ArticleOncogene2007
Gene amplification and associated loss of 5' regulatory sequences of CoAA in human cancers.
Article in Oncogene, 2007. 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.
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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
19 citing papers in PubMed, 40 citations in OpenAlex.
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- The growth hormone receptor interacts with transcriptional regulator HMGN1 upon GH-induced nuclear translocation.Journal of cell communication and signaling · 2023Article
- RBM14 as a novel epigenetic-activated tumor oncogene is implicated in the reprogramming of glycolysis in lung cancer.World journal of surgical oncology · 2023Article
- Decoding cancer and herbal renaissance.Longhua Chinese medicine · 2022Article
- Protein phase separation: A novel therapy for cancer?British journal of pharmacology · 2020Review
- Co-expression networks reveal the tissue-specific regulation of transcription and splicing.Genome research · 2017Article
- RNA processing as an alternative route to attack glioblastoma.Human genetics · 2017Review
- Roles of RNA-Binding Proteins in DNA Damage Response.International journal of molecular sciences · 2016Review
- RNA binding protein RBM14 promotes radio-resistance in glioblastoma by regulating DNA repair and cell differentiation.Oncotarget · 2014Article
- E2/Estrogen receptor/sjogren syndrome-associated autoantigen relieves coactivator activator-induced G1/S arrest to promote breast tumorigenicity.Molecular and cellular biology · 2014Article
- The tumor suppressor annexin A10 is a novel component of nuclear paraspeckles.Cellular and molecular life sciences : CMLS · 2014Article
- TEThered to Runx: novel binding partners for runx factors.Blood cells, molecules & diseases · 2010Article
- Nuclear receptor coregulators in cancer biology.Cancer research · 2009Review
- Co-activator activator (CoAA) prevents the transcriptional activity of Runt domain transcription factors.Journal of cellular biochemistry · 2009Article
- Functional pre- mRNA trans-splicing of coactivator CoAA and corepressor RBM4 during stem/progenitor cell differentiation.The Journal of biological chemistry · 2009Article
- Dual roles for coactivator activator and its counterbalancing isoform coactivator modulator in human kidney cell tumorigenesis.Cancer research · 2008Article
- The extracellular domain of the growth hormone receptor interacts with coactivator activator to promote cell proliferation.Molecular endocrinology (Baltimore, Md.) · 2008Article
- Switched alternative splicing of oncogene CoAA during embryonal carcinoma stem cell differentiation.Nucleic acids research · 2007Article
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 2 institutions in 1 country.
Funding
Abstract
CoAA is an RRM-containing transcriptional coactivator that stimulates transcriptional activation and regulates alternative splicing. We show that the CoAA gene is amplified at the chromosome 11q13 locus in a subset of primary human cancers including non-small cell lung carcinoma, squamous cell skin carcinoma and lymphoma. Analysis of 42 primary tumors suggests that CoAA amplifies independently from the CCND1 locus. Detailed mapping of three CoAA amplicons reveals that the amplified CoAA gene is consistently located at the 5' boundaries of the amplicons. The CoAA coding and basal promoter sequences are retained within the amplicons but upstream silencing sequences are lost. CoAA protein is overexpressed in tumors containing the amplified CoAA gene. RNA dot blot analysis of 100 cases of primary tumors suggests elevated CoAA mRNA expression. CoAA positively regulates its own basal promoter in transfection assays. Thus, gene amplification, loss of silencing sequence and positive feedback regulation may lead to drastic upregulation of CoAA protein. CoAA has transforming activities when tested in soft agar assays, and CoAA is homologous to oncoproteins EWS and TLS, which regulate alternative splicing. These data imply that CoAA may share a similar oncogenic mechanism with oncogene EWS and that CoAA deregulation may alter the alternative splicing of target genes.
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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.