Evidence map›Paper›PMID 30944312›Full record

ArticleCell death & disease2019

Cancer testis antigen 55 deficiency attenuates colitis-associated colorectal cancer by inhibiting NF-κB signaling.

Huan Zhao, Wen-Ming Pan, Hui-Hui Zhang, Yang Song, Jie Chen, Ying Xiang, Bo Gu, Shang-Ze Li, Run-Lei Du, Xiao-Dong Zhang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.5field-weighted citation impact, top 36% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. Vitamin DCancers · 2024
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  2. Differential Toxicity Responses between Hepatopancreas and Gills inAnimals : an open access journal from MDPI · 2023
    Article
  3. Article
  4. 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 3 institutions in 1 country.

Huan ZhaoHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, China.
Wen-Ming PanDepartment of Emergency Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hui-Hui ZhangLaboratory of Molecular Biology, School of Medicine in Hunan Normal University, Changsha, Hunan, China.
Yang SongHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, China.
Jie ChenHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, China.
Ying XiangHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, China.
Bo GuHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, China.
Shang-Ze LiMedical Science Research Center, Zhongnan Hospital of Wuhan University, Wuhan, China. shangze.li@whu.edu.cn.
Run-Lei DuHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, China.
Xiao-Dong ZhangHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, China. zhangxd@whu.edu.cn.ORCID http://orcid.org/0000-0002-5137-7145
Wuhan University · CNHunan Normal University · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colitis-associated cancer (CAC), a prototype of inflammation-associated cancer, is one of the most common gastrointestinal tumors. As a potential cancer testis antigen (CT antigen), cancer testis antigen 55 (CT55) is expressed in different tumors and normal testes. However, its role in CAC remains unknown. Here, we identified CT55 as a new potent promoter of CAC. We discovered that Ct55 deficiency alleviated inflammatory responses, decreased cell proliferation and colitis-associated tumorigenesis in an azoxymethane/dextran sulfate sodium (AOM/DSS) mouse model. Mechanistically, CT55 acts as an accelerator of tumor necrosis factor (TNF)-α-induced nuclear factor-κB (NF-κB) signaling. Upon stimulation with TNF-α, CT55 interacts with the IκB kinase (IKK) complex, which increases the phosphorylation of IKKα/β and activates IKK-p65 signaling, while knockout of CT55 blocks IKK-p65 signaling. Notably, inhibition of IKK abolished the positive effect of CT55 on NF-κB activation. Collectively, our findings strongly indicate that CT55 deficiency suppresses the development of CAC and that the CT55-TNF-α-induced NF-κB axis may represent a promising target for CAC therapy.

Indexed as

AnimalsAntigens, NeoplasmAzoxymethaneCarcinogenesisCell ProliferationColitisColorectal NeoplasmsDextran SulfateDisease Models, AnimalHCT116 CellsHEK293 CellsHumansI-kappa B KinaseMiceMice, Inbred C57BLMice, KnockoutAntigens, NeoplasmAzoxymethaneDextran SulfateI-kappa B KinaseNF-kappa BTumor Necrosis Factor-alpha

Identifiers

PMID30944312
PMCPMC6447546
OpenAlexW2931756573

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.