Evidence map›Paper›PMID 33109187›Full record

ArticleCell communication and signaling : CCS2020

JARID1B promotes colorectal cancer proliferation and Wnt/β-catenin signaling via decreasing CDX2 level.

Da Huang, Fan Xiao, Haibin Hao, Fuzhou Hua, Zhenzhong Luo, Zhaoxia Huang, Qing Li, Sha Chen, Xiuzhi Cheng, Xinyue Zhang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

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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

13 authors at 2 institutions in 1 country.

Da HuangDepartment of Thyroid Surgery, Second Affiliated Hospital of Nanchang University, Nanchang, China.
Fan XiaoJiangxi Province Key Laboratory of Molecular Medicine, Nanchang, China.
Haibin HaoDepartment of General Surgery, Second Affiliated Hospital of Nanchang University, Nanchang, China.
Fuzhou HuaJiangxi Province Key Laboratory of Molecular Medicine, Nanchang, China.
Zhenzhong LuoJiangxi Province Key Laboratory of Molecular Medicine, Nanchang, China.
Zhaoxia HuangCenter for Education Evaluation, Nanchang Normal University, Nanchang, China.
Qing LiDepartment of Pathology, Second Affiliated Hospital of Nanchang University, Nanchang, China.
Sha ChenDepartment of Anesthesiology, Second Affiliated Hospital of Nanchang University, Nanchang, China.
Xiuzhi ChengJiangxi Province Key Laboratory of Molecular Medicine, Nanchang, China.
Xinyue ZhangJiangxi Province Key Laboratory of Molecular Medicine, Nanchang, China.
Weilan FangJiangxi Province Key Laboratory of Molecular Medicine, Nanchang, China.
Xiaoyun HuDepartment of General Surgery, Second Affiliated Hospital of Nanchang University, Nanchang, China. Xiaoyun206@126.com.
Fanrong LiuJiangxi Province Key Laboratory of Molecular Medicine, Nanchang, China. fanrongliu123@163.com.ORCID 0000-0002-9783-492X
Nanchang University · CNNanchang Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundJumonji AT-rich interactive domain 1B(JARID1B) has been shown to be upregulated in many human cancers and plays a critical role in the development of cancers cells. Nevertheless, its functional role in colorectal cancer (CRC) progression is not fully understood.

methodsHerein, JARID1B expression levels were detected in clinical CRC samples by western blotting and qRT-PCR. DLD-1 cells with JARID1B knockdown or overexpression by stably transfected plasmids were used in vitro and in vivo study. Colony formation, 5-ethynyl-20-deoxyuridine (EdU) and Real Time Cellular Analysis (RTCA) assays were used to detect cell proliferation and growth. Transcriptome and CHIP assays were used to examine the molecular biology changes and molecular interaction in these cells. Nude mice was utilized to study the correlation of JARID1B and tumor growth in vivo.

resultsHere, we first observed that JARID1B was significantly upregulated in CRC tissue compared to adjacent normal tissues. In CRC patients, JARID1B high expression was positively relation with poor overall survival. Multivariate analyses revealed that high JARID1B expression was an independent predictive marker for the poor prognosis of CRC. In addition, we found that JARID1B promoted CRC cells proliferation by Wnt/β-catenin signaling pathway. Further studies demonstrated CDX2 as a downstream target of JARID1B, and our data demonstrated that CDX2 is crucial for JARID1B -mediated Wnt/β-catenin signaling pathway. Mechanistically, we demonstrated that JARID1B regulated CDX2 expression through demethylation of H3K4me3.

conclusionsCDX2 inhibited by JARID1B-derived H3K4me3 methylation promoted cells proliferation of CRC via Wnt/β-catenin signaling pathway. Therefore, our studies provided a novel insight into the role of JARID1B in CRC cells proliferation and potential new molecular target for treating CRC. Video abstract.

Indexed as

Wnt Signaling PathwayAnimalsCarcinogenesisCDX2 Transcription FactorCell Line, TumorCell ProliferationColorectal NeoplasmsDisease ProgressionDown-RegulationGene Expression Regulation, NeoplasticHistonesHumansJumonji Domain-Containing Histone DemethylasesLysineMaleMethylationCDX2 protein, humanCDX2 Transcription FactorHistonesJumonji Domain-Containing Histone DemethylasesKDM5B protein, humanLysineNuclear ProteinsRepressor ProteinsCDX2Cell proliferationColorectal cancerH3K4me3JARID1BWnt/β-catenin

Identifiers

PMID33109187
PMCPMC7590656
OpenAlexW3097302386

What OpenQuestion holds

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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.