ArticleCancer letters2009
Mechanisms of decreased expression of transforming growth factor-beta receptor type I at late stages of HPV16-mediated transformation.
Article in Cancer letters, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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
12 citing papers in PubMed, 18 citations in OpenAlex.
- Role and clinical significance of TGF‑β1 and TGF‑βR1 in malignant tumors (Review).International journal of molecular medicine · 2021Review
- Inhibition of Epstein-Barr Virus Replication in Human Papillomavirus-Immortalized Keratinocytes.Journal of virology · 2019Article
- Induction of Interferon Kappa in Human Papillomavirus 16 Infection by Transforming Growth Factor Beta-Induced Promoter Demethylation.Journal of virology · 2018Article
- The human papillomavirus E7 oncoprotein as a regulator of transcription.Virus research · 2017Review
- Transforming growth factor-β1 in carcinogenesis, progression, and therapy in cervical cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- The Interaction Between Human Papillomaviruses and the Stromal Microenvironment.Progress in molecular biology and translational science · 2016Review
- Article
- The translational significance of epithelial-mesenchymal transition in head and neck cancer.Clinical and translational medicine · 2014Article
- TGF-β regulation of gene expression at early and late stages of HPV16-mediated transformation of human keratinocytes.Virology · 2013Article
- Partial loss of Smad signaling during in vitro progression of HPV16-immortalized human keratinocytes.BMC cancer · 2013Article
- Ski protein levels increase during in vitro progression of HPV16-immortalized human keratinocytes and in cervical cancer.Virology · 2013Article
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Transforming growth factor-beta (TGF-beta) signaling is disrupted in many cancers, including cervical cancer, leading to TGF-beta resistance. Although initially sensitive, human papillomavirus type 16 (HPV16) immortalized human keratinocytes (HKc/HPV16) become increasingly resistant to the growth inhibitory effects of TGF-beta during in vitro progression to a differentiation resistant phenotype (HKc/DR). We have previously shown that loss of TGF-beta sensitivity in HKc/DR is attributed to decreased expression of TGF-beta receptor type I (TGF-beta RI), while the levels of TGF-beta receptor type II (TGF-beta RII) remain unchanged. The present study explored molecular mechanisms leading to reduced TGF-beta RI expression in HKc/DR. Using TGF-beta RI and TGF-beta RII promoter reporter constructs, we determined that acute expression of the HPV16 oncogenes E6 and E7 decreased the promoter activity of TGF-beta RI and TGF-beta RII by about 50%. However, promoter activity of TGF-beta RI is decreased to a greater extent than TGF-beta RII as HKc/HPV16 progress to HKc/DR. Reduced TGF-beta RI expression in HKc/DR was found not to be linked to mutations within the TGF-beta RI promoter or to promoter methylation. Electrophoretic mobility shift and supershift assays using probes encompassing Sp1 binding sites in the TGF-beta RI promoter found no changes between HKc/HPV16 and HKc/DR in binding of the transcription factors Sp1 or Sp3 to the probes. Also, Western blots determined that protein levels of Sp1 and Sp3 remain relatively unchanged between HKc/HPV16 and HKc/DR. Overall, these results demonstrate that mutations in or hypermethylation of the TGF-beta RI promoter, along with altered levels of Sp1 or Sp3, are not responsible for the reduced expression of TGF-beta RI we observe in HKc/DR. Rather the HPV16 oncogenes E6 and E7 themselves exhibit an inhibitory effect on TGF-beta receptor promoter activity.
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Registered trials
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