Evidence map›Paper›PMID 26760960›Full record

ArticleOncotarget2016

Adenomatous polyposis coli genotype-dependent toll-like receptor 4 activity in colon cancer.

Feng Wen, Yongmei Liu, Wei Wang, Meng Li, Fuchun Guo, Yaxiong Sang, Qing Qin, Yongsheng Wang, Qiu Li

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

Article in Oncotarget, 2016. 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
0.3field-weighted citation impact, top 38% 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, 4 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. 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

9 authors at 3 institutions in 1 country.

Feng WenThe Department of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, University of Sichuan, Sichuan, China.
Yongmei LiuThe Department of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, University of Sichuan, Sichuan, China.
Wei WangState Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center for Biotherapy, West China Hospital, University of Sichuan, Sichuan, China.
Meng LiState Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center for Biotherapy, West China Hospital, University of Sichuan, Sichuan, China.
Fuchun GuoThe Department of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, University of Sichuan, Sichuan, China.
Yaxiong SangState Key Laboratory of Biotherapy and Cancer Center/Collaborative Innovation Center for Biotherapy, West China Hospital, University of Sichuan, Sichuan, China.
Qing QinThe Department of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, University of Sichuan, Sichuan, China.
Yongsheng WangThe Department of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, University of Sichuan, Sichuan, China.
Qiu LiThe Department of Medical Oncology, Cancer Center, State Key Laboratory of Biotherapy/Collaborative Innovation Center for Biotherapy, West China Hospital, University of Sichuan, Sichuan, China.
State Key Laboratory of BiotherapySichuan University · CNSichuan University of Science and Engineering · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptors (TLRs)/NF-κB activation stimulated by lipopolysaccharide (LPS) was associated with diverse biological response in colon cancer, but the underlying mechanism was largely unknown. In the current study, we reported cell proliferation was elevated in adenomatous polyposis coli (APC) mutated- and APC knockdown cell lines, while the proliferation was inhibited in APC wild-type cell lines. Besides, in vivo experiments showed that LPS promoted APC knockdown tumor growth while inhibited proliferation of APC wild type. Further study confirmed that activation of TLRs/NF-κB signaling pathway by LPS cross regulated with APC/GSK-3β/β-catenin pathway, which were depend on APC status of cell lines. Taken together, APC genotypes play a key role in LPS induced different colon cancer biological response by cross-regulating β-catenin and NF-κB, which may provide a novel strategy for carcinogenesis prevention.

Indexed as

Adenomatous Polyposis Coli ProteinAnimalsApoptosisbeta CateninBlotting, WesternCell ProliferationColonic NeoplasmsFemaleFlow CytometryFluorescent Antibody TechniqueGenotypeGlycogen Synthase Kinase 3 betaHumansImmunoenzyme TechniquesLipopolysaccharidesMiceAdenomatous Polyposis Coli Proteinbeta CateninGlycogen Synthase Kinase 3 betaLipopolysaccharidesNF-kappa BRNA, Small InterferingTLR4 protein, humanToll-Like Receptor 4adenomatous polyposis colicolon cancerNF-κBβ-catenin

Identifiers

PMID26760960
PMCPMC4884952
OpenAlexW2287005606

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.