Evidence map›Paper›PMID 28042499›Full record

ArticleAmerican journal of cancer research2016

PCAF acts as a gastric cancer suppressor through a novel PCAF-p16-CDK4 axis.

Hong-Jun Fei, Li-Dong Zu, Jun Wu, Xiao-Shu Jiang, Jing-Long Wang, Y Eugene Chin, Guo-Hui Fu

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. PCAF Accelerates Vascular Senescence via the Hippo Signaling Pathway.Oxidative medicine and cellular longevity · 2022
    Article
  10. Complex functions of Gcn5 and Pcaf in development and disease.Biochimica et biophysica acta. Gene regulatory mechanisms · 2021
    Review
  11. Article
  12. Review
  13. Article
  14. Role of p27Oncotarget · 2018
    Review
  15. 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

7 authors at 2 institutions in 1 country.

Hong-Jun FeiPathology Center, Shanghai General Hospital/Faculty of Basic Medicine, School of Medicine, Shanghai Jiao Tong University Shanghai 200025, P. R. China.
Li-Dong ZuPathology Center, Shanghai General Hospital/Faculty of Basic Medicine, School of Medicine, Shanghai Jiao Tong University Shanghai 200025, P. R. China.
Jun WuPathology Center, Shanghai General Hospital/Faculty of Basic Medicine, School of Medicine, Shanghai Jiao Tong University Shanghai 200025, P. R. China.
Xiao-Shu JiangDepartment of Pathophysiology, Harbin Medical University Harbin 150081, P. R. China.
Jing-Long WangPathology Center, Shanghai General Hospital/Faculty of Basic Medicine, School of Medicine, Shanghai Jiao Tong University Shanghai 200025, P. R. China.
Y Eugene ChinInstitute of Health Sciences, Shanghai Institutes of Biological Sciences, Chinese Academy of Sciences Shanghai, P. R. China.
Guo-Hui FuPathology Center, Shanghai General Hospital/Faculty of Basic Medicine, School of Medicine, Shanghai Jiao Tong University Shanghai 200025, P. R. China.
Harbin Medical University · CNShanghai Institutes for Biological Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) is a leading cause of cancer-related death worldwide and the pathogenesis of GC remains largely unknown. Here, we demonstrate a novel mechanism by which P300/CBP associating factor (PCAF) acts as a tumor suppressor in GC cells. We showed that both PCAF mRNA and protein were downregulated in GC cells, and that this downregulation correlated with poor survival. Meanwhile, the interaction between human anion exchanger 1 (AE1) and p16 is a key event in GC development. We found that PCAF inhibited GC growth by interacting with AE1 and p16 to promote ubiquitin-mediated degradation of AE1 and p16 upregulation and translocation into the nucleus. Binding of nuclear p16 to CDK4 prevented the CDK4-Cyclin D1 interaction to inhibit GC proliferation. Furthermore, reduced PCAF levels in GC cells were associated with intracellular alkalinization and decreased immunity. Together these results suggest that PCAF acts as a GC suppressor through a novel PCAF-p16-CDK4 axis. The downregulation of PCAF expression in GC cells that follows intracellular alkalinization and decreased immune response, indicates that GC therapies should focus on restoring PCAF levels.

Indexed as

AE1GCPCAF-P16-CDK4 axisproliferation

Identifiers

PMID28042499
PMCPMC5199753
OpenAlexW2572430043

What OpenQuestion holds

Textmetadata
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.