ArticleMolecular and cellular biology2003
Increased expression of TATA-binding protein, the central transcription factor, can contribute to oncogenesis.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 66 citations in OpenAlex.
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- An interaction network driven approach for identifying biomarkers for progressing cervical intraepithelial neoplasia.Scientific reports · 2018Article
- Mechanisms of Oncogene-Induced Replication Stress: Jigsaw Falling into Place.Cancer discovery · 2018Review
- Maf1 phenotypes and cell physiology.Biochimica et biophysica acta. Gene regulatory mechanisms · 2018Review
- Abnormal expression of TFIIIB subunits and RNA Pol III genes is associated with hepatocellular carcinoma.Liver research (Beijing, China) · 2017Article
- Elevated TATA-binding protein expression drives vascular endothelial growth factor expression in colon cancer.Oncotarget · 2017Article
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- Increased global transcription activity as a mechanism of replication stress in cancer.Nature communications · 2016Article
- Therapeutic interventions to disrupt the protein synthetic machinery in melanoma.Pigment cell & melanoma research · 2015Review
- Emerging Roles for Maf1 beyond the Regulation of RNA Polymerase III Activity.Journal of molecular biology · 2015Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Despite the central role of TATA-binding protein (TBP) in transcription, changes in cellular TBP concentration produce selective effects on gene expression. Moreover, TBP is up-regulated by oncogenic signaling pathways. These findings suggest that TBP could be a nexus in pathways that regulate cell proliferation and that genetic lesions that result in cellular transformation may produce their effects at least in part through TBP. We provide evidence consistent with this hypothesis, demonstrating that increases in TBP expression contribute to cellular transformation. A Ras-mediated increase in TBP expression is required for full Ras transforming activity. TBP overexpression induces cells to grow in an anchorage-independent manner and to form tumors in athymic mice. These effects on cellular transformation require changes in RNA polymerase II-dependent transcription and on the selective recruitment of TBP to promoters via its DNA binding activity. TBP expression is elevated in human colon carcinomas relative to normal colon epithelium. Both Ras-dependent and Ras-independent mechanisms mediate increases in TBP expression in colon carcinoma cell lines. We conclude that TBP may be a critical component in dysregulated signaling that occurs downstream of genetic lesions that cause tumors.
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