ArticleCancer research2007
Cancer cells and normal cells differ in their requirements for Thoc1.
Article in Cancer research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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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
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Background gene expression networks significantly enhance drug response prediction by transcriptional profiling.The pharmacogenomics journal · 2012Pooled it
- Comprehensive Analysis of the Expression and Clinical Significance of THO Complex Members in Hepatocellular Carcinoma.International journal of general medicine · 2022Article
- Article
- THOC1 deficiency leads to late-onset nonsyndromic hearing loss through p53-mediated hair cell apoptosis.PLoS genetics · 2020Article
- Knockdown of THOC1 reduces the proliferation of hepatocellular carcinoma and increases the sensitivity to cisplatin.Journal of experimental & clinical cancer research : CR · 2020Article
- An F-Box Protein, Mdm30, Interacts with TREX Subunit Sub2 To Regulate Cellular Abundance Cotranscriptionally in Orchestrating mRNA Export Independently of Splicing and Mitochondrial Function.Molecular and cellular biology · 2020Article
- Targeted Next-Generation Sequencing Identified Compound Heterozygous Mutations inNeural plasticity · 2020Article
- The plasma peptides of breast versus ovarian cancer.Clinical proteomics · 2019Article
- The role of TREX in gene expression and disease.The Biochemical journal · 2016Review
- The Transcription Factor THO Promotes Transcription Initiation and Elongation by RNA Polymerase I.The Journal of biological chemistry · 2016Article
- Luzp4 defines a new mRNA export pathway in cancer cells.Nucleic acids research · 2015Article
- The Thoc1 ribonucleoprotein and prostate cancer progression.Journal of the National Cancer Institute · 2014Article
- THOC5, a member of the mRNA export complex: a novel link between mRNA export machinery and signal transduction pathways in cell proliferation and differentiation.Cell communication and signaling : CCS · 2014Review
- The Thoc1 encoded ribonucleoprotein is required for myeloid progenitor cell homeostasis in the adult mouse.PloS one · 2014Article
- Transcriptional regulation of immediate-early gene response by THOC5, a member of mRNA export complex, contributes to the M-CSF-induced macrophage differentiation.Cell death & disease · 2013Article
- The THO ribonucleoprotein complex is required for stem cell homeostasis in the adult mouse small intestine.Molecular and cellular biology · 2013Article
- Intellectual disability associated with a homozygous missense mutation in THOC6.Orphanet journal of rare diseases · 2013Article
- The Thoc1 encoded ribonucleoprotein is a substrate for the NEDD4-1 E3 ubiquitin protein ligase.PloS one · 2013Article
- Identification of mRNAs that are spliced but not exported to the cytoplasm in the absence of THOC5 in mouse embryo fibroblasts.RNA (New York, N.Y.) · 2011Article
- Differential expression of THOC1 and ALY mRNP biogenesis/export factors in human cancers.BMC cancer · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The evolutionarily conserved TREX (Transcription/Export) complex physically couples transcription, messenger ribonucleoprotein particle biogenesis, RNA processing, and RNA export for a subset of genes. HPR1 encodes an essential component of the S. cerevisiae TREX complex. HPR1 loss compromises transcriptional elongation, nuclear RNA export, and genome stability. Yet, HPR1 is not required for yeast viability. Thoc1 is the recently discovered human functional orthologue of HPR1. Thoc1 is expressed at higher levels in breast cancer than in normal epithelia, and expression levels correlate with tumor size and metastatic potential. Depletion of Thoc1 protein (pThoc1) in human cancer cell lines compromises cell proliferation. It is currently unclear whether Thoc1 is essential for all mammalian cells or whether cancer cells may differ from normal cells in their dependence on Thoc1. To address this issue, we have compared the requirements for Thoc1 in the proliferation and survival of isogenic normal and oncogene-transformed cells. Neoplastic cells rapidly lose viability via apoptotic cell death on depletion of pThoc1. Induction of apoptotic cell death is coincident with increased DNA damage as indicated by the appearance of phosphorylated histone H2AX. In contrast, the viability of normal cells is largely unaffected by pThoc1 loss. Normal cells lacking Thoc1 cannot be transformed by forced expression of E1A and Ha-ras, suggesting that Thoc1 may be important for neoplastic transformation. In sum, our data are consistent with the hypothesis that cancer cells require higher levels of pThoc1 for survival than normal cells. If true, pThoc1 may provide a novel molecular target for cancer therapy.
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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.