Evidence map›Paper›PMID 33061642›Full record

ArticleCancer management and research2020

CircCSNK1G1 Contributes to the Development of Colorectal Cancer by Increasing the Expression of MYO6 via Competitively Targeting miR-455-3p.

Xianming Huang, Xiaohua Shen, Lixiang Peng, Wenli Mai, Yiye Wan, Huiqing Zhang

Abstract read
In one paragraph

Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

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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

11 citing papers in PubMed.

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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

6 authors.

Xianming HuangDepartment of Pathology, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029, People's Republic of China.
Xiaohua ShenDepartment of Gastrointestinal Medical Oncology, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029, People's Republic of China.
Lixiang PengDepartment of Gastrointestinal Medical Oncology, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029, People's Republic of China.
Wenli MaiDepartment of Gastrointestinal Medical Oncology, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029, People's Republic of China.
Yiye WanDepartment of Gastrointestinal Medical Oncology, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029, People's Republic of China.
Huiqing ZhangDepartment of Gastrointestinal Medical Oncology, Jiangxi Cancer Hospital, Nanchang, Jiangxi 330029, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNumerous circular RNAs (circRNAs) are functionally investigated in various human cancers, including colorectal cancer (CRC). In this study, we explored the function of circCSNK1G1 and mechanism of action in CRC, aiming to provide evidence for circCSNK1G1 involving in CRC pathogenesis.

methodsThe expression of circCSNK1G1, miR-455-3p and Myosin VI (MYO6) were examined using quantitative real-time polymerase chain reaction (qRT-PCR). The functions of circCSNK1G1 on cell proliferation, apoptosis, cycle and migration/invasion were investigated using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, colony formation assay, flow cytometry assay and transwell assay, respectively. The targeted relationship between miR-455-3p and circCSNK1G1 or MYO6 predicted by bioinformatics analysis was validated using dual-luciferase reporter assay and RNA pull-down assay. The role of circCSNK1G1 was also explored in nude mice in vivo.

resultsThe expression of circCSNK1G1 and MYO6 was elevated, while the expression of miR-455-3p was declined in CRC tissues and cells. Silencing circCSNK1G1 inhibited CRC cell proliferation, migration and invasion and induced cell apoptosis and cell cycle arrest. MiR-455-3p was a target of circCSNK1G1, and miR-455-3p could bind to MYO6. CircCSNK1G1 positively regulated MYO6 expression by targeting miR-455-3p. Inhibition of miR-455-3p reversed the effects of circCSNK1G1 silencing in CRC cells. Besides, miR-455-3p restoration blocked CRC cell growth and metastasis, which were abolished by MYO6 overexpression. Moreover, circCSNK1G1 regulated the miR-455-3p/MYO6 axis to block tumor growth in vivo.

conclusionCircCSNK1G1 participated in the progression of CRC partly by modulating the miR-455-3p/MYO6 network, which provided a theoretical basis for circCSNK1G1 involving in CRC pathogenesis, hinting that circCSNK1G1 might be a useful biomarker for CRC treatment.

Indexed as

circCSNK1G1colorectal cancermiR-455-3pMYO6

Identifiers

PMID33061642
PMCPMC7538009

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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.