Evidence map›Paper›PMID 34544413›Full record

ArticleCancer cell international2021

LINC01605, regulated by the EP300-SMYD2 complex, potentiates the binding between METTL3 and SPTBN2 in colorectal cancer.

Meng Yue, Tao Liu, Guoqiang Yan, Xiaofan Luo, Lei Wang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

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  17. The emerging role of mFrontiers in cell and developmental biology · 2023
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  20. The Interaction Between NFrontiers in oncology · 2021
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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

5 authors at 1 institution in 1 country.

Meng YueDepartment of Colorecal and Anal Surgery, The First Hospital of Jilin University, No. 71, Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, People's Republic of China.
Tao LiuDepartment of Colorecal and Anal Surgery, The First Hospital of Jilin University, No. 71, Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, People's Republic of China.
Guoqiang YanDepartment of Colorecal and Anal Surgery, The First Hospital of Jilin University, No. 71, Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, People's Republic of China.
Xiaofan LuoDepartment of Colorecal and Anal Surgery, The First Hospital of Jilin University, No. 71, Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, People's Republic of China.
Lei WangDepartment of Colorecal and Anal Surgery, The First Hospital of Jilin University, No. 71, Xinmin Street, Chaoyang District, Changchun, 130021, Jilin, People's Republic of China. leiwang1967@163.com.ORCID http://orcid.org/0000-0002-6302-3715
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundColorectal cancer (CC) is one of the major contributors to tumor-related death worldwide, and its main cause of death is distant metastasis. Dysregulation of long non-coding RNA (lncRNA) LINC01605 has been implicated in CC. However, its role in metastasis of CC remains elusive. The goal of the study is to uncover the biological function and molecular mechanism of LINC01605 in CC.

methodsThe differentially expressed lncRNAs were first screened from GSE97300, GSE84983, GSE110715, GSE70880, and GSE75970 microarrays. The correlation between the expression of LINC01605 and the clinical phenotypes of enrolled CC patients (n = 134) was subsequently analyzed. The upstream and downstream regulatory mechanisms of LINC01605 in CC were identified through bioinformatics and RNA-seq analyses. Finally, the effects of related factors on CC cell growth and metastasis were confirmed through functional validation experiments.

resultsLINC01605, significantly highly expressed in CC, was a prognostic factor for patients with CC. Functional experiments revealed that LINC01605 knockdown inhibited the proliferatory and metastatic potential of CC cells in vitro and in vivo. Moreover, LINC01605 was regulated by SMYD2-EP300-mediated modifications of histone H3K4me3 as well as H3K27ac. LINC01605 was found to bind to METTL3 and promote the m6A modification of SPTBN2 mRNA, thereby facilitating the translation of SPTBN2.

conclusionsOverexpression of LINC01605, regulated by SMYD2-EP300-mediated H3K27ac and H3K4me3 modifications, bound to METTL3 protein to promote m6A modification of SPTBN2 mRNA, leading to the development of CC.

Indexed as

Colorectal cancerH3K27acH3K4me3LINC01605m6AMETTL3SPTBN2

Identifiers

PMID34544413
PMCPMC8451128
OpenAlexW3200255526

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LicenceCC BY
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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.