Evidence map›Paper›PMID 28523736›Full record

ArticleCell proliferation2017

Hyper activation of β-catenin signalling induced by IKKε inhibition thwarts colorectal cancer cell proliferation.

Jie Chen, Jun Zhao, Xuan Chen, Chengming Ding, Katie Lee, Zeming Jia, Yaoting Zhang, Yuzheng Zhou, Chaoying Wei, Jiantai He and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell proliferation, 2017. 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
0.4field-weighted citation impact, top 43% 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, 12 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

12 authors at 2 institutions in 2 countries.

Jie ChenDivision of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Jun ZhaoDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, 90033, USA.
Xuan ChenDivision of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Chengming DingDivision of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.ORCID http://orcid.org/0000-0002-6979-1221
Katie LeeDepartment of Molecular Microbiology and Immunology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA, 90033, USA.
Zeming JiaDivision of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Yaoting ZhangDivision of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Yuzheng ZhouState Key Laboratory of Medical Genetics and School of Life Sciences, Central South University, Changsha, Hunan, 410008, China.
Chaoying WeiState Key Laboratory of Medical Genetics and School of Life Sciences, Central South University, Changsha, Hunan, 410008, China.
Jiantai HeDivision of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.
Zanxian XiaState Key Laboratory of Medical Genetics and School of Life Sciences, Central South University, Changsha, Hunan, 410008, China.
Jian PengDivision of General Surgery, Xiangya Hospital, Central South University, Changsha, Hunan, 410008, China.ORCID http://orcid.org/0000-0003-0991-3896
Central South University · CNUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveAberrant activation of Wnt/β-catenin signalling contributes significantly to the development of human colorectal cancers and β-catenin is the key signalling molecule transducing canonical Wnt/β-catenin signalling. Therefore, β-catenin is a promising therapeutic target for cancer treatment. This study demonstrates that the oncogenic IKKε kinase phosphorylates β-catenin to restrain its hyper activation, therefore promoting colorectal cancer (CRC) cell proliferation. MATERIALS AND

methodsIKKε and β-catenin expression levels in human colorectal cancer tissues and cell lines were analysed by immunohistochemical staining and Western blotting. The regulation of IKKε on Wnt/β-catenin signalling pathway was studied by reporter assay and real-time PCR analysis in the context of IKKε stably knocking down. Co-immunoprecipitation was conducted to monitor the interaction between IKKε and β-catenin. Kinase assay was performed to measure β-catenin post-translational modifications induced by IKKε.

resultsOncogenic IKKε kinase is required for the proliferation of colorectal cancer cells. Mechanistically, inhibition of IKKε results in β-catenin hyper activation and thwarts CRC cell proliferation. Furthermore, IKKε phosphorylates β-catenin and inhibits the activation of β-catenin signalling.

conclusionOur study suggests that IKKε is a potential target to combat CRC induced by aberrant Wnt/β-catenin signalling.

Indexed as

Amino Acid Sequencebeta CateninCell Line, TumorCell ProliferationColonColorectal NeoplasmsHEK293 CellsHumansI-kappa B KinaseImmunoprecipitationPhosphorylationReal-Time Polymerase Chain ReactionRNA InterferenceRNA, Small InterferingTranscription, GeneticWnt Signaling Pathwaybeta CateninI-kappa B KinaseRNA, Small Interfering

Identifiers

PMID28523736
PMCPMC6529108
OpenAlexW2615122877

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.