ArticleOncology letters2016
Entrance of the Tat protein of HIV-1 into human uterine cervical carcinoma cells causes upregulation of HPV-E6 expression and a decrease in p53 protein levels.
Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Global research trends and hotspots in human immunodeficiency virus-associated cervical cancer (1990-2025): a multi-database bibliometric analysis.Frontiers in immunology · 2026Pooled it
- Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026Review
- Association of Immunodeficiency and HIV Viremia With Cervical Precancer and Cancer Risk Among Women With HIV in South Africa.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2026Article
- A tailored phosphorothioate coordinator enables CRISPR/Cas in-situ amplification.Nucleic acids research · 2026Article
- Article
- Immune Dysregulation and Viral Persistence in HPV-HIV Coinfection: Oncogenic and Clinical Implications.HIV/AIDS (Auckland, N.Z.) · 2026Review
- Molecular epidemiology of high-risk human papillomavirus infection and its predictive factors among women living with HIV in Northeast Ethiopia: a facility-based cross-sectional study.BMC infectious diseases · 2025Article
- Berberine: A dual anti-HIV and anti- cervical cancer compound.Research square · 2024Article
- Clinical Predictors and Outcomes of Invasive Anal Cancer for People With HIV in an Inception Cohort.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2024Article
- Article
- Impact of HIV on HPV-related cancers in men who have sex with men: a review.Frontiers in cellular and infection microbiology · 2024Review
- The Role of p53 in HIV Infection.Current HIV/AIDS reports · 2023Review
- HIV-1-related factors interact with p53 to influence cellular processes.AIDS research and therapy · 2023Review
- Network modeling suggests HIV infection phenocopies PI3K-AKT pathway mutations to enhance HPV-associated cervical cancer.Molecular omics · 2023Article
- HIV-1 exploits Hes-1 expression during pre-existing HPV-16 infection for cancer progression.Virusdisease · 2023Article
- Human papillomavirus in the setting of immunodeficiency: Pathogenesis and the emergence of next-generation therapies to reduce the high associated cancer risk.Frontiers in immunology · 2023Review
- Long noncoding RNAs (lncRNAs) in HIV-mediated carcinogenesis: Role in cell homeostasis, cell survival processes and drug resistance.Non-coding RNA research · 2022Review
- Update on the Epidemiological Features and Clinical Implications of Human Papillomavirus Infection (HPV) and Human Immunodeficiency Virus (HIV) Coinfection.Microorganisms · 2022Review
- The Role of Inflammation in Anal Cancer.Diseases (Basel, Switzerland) · 2022Review
- Characterisation of anal intraepithelial neoplasia and anal cancer in HIV-positive men by immunohistochemical markers p16, Ki-67, HPV-E4 and DNA methylation markers.International journal of cancer · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The infection of uterine cervical epithelial cells by oncogenic, high-risk human papilloma viruses (HR-HPVs) may lead to the development of cervical carcinoma. Of note, the incidence of this tumor is significantly increased in women infected by both HR-HPV and human immunodeficiency virus (HIV)-1. In this regard, previous studies have linked the HIV-1 Tat protein, a trans-activator of viral gene expression, to the pathogenesis of HIV-associated malignancies. In particular, it has been shown that upon its release by acutely infected cells, Tat protein can enter human cells, thus modifying their phenotype. Based on these findings, the present study evaluated whether extracellular Tat protein could be taken up by human uterine cervical carcinoma cells, and whether this could affect the expression of HPV (E6 or E7) or cellular (p16 or p53) molecules, which are key to cervical carcinoma development or progression. The results indicated that extracellular, biologically active HIV-1 Tat protein is taken up by human uterine cervical carcinoma cells, and that this is followed by an increase in the expression of the E6 protein of HPV, and by a reduction in the protein levels of the cellular oncosuppressor p53. Since p53 loss is associated with cell dedifferentiation and immortalization, these findings suggest a possible link between extracellular Tat protein and the high incidence and clinical aggressiveness of uterine cervical carcinoma observed in HIV/HPV doubly infected women.
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