Evidence map›Paper›PMID 26267535›Full record

ArticleCancer cell2015

ERK2-Dependent Phosphorylation of CSN6 Is Critical in Colorectal Cancer Development.

Lekun Fang, Weisi Lu, Hyun Ho Choi, Sai-Ching J Yeung, Jung-Yu Tung, Chwan-Deng Hsiao, Enrique Fuentes-Mattei, David Menter, Chuangqi Chen, Lei Wang and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

58 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
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  6. CSN6-SPOP-HMGCS1 Axis Promotes Hepatocellular Carcinoma Progression via YAP1 Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
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  9. Computational exploration of the significance ofWorld journal of clinical oncology · 2023
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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 4 institutions in 3 countries.

Lekun FangDepartment of Colorectal Surgery, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou 510655, China; Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou 510655, China; Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Weisi LuState Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou 510060, China; Key Laboratory of Gene Engineering of the Ministry of Education, School of Life Sciences, Sun Yat-sen University, Guangzhou 510275, China; Program in Genes and Development, The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA.
Hyun Ho ChoiDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Sai-Ching J YeungDepartment of Endocrine Neoplasia and Hormonal Disorders, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Jung-Yu TungInstitute of Molecular Biology, Academia Sinica, Taipei 11529, Taiwan.
Chwan-Deng HsiaoInstitute of Molecular Biology, Academia Sinica, Taipei 11529, Taiwan.
Enrique Fuentes-MatteiDepartment of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
David MenterDepartment of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Chuangqi ChenDepartment of Surgery, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou 510080, China.
Lei WangDepartment of Colorectal Surgery, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou 510655, China; Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou 510655, China.
Jianping WangDepartment of Colorectal Surgery, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou 510655, China; Guangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou 510655, China. Electronic address: wangjpgz@163.com.
Mong-Hong LeeGuangdong Provincial Key Laboratory of Colorectal and Pelvic Floor Disease, The Sixth Affiliated Hospital of Sun Yat-sen University, Guangzhou 510655, China; Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA; Program in Cancer Biology, The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA; Program in Genes and Development, The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TX 77030, USA. Electronic address: mhlee@mdanderson.org.
The University of Texas MD Anderson Cancer Center · USInstitute of Molecular Biology, Academia Sinica · TWSixth Affiliated Hospital of Sun Yat-sen University · CNSun Yat-sen University · CN

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Regulation of cyclin-dependent kinase inhibitor p27 in cancerR01CA089266 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LEE, MONG-HONG · 2002 to 2013
$2.8M
NCI NIH HHS CA16672NCI NIH HHS L30 CA199587NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA089266NCI NIH HHS R01CA089266PHS HHS KG081048
6 · The paper itself

Abstract

Biomarkers for predicting prognosis are critical to treating colorectal cancer (CRC) patients. We found that CSN6, a subunit of COP9 signalosome, is overexpressed in CRC samples and that CSN6 overexpression is correlated with poor patient survival. Mechanistic studies revealed that CSN6 is deregulated by epidermal growth factor receptor (EGFR) signaling, in which ERK2 binds directly to CSN6 Leu163/Val165 and phosphorylates CSN6 at Ser148. Furthermore, CSN6 regulated β-Trcp and stabilized β-catenin expression by blocking the ubiquitin-proteasome pathway, thereby promoting CRC development. High CSN6 expression was positively correlated with ERK2 activation and β-catenin overexpression in CRC samples, and inhibiting CSN6 stability with cetuximab reduced colon cancer growth. Taken together, our study's findings indicate that the deregulation of β-catenin by ERK2-activated CSN6 is important for CRC development.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAntineoplastic Agentsbeta CateninBlotting, WesternCell Line, TumorCetuximabColorectal NeoplasmsCOP9 Signalosome ComplexFemaleGene Expression ProfilingHCT116 CellsHumansMaleMice, Inbred BALB CMice, NudeAdaptor Proteins, Signal TransducingAntineoplastic Agentsbeta CateninCetuximabCOP9 Signalosome ComplexCOPS6 protein, humanMAPK1 protein, humanMitogen-Activated Protein Kinase 1

Identifiers

PMID26267535
PMCPMC4560098
OpenAlexW1959684413

What OpenQuestion holds

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Registered trials

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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.