Evidence map›Paper›PMID 26544625›Full record

ArticleOncotarget2015

Oncogenic Ras suppresses ING4-TDG-Fas axis to promote apoptosis resistance.

Jie Sun, Qi Shen, Haiqi Lu, Zhinong Jiang, Wenxia Xu, Lifeng Feng, Ling Li, Xian Wang, Xiujun Cai, Hongchuan Jin

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

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Inhibitor of growth-4 is a potential target for cancer therapy.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Review
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 3 institutions in 2 countries.

Jie SunLaboratory of Cancer Biology, Provincial Key Lab of Biotherapy in Zhejiang, Sir Runrun Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Qi ShenDepartment of Medical Oncology, Sir Runrun Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Haiqi LuDepartment of Medical Oncology, Sir Runrun Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Zhinong JiangDepartment of Pathology, Sir Runrun Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Wenxia XuLaboratory of Cancer Biology, Provincial Key Lab of Biotherapy in Zhejiang, Sir Runrun Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Lifeng FengLaboratory of Cancer Biology, Provincial Key Lab of Biotherapy in Zhejiang, Sir Runrun Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Ling LiDivision of Hematopoietic Stem Cell and Leukemia Research, City of Hope National Medical Center, Duarte, CA, USA.
Xian WangDepartment of Medical Oncology, Sir Runrun Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Xiujun CaiDepartment of General Surgery, Sir Runrun Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Hongchuan JinLaboratory of Cancer Biology, Provincial Key Lab of Biotherapy in Zhejiang, Sir Runrun Shaw Hospital, Medical School of Zhejiang University, Hangzhou, China.
Zhejiang University · CNSir Run Run Shaw Hospital · CNCity Of Hope National Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ras is aberrantly activated in many cancers and active DNA demethylation plays a fundamental role to establish DNA methylation pattern which is of importance to cancer development. However, it was unknown whether and how Ras regulate DNA demethylation during carcinogenesis. Here we found that Ras downregulated thymine-DNA glycosylase (TDG), a DNA demethylation enzyme, by inhibiting the interaction of transcription activator ING4 with TDG promoter. TDG recruited histone lysine demethylase JMJD3 to the Fas promoter and activated its expression, thus restoring sensitivity to apoptosis. TDG suppressed in vivo tumorigenicity of xenograft pancreatic cancer. Thus, we speculate that reversing Ras-mediated ING4 inhibition to activate Fas expression is a potential therapeutic approach for Ras-driven cancers.

Indexed as

AnimalsApoptosisBlotting, WesternCell Cycle ProteinsCell Line, TumorDrug Resistance, Neoplasmfas ReceptorGene Expression Regulation, NeoplasticHomeodomain ProteinsHumansImmunohistochemistryJumonji Domain-Containing Histone DemethylasesMiceMice, NudeNIH 3T3 CellsPancreatic NeoplasmsCell Cycle ProteinsFAS protein, humanfas ReceptorHomeodomain ProteinsING4 protein, humanJumonji Domain-Containing Histone DemethylasesKDM6B protein, humanras ProteinsThymine DNA GlycosylaseTumor Suppressor ProteinsING4oncogenesisRasTDG

Identifiers

PMID26544625
PMCPMC4747204
OpenAlexW2273127277

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.