Evidence map›Paper›PMID 30079588›Full record

ArticleJournal of cellular and molecular medicine2018

The lysine acetyltransferase GCN5 contributes to human papillomavirus oncoprotein E7-induced cell proliferation via up-regulating E2F1.

Lijun Qiao, Qishu Zhang, Weifang Zhang, Jason J Chen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. The role of acetylation and deacetylation in cancer metabolism.Clinical and translational medicine · 2025
    Review
  5. Review
  6. Genes · 2022
    Article
  7. Review
  8. Oncogenic HPV promotes the expression of the long noncoding RNA lnc-FANCI-2 through E7 and YY1.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
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

4 authors at 1 institution in 1 country.

Lijun QiaoThe Cancer Research Center and Department of Microbiology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, China.
Qishu ZhangThe Cancer Research Center and Department of Microbiology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, China.
Weifang ZhangDepartment of Microbiology and Key Laboratory of Infection and Immunity of Shandong Province, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, China.ORCID 0000-0003-4675-656X
Jason J ChenThe Cancer Research Center and Department of Microbiology, School of Basic Medical Sciences, Shandong University, Jinan, Shandong, China.ORCID 0000-0001-9703-6621
Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

General control nondepressible 5 (GCN5), the first identified transcription-related lysine acetyltransferase (KAT), is an important catalytic component of a transcriptional regulatory SAGA (Spt-Ada-GCN5-Acetyltransferase) and ATAC (ADA2A-containing) complex. While GCN5 has been implicated in cancer development, its role in cervical cancer is not known. The human papillomavirus (HPV) oncoprotein E7 abrogates the G1 cell cycle checkpoint and induces genomic instability, which plays a central role in cervical carcinogenesis. In this study, we observed that GCN5 was up-regulated in HPV E7-expressing cells, knockdown of GCN5 inhibited cell cycle progression and DNA synthesis in HPV E7-expressing cells. Notably, GCN5 knockdown reduced the steady-state levels of transcription factor E2F1. Depletion of E2F1 caused G1 arrest while overexpression of E2F1 rescued the inhibitory effects of GCN5 knockdown on G1/S progression in HPV E7-expressing cells. Results from chromatin immunoprecipitation (ChIP) assays demonstrated that GCN5 bound to the E2F1 promoter and increased the extent of histone acetylation within these regions. GCN5 also acetylated c-Myc and increased its ability to bind to the E2F1 promoter. Knockdown of c-Myc reduced the steady-state levels of E2F1 and caused G1 arrest. These results revealed a novel mechanism of E7 function whereby elevated GCN5 acetylates histones and c-Myc to regulate E2F1 expression and cell cycle progression.

Indexed as

CarcinogenesisCell Line, TumorCell ProliferationChromatin ImmunoprecipitationDNA-Binding ProteinsE2F1 Transcription FactorFemaleG1 Phase Cell Cycle CheckpointsGene Expression Regulation, NeoplasticGene Knockdown TechniquesGenomic InstabilityHumansp300-CBP-Associated Factorp300-CBP Transcription FactorsPapillomaviridaePapillomavirus E7 ProteinsDNA-Binding ProteinsE2F1 protein, humanE2F1 Transcription FactorMYC protein, humanp300-CBP-Associated Factorp300-CBP Transcription FactorsPapillomavirus E7 ProteinsProto-Oncogene Proteins c-mycCdk1E2F1G1 checkpointGCN5human papillomavirus

Identifiers

PMID30079588
PMCPMC6201343
OpenAlexW2886787121

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.