ArticlePloS one2009
Human papillomavirus-16 E7 interacts with glutathione S-transferase P1 and enhances its role in cell survival.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 34 citations in OpenAlex.
- Head and neck tumor organoid biobank for modelling individual responses to radiation therapy according to the TP53/HPV status.Journal of experimental & clinical cancer research : CR · 2025Article
- The Hallmarks of Cervical Cancer: Molecular Mechanisms Induced by Human Papillomavirus.Biology · 2024Review
- The human papillomavirus oncoproteins: a review of the host pathways targeted on the road to transformation.The Journal of general virology · 2021Review
- GSTpi regulates VE-cadherin stabilization through promoting S-glutathionylation of Src.Redox biology · 2020Article
- An evolving understanding of the S-glutathionylation cycle in pathways of redox regulation.Free radical biology & medicine · 2018Review
- Article
- Cervical Cancer Cell Line Secretome Highlights the Roles of Transforming Growth Factor-Beta-Induced Protein ig-h3, Peroxiredoxin-2, and NRF2 on Cervical Carcinogenesis.BioMed research international · 2017Article
- Interaction between the human papillomavirus 16 E7 oncoprotein and gelsolin ignites cancer cell motility and invasiveness.Oncotarget · 2016Article
- Glutathione S-transferase mediates an ageing response to mitochondrial dysfunction.Mechanisms of ageing and development · 2016Article
- Article
- The papillomavirus E7 proteins.Virology · 2013Review
- Oxidative stress and HPV carcinogenesis.Viruses · 2013Review
- Glutathione-s-transferases as determinants of cell survival and death.Antioxidants & redox signaling · 2012Review
- Article
- Cellular transformation by human papillomaviruses: lessons learned by comparing high- and low-risk viruses.Virology · 2012Review
- Current approaches on viral infection: proteomics and functional validations.Frontiers in microbiology · 2012Article
- The role of glutathione S-transferase P in signaling pathways and S-glutathionylation in cancer.Free radical biology & medicine · 2011Review
- Retinoblastoma-independent antiproliferative activity of novel intracellular antibodies against the E7 oncoprotein in HPV 16-positive cells.BMC cancer · 2011Article
- Glutathione s-transferases in pediatric cancer.Frontiers in oncology · 2011Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHuman Papillomavirus (HPV)-16 is a paradigm for "high-risk" HPVs, the causative agents of virtually all cervical carcinomas. HPV E6 and E7 viral genes are usually expressed in these tumors, suggesting key roles for their gene products, the E6 and E7 oncoproteins, in inducing malignant transformation. METHODOLOGY/PRINCIPAL
findingsBy protein-protein interaction analysis, using mass spectrometry, we identified glutathione S-transferase P1-1 (GSTP1) as a novel cellular partner of the HPV-16 E7 oncoprotein. Following mapping of the region in the HPV-16 E7 sequence that is involved in the interaction, we generated a three-dimensional molecular model of the complex between HPV-16 E7 and GSTP1, and used this to engineer a mutant molecule of HPV-16 E7 with strongly reduced affinity for GSTP1.When expressed in HaCaT human keratinocytes, HPV-16 E7 modified the equilibrium between the oxidized and reduced forms of GSTP1, thereby inhibiting JNK phosphorylation and its ability to induce apoptosis. Using GSTP1-deficient MCF-7 cancer cells and siRNA interference targeting GSTP1 in HaCaT keratinocytes expressing either wild-type or mutant HPV-16 E7, we uncovered a pivotal role for GSTP1 in the pro-survival program elicited by its binding with HPV-16 E7. CONCLUSIONS/SIGNIFICANCE: This study provides further evidence of the transforming abilities of this oncoprotein, setting the groundwork for devising unique molecular tools that can both interfere with the interaction between HPV-16 E7 and GSTP1 and minimize the survival of HPV-16 E7-expressing cancer cells.
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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.