immune checkpoints suppress the surveillance of senescent cells promoting their accumulation with aging and in age-related diseases.Biogerontology · 2024Review
- Acquired resistance to immunotherapy and chemoradiation in MYC amplified head and neck cancer.NPJ precision oncology · 2024Article
- The Wheel of p53 Helps to Drive the Immune System.International journal of molecular sciences · 2023Review
- ZBTB2 links p53 deficiency to HIF-1-mediated hypoxia signaling to promote cancer aggressiveness.EMBO reports · 2023Article
- Elongation factor-2 kinase is a critical determinant of the fate and antitumor immunity of CD8Science advances · 2022Article
- The Role of Senescent Cells in Acquired Drug Resistance and Secondary Cancer in BRAFi-Treated Melanoma.Cancers · 2021Review
- Dissecting phenotypic transitions in metastatic disease via photoconversion-based isolation.eLife · 2021Article
- Efficient mutation screening for cervical cancers from circulating tumor DNA in blood.BMC cancer · 2020Article
- Tumor intrinsic immunity related proteins may be novel tumor suppressors in some types of cancer.Scientific reports · 2019Article
- The role of CEA-related cell adhesion molecule-1 (CEACAM1) in vascular homeostasis.Histochemistry and cell biology · 2016Review
- Glycosylation Alters Dimerization Properties of a Cell-surface Signaling Protein, Carcinoembryonic Antigen-related Cell Adhesion Molecule 1 (CEACAM1).The Journal of biological chemistry · 2016Article
- Loss of CEACAM1, a Tumor-Associated Factor, Attenuates Post-infarction Cardiac Remodeling by Inhibiting Apoptosis.Scientific reports · 2016Article
- A549 cells adapted to high nitric oxide show reduced surface CEACAM expression and altered adhesion and migration properties.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- A comprehensive phylogenetic and structural analysis of the carcinoembryonic antigen (CEA) gene family.Genome biology and evolution · 2014Article
- Condurango-glycoside-A fraction of Gonolobus condurango induces DNA damage associated senescence and apoptosis via ROS-dependent p53 signalling pathway in HeLa cells.Molecular and cellular biochemistry · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The p53 tumor-suppressor protein has a key role in the induction of cellular senescence, an important barrier to cancer development. However, very little is known about the physiological mediators of cellular senescence induced by p53. CEACAM1 is an immunoglobulin superfamily member whose expression is frequently lost in human tumors and exhibits tumor-suppressor features in several experimental systems, including Ceacam1 knockout mice. There is currently little understanding of the pathways and mechanisms by which CEACAM1 exerts its tumor-suppressor function. Here we report that CEACAM1 is strongly upregulated during the cellular response to DNA double-strand breaks (DSBs) starting from the lowest doses of DSB inducers used, and that upregulation is mediated by the ataxia telangiectasia mutated (ATM)/p53 pathway. Stable silencing of CEACAM1 showed that CEACAM1 is required for p53-mediated cellular senescence, but not initial cell growth arrest, in response to DNA damage. These findings identify CEACAM1 as a key component of the ATM/p53-mediated cellular response to DNA damage, and as a tumor suppressor mediating cellular senescence downstream of p53.
Identifiers
What OpenQuestion holds
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.