ArticleJournal of virology2003
Endogenous human papillomavirus E6 and E7 proteins differentially regulate proliferation, senescence, and apoptosis in HeLa cervical carcinoma cells.
Article in Journal of virology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers.
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Who cites it
168 citing papers in PubMed, 344 citations in OpenAlex.
- Therapy resistance-related ncRNAs in cervical cancer: biomarkers and therapeutic targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Review
- Integrated transcriptomic and functional analysis reveals selective cytotoxicity and HPV oncogene suppression induced by cinnamon essential oil in cervical cancer cells.BMC complementary medicine and therapies · 2026Article
- Lipid reprogramming of stratified squamous epithelium by the high-risk HPV E6 and E6/E7 oncoproteins.Metabolomics : Official journal of the Metabolomic Society · 2026Article
- The MYB-related transcription factor MYPOP acts as a selective regulator of cancer cell growth.Communications biology · 2026Article
- HPV Infection and Oxidative Stress in Cervical Carcinogenesis: Linking Apoptosis, Senescence, SASP, and EMT.Antioxidants (Basel, Switzerland) · 2026Review
- A genome-wide analysis of YY1 and TFAP2 competition on overlapping motifs reveals their roles in HPV-induced carcinogenesis.PLoS pathogens · 2025Article
- E6AP is essential for the proliferation of HPV-positive cancer cells by preventing senescence.PLoS pathogens · 2025Article
- Resolution of oncogene-induced senescence markers in HPV-infected cervical cancer tissue.BMC cancer · 2025Article
- PLOD2 exacerbates cervical squamous cell carcinoma by suppressing p53 by binding to YAP1.Molecular medicine reports · 2025Article
- The Natural History of Cervical Cancer and the Case for MicroRNAs: Is Human Papillomavirus Infection the Whole Story?International journal of molecular sciences · 2024Review
- Fibroblasts Regulate the Transformation Potential of Human Papillomavirus-positive Keratinocytes.bioRxiv : the preprint server for biology · 2024Article
- Listeria-vectored cervical cancer vaccine candidate strains reduce MDSCs via the JAK-STAT signaling pathway.BMC biology · 2024Article
- A novel method for colposcopic shunting in HPV-positive women: Quantitative detection of HPV E7 oncoprotein.Heliyon · 2024Article
- Editorial: Lipids, lipid oxidation, and cancer: from biology to therapeutics.Frontiers in oncology · 2024Article
- Targeted inhibition of BET proteins in HPV16-positive head and neck squamous cell carcinoma reveals heterogeneous transcriptional responses.Frontiers in oncology · 2024Article
- HPV E6/E7: insights into their regulatory role and mechanism in signaling pathways in HPV-associated tumor.Cancer gene therapy · 2024Review
- For Better or Worse: Modulation of the Host DNA Damage Response by Human Papillomavirus.Annual review of virology · 2023Review
- When Bacteria and Viruses Collide: A Tale ofViruses · 2023Review
- Preferential killing of melanoma cells by a p16-related peptide.Biology open · 2023Article
- NSP4 as adjuvant for immunogenicity and design of effective therapeutic HPV16 E6/E7/L1 DNA vaccine in tumor-bearing and healthy C57BL/6 mice.BMC research notes · 2023Article
108 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cervical cancer cells express high-risk human papillomavirus (HPV) E6 and E7 proteins, and repression of HPV gene expression causes the cells to cease proliferation and undergo senescence. However, it is not known whether both HPV proteins are required to maintain the proliferative state of cervical cancer cells, or whether mutations that accumulate during carcinogenesis eliminate the need for one or the other of them. To address these questions, we used the bovine papillomavirus E2 protein to repress the expression of either the E6 protein or the E7 protein encoded by integrated HPV18 DNA in HeLa cervical carcinoma cells. Repression of the E7 protein activated the Rb pathway but not the p53 pathway and triggered senescence, whereas repression of the E6 protein activated the p53 pathway but not the Rb pathway and triggered both senescence and apoptosis. Telomerase activity, cyclin-dependent kinase activity, and expression of c-myc were markedly inhibited by repression of either E6 or E7. These results demonstrate that continuous expression of both the E6 and the E7 protein is required for optimal proliferation of cervical carcinoma cells and that the two viral proteins exert distinct effects on cell survival and proliferation. Therefore, strategies that inhibit the expression or activity of either viral protein are likely to inhibit the growth of HPV-associated cancers.
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