ArticleProceedings of the National Academy of Sciences of the United States of America2017
Induction of dormancy in hypoxic human papillomavirus-positive cancer cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed.
- COVID-19 triggers pulmonary tumor outgrowth through hypoxia- and inflammation-induced VEGF-dependent angiogenesis.Signal transduction and targeted therapy · 2026Article
- Th17 cells favor migration and invasiveness of cervical cancer cells under hypoxia in an IGF2BP2-dependent manner.International journal of cancer · 2026Article
- Intratumoral spatiotemporal heterogeneity of HPV DNA status in HPV-associated oropharyngeal squamous cell carcinoma with clinical record.Journal of translational medicine · 2026Article
- Ferroptosis as a novel targeted therapy in gynecological malignant tumors.Discover oncology · 2026Review
- The enigmatic role of tumor dormancy cells in gynecologic cancers.Frontiers in immunology · 2026Review
- REDD1 Affects Proliferation, Apoptosis, Migration, and Colony Formation via p-ERK and p-JNK Signaling in Lung Adenocarcinoma Cells Under Hypoxia.Biomedicines · 2025Article
- Hypoxia drives cervical cancer progression via OCT4/ORAI3-dependent glycolysis and CaCellular and molecular life sciences : CMLS · 2025Article
- Attributes of HPV associated cancers.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Review
- Hypoxic HPV-Positive Cancer Cells Are Particularly Sensitive to the Pro-Senescent Effects of B-MYB Repression Due to the Lack of Compensatory A-MYB Induction.Journal of medical virology · 2025Article
- Pleiotropic Effects of Metformin on the Chemotherapy Response of HPV-Positive Cancer Cells.Journal of medical virology · 2025Article
- Towards understanding cancer dormancy over strategic hitching up mechanisms to technologies.Molecular cancer · 2025Review
- E6AP is essential for the proliferation of HPV-positive cancer cells by preventing senescence.PLoS pathogens · 2025Article
- The ability of clostridium novyi-NT spores to induce apoptosis via the mitochondrial pathway in mice with HPV-positive cervical cancer tumors derived from the TC-1 cell line.BMC complementary medicine and therapies · 2024Article
- Review
- The potential role of HPV oncoproteins in the PD-L1/PD-1 pathway in cervical cancer: new perspectives on cervical cancer immunotherapy.Frontiers in oncology · 2024Review
- Article
- Anti-tumor Effects of Cisplatin Synergist in Combined Treatment withAdvanced pharmaceutical bulletin · 2023Article
- Article
- Tracking HPV Infection, Associated Cancer Development, and Recent Treatment Efforts-A Comprehensive Review.Vaccines · 2023Review
Corrections and comments
- Commented on by
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oncogenic human papillomaviruses (HPVs) are closely linked to major human malignancies, including cervical and head and neck cancers. It is widely assumed that HPV-positive cancer cells are under selection pressure to continuously express the viral E6/E7 oncogenes, that their intracellular p53 levels are reconstituted on E6/E7 repression, and that E6/E7 inhibition phenotypically results in cellular senescence. Here we show that hypoxic conditions, as are often found in subregions of cervical and head and neck cancers, enable HPV-positive cancer cells to escape from these regulatory principles: E6/E7 is efficiently repressed, yet, p53 levels do not increase. Moreover, E6/E7 repression under hypoxia does not result in cellular senescence, owing to hypoxia-associated impaired mechanistic target of rapamycin (mTOR) signaling via the inhibitory REDD1/TSC2 axis. Instead, a reversible growth arrest is induced that can be overcome by reoxygenation. Impairment of mTOR signaling also interfered with the senescence response of hypoxic HPV-positive cancer cells toward prosenescent chemotherapy in vitro. Collectively, these findings indicate that hypoxic HPV-positive cancer cells can induce a reversible state of dormancy, with decreased viral antigen synthesis and increased therapeutic resistance, and may serve as reservoirs for tumor recurrence on reoxygenation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.