Evidence map›Paper›PMID 24874735›Full record

Trial reportCell death & disease2014

Elf3 drives β-catenin transactivation and associates with poor prognosis in colorectal cancer.

J-L Wang, Z-F Chen, H-M Chen, M-Y Wang, X Kong, Y-C Wang, T-T Sun, J Hong, W Zou, J Xu and 1 more

Erratum issuedOpen access · goldAbstract readClinical Trial
In one paragraph

Trial report in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
2.8field-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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

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  13. mCancer gene therapy · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

J-L WangState Key Laboratory of Oncogene and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Department of Gastroenterology and Hepatology, Ren-Ji Hospital, School of Medicine, Shanghai Jiao-Tong University, Shanghai Cancer Institute, Shanghai Institute of Digestive Disease, 145 Middle Shandong Road, Shanghai, China.
Z-F ChenState Key Laboratory of Oncogene and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Department of Gastroenterology and Hepatology, Ren-Ji Hospital, School of Medicine, Shanghai Jiao-Tong University, Shanghai Cancer Institute, Shanghai Institute of Digestive Disease, 145 Middle Shandong Road, Shanghai, China.
H-M ChenState Key Laboratory of Oncogene and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Department of Gastroenterology and Hepatology, Ren-Ji Hospital, School of Medicine, Shanghai Jiao-Tong University, Shanghai Cancer Institute, Shanghai Institute of Digestive Disease, 145 Middle Shandong Road, Shanghai, China.
M-Y WangState Key Laboratory of Oncogene and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Department of Gastroenterology and Hepatology, Ren-Ji Hospital, School of Medicine, Shanghai Jiao-Tong University, Shanghai Cancer Institute, Shanghai Institute of Digestive Disease, 145 Middle Shandong Road, Shanghai, China.
X KongState Key Laboratory of Oncogene and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Department of Gastroenterology and Hepatology, Ren-Ji Hospital, School of Medicine, Shanghai Jiao-Tong University, Shanghai Cancer Institute, Shanghai Institute of Digestive Disease, 145 Middle Shandong Road, Shanghai, China.
Y-C WangState Key Laboratory of Oncogene and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Department of Gastroenterology and Hepatology, Ren-Ji Hospital, School of Medicine, Shanghai Jiao-Tong University, Shanghai Cancer Institute, Shanghai Institute of Digestive Disease, 145 Middle Shandong Road, Shanghai, China.
T-T SunState Key Laboratory of Oncogene and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Department of Gastroenterology and Hepatology, Ren-Ji Hospital, School of Medicine, Shanghai Jiao-Tong University, Shanghai Cancer Institute, Shanghai Institute of Digestive Disease, 145 Middle Shandong Road, Shanghai, China.
J HongState Key Laboratory of Oncogene and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Department of Gastroenterology and Hepatology, Ren-Ji Hospital, School of Medicine, Shanghai Jiao-Tong University, Shanghai Cancer Institute, Shanghai Institute of Digestive Disease, 145 Middle Shandong Road, Shanghai, China.
W ZouDepartment of Surgery, University of Michigan, Ann Arbor, MI, USA.
J XuState Key Laboratory of Oncogene and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Department of Gastroenterology and Hepatology, Ren-Ji Hospital, School of Medicine, Shanghai Jiao-Tong University, Shanghai Cancer Institute, Shanghai Institute of Digestive Disease, 145 Middle Shandong Road, Shanghai, China.
J-Y FangState Key Laboratory of Oncogene and Related Genes, Key Laboratory of Gastroenterology & Hepatology, Ministry of Health, Department of Gastroenterology and Hepatology, Ren-Ji Hospital, School of Medicine, Shanghai Jiao-Tong University, Shanghai Cancer Institute, Shanghai Institute of Digestive Disease, 145 Middle Shandong Road, Shanghai, China.
Shanghai Jiao Tong University · CNState Key Laboratory of Oncogene and Related Genes · CNUniversity of Michigan–Ann Arbor · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aberrant regulation of the Wnt/β-catenin pathway plays important roles in colorectal carcinogenesis, with over 90% of cases of sporadic colon cancer featuring β-catenin accumulation. While ubiquitination-mediated degradation is widely accepted as a major route for β-catenin protein turnover, little is known about the regulation of β-catenin in transcriptional level. Here we show that Elf3, a member of the E-twenty-six family of transcription factors, drives β-catenin transactivation and associates with poor survival of colorectal cancer (CRC) patients. We first found recurrent amplification and upregulation of Elf3 in CRC tissues, and further Gene Set Enrichment Analysis identified significant association between Elf3 expression and activity of WNT/β-catenin pathway. Chromatin immunoprecipitation and electrophoretic mobility shift assay consistently revealed that Elf3 binds to and transactivates β-catenin promoter. Ectopic expression of Elf3 induces accumulation of β-catenin in both nucleus and cytoplasm, causing subsequent upregulation of several effector genes including c-Myc, VEGF, CCND1, MMP-7 and c-Jun. Suppressing Elf3 in CRC cells attenuates β-catenin signaling and decreases cell proliferation, migration and survival. Targeting Elf3 in xenograft tumors suppressed tumor progression in vivo. Taken together, our data identify Elf3 as a pivotal driver for β-catenin signaling in CRC, and highlight potential prognostic and therapeutic significance of Elf3 in CRC.

Indexed as

Gene Expression Regulation, NeoplasticTranscriptional Activationbeta CateninColorectal NeoplasmsDNA-Binding ProteinsFemaleHumansMaleNeoplasm ProteinsPrognosisProto-Oncogene Proteins c-etsTranscription Factorsbeta CateninDNA-Binding ProteinsELF3 protein, humanNeoplasm ProteinsProto-Oncogene Proteins c-etsTranscription Factors

Identifiers

PMID24874735
PMCPMC4047871
OpenAlexW1997598840

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.