ArticlePloS one2012
Overexpression of CD157 contributes to epithelial ovarian cancer progression by promoting mesenchymal differentiation.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- Histone methyltransferase SET-18/SMYD2-mediated activation of NADase TIR-1d/SARM1 increases mtROS to promote aging.iScience · 2026Article
- Bioinformatics analysis identifies BST1 as a potential therapeutic target linked to neutrophil extracellular traps in patients with acute liver failure.Scientific reports · 2025Article
- Biological Functions and Therapeutic Potential of NADCancers · 2024Review
- Identification of novel pQTL-SNPs associated with lung adenocarcinoma risk: A multi-stage study.Cancer medicine · 2024Article
- Article
- Cancer-mesothelial and cancer-macrophage interactions in the ovarian cancer microenvironment.American journal of physiology. Cell physiology · 2023Review
- Genetic polymorphisms of bone marrow stromal cell antigen-1 (BST-1/CD157): implications for immune/inflammatory dysfunction in neuropsychiatric disorders.Frontiers in immunology · 2023Review
- Bone marrow stromal cell antigen-1 (CD157) regulated by sphingosine kinase 2 mediates kidney fibrosis.Frontiers in medicine · 2022Article
- CD157 signaling promotes survival of acute myeloid leukemia cells and modulates sensitivity to cytarabine through regulation of anti-apoptotic Mcl-1.Scientific reports · 2021Article
- Identification ofOncology letters · 2021Article
- CD157 and Brain Immune System in (Patho)physiological Conditions: Focus on Brain Plasticity.Frontiers in immunology · 2020Review
- The Roles of CD38 and CD157 in the Solid Tumor Microenvironment and Cancer Immunotherapy.Cells · 2019Review
- CD157: From Myeloid Cell Differentiation Marker to Therapeutic Target in Acute Myeloid Leukemia.Cells · 2019Review
- CD157 and CD200 at the crossroads of endothelial remodeling and immune regulation.Stem cell investigation · 2019Article
- Soluble CD157 in pleural effusions: a complementary tool for the diagnosis of malignant mesothelioma.Oncotarget · 2018Article
- NAD Metabolism in Cancer Therapeutics.Frontiers in oncology · 2018Review
- Human canonical CD157/Bst1 is an alternatively spliced isoform masking a previously unidentified primate-specific exon included in a novel transcript.Scientific reports · 2017Article
- Unveiling differentially expressed genes upon regulation of transcription factors in sepsis.3 Biotech · 2017Article
- An integrated proteomic and glycoproteomic approach uncovers differences in glycosylation occupancy from benign and malignant epithelial ovarian tumors.Clinical proteomics · 2017Article
- Spheroid-Formation (Colonosphere) Assay for in Vitro Assessment and Expansion of Stem Cells in Colon Cancer.Stem cell reviews and reports · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial ovarian carcinoma (EOC) is an aggressive tumor often diagnosed at an advanced stage, when there is little or no prospect of cure. Despite advances in surgical and chemotherapeutic strategies, only marginal improvements in patient outcome have been obtained. Hence, unraveling the biological mechanisms underpinning EOC progression is critical for improving patients' survival. Recently, we reported that CD157 (an ectoenzyme regulating leukocyte diapedesis) is expressed in EOC and that high expression of the molecule is negatively correlated with the disease outcome in patients. Here, we demonstrate that forced overexpression of CD157 in OVCAR-3, TOV-21G, A2780 and OV-90 ovarian cancer cell lines promotes morphological and phenotypic changes characterized by disruption of intercellular junctions, downregulation of epithelial markers and upregulation of mesenchymal ones. These changes in cell shape and phenotype bring to reduced sensitivity to anoikis, increased anchorage-independent growth, cell motility and mesothelial invasion. Conversely, knockdown of CD157 in OV-90 and OC314 cells reverts the mesenchymal phenotype and reduces the cells' migratory potential. Transcriptome profiling analysis highlighted 378 significantly differentially expressed genes, representing the signature of CD157-overexpressing OVCAR-3 and OV-90 cells. The modulation of selected genes translates into alteration of protein expression that give cells a highly malignant phenotype. The overall picture deduced from the analysis of the modulated transcripts is that high expression of CD157 strengthens a number of biological processes favoring tumor progression (including development and cell motility), and weakens several biological processes hindering tumor progression (such as apoptosis, cell death and response to stress). Together, these findings implicate CD157 in the progression of EOC to metastatic disease and suggest that CD157 may represent a valuable therapeutic target.
Indexed as
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.