ArticleCellular oncology (Dordrecht, Netherlands)2012
CSE1L, DIDO1 and RBM39 in colorectal adenoma to carcinoma progression.
Article in Cellular oncology (Dordrecht, Netherlands), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Tissue-Specific Multi-Omics Integration Demonstrates Molecular Signatures Connecting Obesity to Immune Vulnerability.Metabolites · 2026Article
- RBM39 Functions as a Potential Oncogene Through the NF-κB Signaling Pathway in Colorectal Cancer Cells.Journal of Cancer · 2025Article
- MORC2 regulates RBM39-mediated CDK5RAP2 alternative splicing to promote EMT and metastasis in colon cancer.Cell death & disease · 2024Article
- RBM39 is a potential prognostic biomarker with functional significance in hepatocellular carcinoma.Translational cancer research · 2024Article
- Indisulam synergizes with melphalan to inhibit Multiple Myeloma malignancy via targeting TOP2A.PloS one · 2024Article
- Data mining identifies novel RNA-binding proteins involved in colon and rectal carcinomas.Frontiers in cell and developmental biology · 2023Article
- Systematic pan-cancer analysis identifies RBM39 as an immunological and prognostic biomarker.Journal of cellular and molecular medicine · 2022Article
- Analysis and identification of mMolecular therapy. Nucleic acids · 2022Article
- RNA-binding protein 39: a promising therapeutic target for cancer.Cell death discovery · 2021Review
- The conserved alternative splicing factor caper regulates neuromuscular phenotypes during development and aging.Developmental biology · 2021Article
- RNA Regulators in Leukemia and Lymphoma.Cold Spring Harbor perspectives in medicine · 2020Review
- Development of CAPER peptides for the treatment of triple negative breast cancer.Cell cycle (Georgetown, Tex.) · 2020Article
- Cancer the'RBP'eutics-RNA-binding proteins as therapeutic targets for cancer.Pharmacology & therapeutics · 2019Review
- Exome sequencing in 51 early onset non-familial CRC cases.Molecular genetics & genomic medicine · 2019Article
- CAPER as a therapeutic target for triple negative breast cancer.Oncotarget · 2018Article
- Discovering sparse transcription factor codes for cell states and state transitions during development.eLife · 2017Article
- Distinct prostate cancer-related mRNA cargo in extracellular vesicle subsets from prostate cell lines.BMC cancer · 2017Article
- Knockdown of CSE1L Gene in Colorectal Cancer Reduces Tumorigenesis in Vitro.The American journal of pathology · 2016Article
- CAS (CSE1L) signaling pathway in tumor progression and its potential as a biomarker and target for targeted therapy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Quantitative analysis of gene expression in fixed colorectal carcinoma samples as a method for biomarker validation.Molecular medicine reports · 2016Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGain of chromosome 20q is an important factor in the progression from colorectal adenomas to carcinomas. Genes that drive 20q gain are expected to show correlation of mRNA and protein expression levels with 20q DNA copy number status while functionally influencing cancer processes. CSE1L, DIDO1 and RBM39 are located on the 20q amplicon and affect processes such as cell viability and anchorage-independent growth in colorectal cancer. This study aimed to investigate whether CSE1L, DIDO1 and RBM39 may drive 20q amplification.
methodsProtein expression levels were examined by immunohistochemical evaluation of tissue microarrays containing a series of colorectal adenoma and carcinoma samples, which were characterized by genome-wide (microarray-based) DNA and mRNA profiling.
resultsCSE1L, DIDO1 and RBM39 mRNA expression levels correlated with chromosome 20q DNA copy number status. CSE1L protein expression was not associated with 20q gain, although its expression was increased in carcinomas compared to adenomas. DIDO1 and RBM39 protein expression was quite strong in the majority of tumors irrespective of 20q DNA copy number status.
conclusionThe lack of correlation between protein expression levels and 20q DNA copy number status implies that CSE1L, DIDO1 and RBM39 are merely passengers rather than drivers of chromosome 20q gain in colorectal adenoma-to-carcinoma progression.
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