Evidence map›Paper›PMID 21822357›Full record

ArticleMediators of inflammation2011

HPV16E6-dependent c-fos expression contributes to AP-1 complex formation in SiHa cells.

Feixin Liang, Shinichiro Kina, Hiroyuki Takemoto, Akira Matayoshi, Thongsavanh Phonaphonh, Nao Sunagawa, Keiichi Arakaki, Akira Arasaki, Hai Kuang, Hajime Sunakawa

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.1field-weighted citation impact, top 46% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Review
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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

10 authors at 2 institutions in 2 countries.

Feixin LiangDepartment of Clinical Neuroscience Oral and Maxillofacial Functional Rehabilitation, University of Ryukyus, 207 Uehara, Nishihara, Okinawa 903-0215, Japan.
Shinichiro Kina
Hiroyuki Takemoto
Akira Matayoshi
Thongsavanh Phonaphonh
Nao Sunagawa
Keiichi Arakaki
Akira Arasaki
Hai Kuang
Hajime Sunakawa
University of the Ryukyus · JPGuangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To date, the major role of HPV16E6 in cancer has been considered to be its ability to inhibit the p53 tumor-suppressor protein, thereby thwarting p53-mediated cytotoxic responses to cellular stress signals. Here, we show that HPV16E6-dependent c-fos oncogenic protein expression contributes to AP-1 complex formation under oxidative stress in SiHa cells (HPV16-positive squamous cell carcinoma of the cervix). In addition, we examined the role of HPV16E6 in TGF-α-induced c-fos expression and found that the c-fos protein expression induced by TGF-α is HPV16E6 dependent. Thus, our results provide the first evidence that HPV16E6 contributes to AP-1 complex formation after both ligand-dependent and independent EGFR activation, suggesting a new therapeutic approach to the treatment of HPV-associated tumors.

Indexed as

Cell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansOncogene Proteins, ViralProto-Oncogene Proteins c-fosRepressor ProteinsRNA, Small InterferingTranscription Factor AP-1Transforming Growth Factor alphaUterine Cervical NeoplasmsE6 protein, Human papillomavirus type 16Oncogene Proteins, ViralProto-Oncogene Proteins c-fosRepressor ProteinsRNA, Small InterferingTranscription Factor AP-1Transforming Growth Factor alpha

Identifiers

PMID21822357
PMCPMC3147133
OpenAlexW2120827974

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.