Evidence map›Paper›PMID 30185232›Full record

ArticleJournal of hematology & oncology2018

The lncRNA NEAT1 activates Wnt/β-catenin signaling and promotes colorectal cancer progression via interacting with DDX5.

Meng Zhang, Weiwei Weng, Qiongyan Zhang, Yong Wu, Shujuan Ni, Cong Tan, Midie Xu, Hui Sun, Chenchen Liu, Ping Wei and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of hematology & oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 228 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
228citing papers in PubMed, 1 pooled it
10.1field-weighted citation impact, top 1% 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

228 citing papers in PubMed, 1 synthesis or guideline pooled it, 364 citations in OpenAlex.

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168 more citing papers are in PubMed but not listed here.

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

11 authors at 3 institutions in 1 country.

Meng ZhangDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Weiwei WengDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Qiongyan ZhangDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Yong WuInstitute of Pathology, Fudan University, Shanghai, China.
Shujuan NiDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Cong TanDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Midie XuDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Hui SunDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Chenchen LiuDepartment of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Ping WeiDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. weiping@fudan.edu.cn.
Xiang DuDepartment of Pathology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. dx2008cn@163.com.
Shanghai Medical College of Fudan University · CNFudan University · CNFudan University Shanghai Cancer Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) has been reported to be overexpressed in colorectal cancer (CRC). However, its underlying mechanisms in the progression of CRC have not been well studied.

methodsTo investigate the clinical significance of NEAT1, we analyzed its expression levels in a publicly available dataset and in 71 CRC samples from Fudan University Shanghai Cancer Center. Functional assays, including the CCK8, EdU, colony formation, wound healing, and Transwell assays, were used to determine the oncogenic role of NEAT1 in human CRC progression. Furthermore, RNA pull-down, mass spectrometry, RNA immunoprecipitation, and Dual-Luciferase Reporter Assays were used to determine the mechanism of NEAT1 in CRC progression. Animal experiments were used to determine the role of NEAT1 in CRC tumorigenicity and metastasis in vivo.

resultsNEAT1 expression was significantly upregulated in CRC tissues compared with its expression in normal tissues. Altered NEAT1 expression led to marked changes in proliferation, migration, and invasion of CRC cells both in vitro and in vivo. Mechanistically, we found that NEAT1 directly bound to the DDX5 protein, regulated its stability, and sequentially activated Wnt signaling. Our study showed that NEAT1 indirectly activated the Wnt/β-catenin signaling pathway via DDX5 and fulfilled its oncogenic functions in a DDX5-mediated manner. Clinically, concomitant NEAT1 and DDX5 protein levels negatively correlated with the overall survival and disease-free survival of CRC patients.

conclusionsOur findings indicated that NEAT1 activated Wnt signaling to promote colorectal cancer progression and metastasis. The NEAT1/DDX5/Wnt/β-catenin axis could be a potential therapeutic target of pharmacological strategies.

Indexed as

Wnt Signaling PathwayAnimalsbeta CateninColorectal NeoplasmsDEAD-box RNA HelicasesDisease ProgressionHCT116 CellsHeterograftsHumansMaleMiceMice, Inbred BALB CMice, NudeRNA, Long NoncodingTransfectionbeta CateninCTNNB1 protein, humanDdx5 protein, humanDEAD-box RNA HelicasesNEAT1 long non-coding RNA, humanRNA, Long NoncodingColorectal cancerDDX5lncRNANEAT1β-Catenin

Identifiers

PMID30185232
PMCPMC6125951
OpenAlexW2890602782

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.