ArticleMolecular biology of the cell2002
Downstream E-box-mediated regulation of the human telomerase reverse transcriptase (hTERT) gene transcription: evidence for an endogenous mechanism of transcriptional repression.
Article in Molecular biology of the cell, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 88 citations in OpenAlex.
- Molecular profiling reveals novel therapeutic targets and clonal evolution in ovarian clear cell carcinoma.BMC cancer · 2024Article
- Fabricating niosomal-PEG nanoparticles co-loaded with metformin and silibinin for effective treatment of human lung cancer cells.Frontiers in oncology · 2023Article
- Timing the Landmark Events in the Evolution of Clear Cell Renal Cell Cancer: TRACERx Renal.Cell · 2018Article
- TIP60 represses telomerase expression by inhibiting Sp1 binding to the TERT promoter.PLoS pathogens · 2017Article
- Telomerase Induction in HPV Infection and Oncogenesis.Viruses · 2017Review
- MR molecular imaging of tumors based on an optimal hTERT promoter tyrosinase expression system.Oncotarget · 2016Article
- Human Telomerase Reverse Transcriptase (hTERT) Transcription Requires Sp1/Sp3 Binding to the Promoter and a Permissive Chromatin Environment.The Journal of biological chemistry · 2015Article
- A Combinatory Strategy for Detection of Live CTCs Using Microfiltration and a New Telomerase-Selective Adenovirus.Molecular cancer therapeutics · 2015Article
- A co-culture genome-wide RNAi screen with mammary epithelial cells reveals transmembrane signals required for growth and differentiation.Breast cancer research : BCR · 2015Article
- Genetic mapping and comparative expression analysis of transcription factors in cotton.PloS one · 2015Article
- Variations in telomere maintenance and the role of telomerase inhibition in gastrointestinal cancer.Pharmacogenomics and personalized medicine · 2015Review
- PI3K/Akt/uncoupling protein 2 signaling pathway may be involved in cell senescence and apoptosis induced by angiotensin II in human vascular endothelial cells.Molecular biology reports · 2014Article
- Poly (ADP-ribose) polymerase 3 (PARP3), a potential repressor of telomerase activity.Journal of experimental & clinical cancer research : CR · 2014Article
- Dual roles of c-Myc in the regulation of hTERT gene.Nucleic acids research · 2014Article
- Upstream stimulatory factor 2 and hypoxia-inducible factor 2α (HIF2α) cooperatively activate HIF2 target genes during hypoxia.Molecular and cellular biology · 2012Article
- Human telomerase reverse transcriptase (hTERT) is a novel target of the Wnt/β-catenin pathway in human cancer.The Journal of biological chemistry · 2012Article
- Tumor suppressors p53, p63TAα, p63TAy, p73α, and p73β use distinct pathways to repress telomerase expression.The Journal of biological chemistry · 2012Article
- Review
- Regulation of hTERT by BCR-ABL at multiple levels in K562 cells.BMC cancer · 2011Article
- High-mobility group A2 protein modulates hTERT transcription to promote tumorigenesis.Molecular and cellular biology · 2011Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Regulation of the hTERT gene encoding the telomerase catalytic subunit plays an important role in human cell senescence, immortalization, and carcinogenesis. By examining the activity of various deleted or mutated hTERT promoter fragments, we show that an E-box element downstream of the transcription initiation site is critical to differential hTERT transcription between the telomerase/hTERT-positive renal cell carcinoma cell line (RCC23) and its telomerase/hTERT-negative counterpart containing a transferred, normal chromosome 3 (RCC23+3). This E-box element mediated repression of hTERT transcription in RCC23+3 but not in RCC23. A copy number-dependent enhancement of the repression suggested active repression, rather than loss of activation, in RCC23+3. Endogenous expression levels of c-Myc or Mad1, which could activate or repress hTERT transcription when overexpressed, did not account for the differential hTERT transcription. Gel mobility shift assays identified the upstream stimulatory factors (USFs) as a major E-box-binding protein complex in both RCC23 and RCC23+3 and, importantly, detected an RCC23+3-specific, E-box-binding factor that was distinct from the USF and Myc/Mad families. The E-box-mediated repression was also active in normal human fibroblasts and epithelial cells and inactive in some, but not all, telomerase/hTERT-positive cancer cells. These findings provide evidence for an endogenous, repressive mechanism that actively functions in telomerase/hTERT-negative normal cells and becomes defective during carcinogenic processes, e.g., by an inactivation of the telomerase repressor gene on chromosome 3.
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