Evidence map›Paper›PMID 31058807›Full record

ReviewInternational journal of molecular sciences2019

PI3K/AKT/mTOR Signaling Regulates the Virus/Host Cell Crosstalk in HPV-Positive Cervical Cancer Cells.

Felicitas Bossler, Karin Hoppe-Seyler, Felix Hoppe-Seyler

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.

  1. Pooled it
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  17. Advancing influenza virus treatment:Materials today. Bio · 2025
    Article
  18. Molecular medicine reports · 2025
    Article
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26 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Felicitas BosslerMolecular Therapy of Virus-Associated Cancers (F065), German Cancer Research Center (DKFZ), D-69120 Heidelberg, Germany. f.bossler@dkfz.de.
Karin Hoppe-SeylerMolecular Therapy of Virus-Associated Cancers (F065), German Cancer Research Center (DKFZ), D-69120 Heidelberg, Germany. k.hoppe-seyler@dkfz.de.
Felix Hoppe-SeylerMolecular Therapy of Virus-Associated Cancers (F065), German Cancer Research Center (DKFZ), D-69120 Heidelberg, Germany. hoppe-seyler@dkfz.de.
Heidelberg University · DEGerman Cancer Research Center · DE

Funding

Deutsche Krebshilfe 112132Wilhelm Sander-Stiftung 2015.137.1Wilhelm Sander-Stiftung 2015.137.2
6 · The paper itself

Abstract

Human papillomavirus (HPV)-induced cancers will remain a significant clinical challenge for decades. Thus, the development of novel treatment strategies is urgently required, which should benefit from improving our understanding of the mechanisms of HPV-induced cell transformation. This should also include analyses of hypoxic tumor cells, which represent a major problem for cancer therapy. Recent evidence indicates that the PI3K/AKT/mTOR network plays a key role for the virus/host cell crosstalk in both normoxic and hypoxic HPV-positive cancer cells. In normoxic cells, the efficacy of the senescence induction upon experimental E6/E7 repression depends on active mTORC1 signaling. Under hypoxia, however, HPV-positive cancer cells can evade senescence due to hypoxic impairment of mTORC1 signaling, albeit the cells strongly downregulate E6/E7. Hypoxic repression of E6/E7 is mediated by the AKT kinase, which is activated under hypoxia by its canonical upstream regulators mTORC2 and PI3K. This review highlights our current knowledge about the oxygen-dependent crosstalk of the PI3K/AKT/mTOR signaling circuit with the HPV oncogenes and the phenotypic state of the host cell. Moreover, since the PI3K/AKT/mTOR pathway is considered to be a promising target for anticancer therapy, we discuss clinical implications for the treatment of HPV-positive cervical and head and neck squamous cell carcinomas.

Indexed as

Host-Pathogen InteractionsSignal TransductionAlphapapillomavirusAnimalsDisease SusceptibilityFemaleHumansOncogene Proteins, ViralPapillomavirus InfectionsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesUterine Cervical NeoplasmsOncogene Proteins, ViralPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesAKTcervical cancerhead and neck cancerhuman papillomavirushypoxiaimmunotherapymTORPI3Ksenescencetumor virus

Identifiers

PMID31058807
PMCPMC6539191
OpenAlexW2943322259

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.