Evidence map›Paper›PMID 33469369›Full record

ArticleCancer management and research2021

CircSND1 Regulated by TNF-α Promotes the Migration and Invasion of Cervical Cancer Cells.

Lili Bai, Wangjie Sun, Zhe Han, Hua Tang

Open access · goldAbstract read
In one paragraph

Article in Cancer management and research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

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  6. Noncoding RNAs as sensors of tumor microenvironmental stress.Journal of experimental & clinical cancer research : CR · 2022
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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

4 authors at 1 institution in 1 country.

Lili Bai *Tianjin Life Science Research Center, Tianjin Key Laboratory of Inflammation Biology, Collaborative Innovation Center of Tianjin for Medical Epigenetics, Department of Pathogen Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, People's Republic of China.
Wangjie Sun *Tianjin Life Science Research Center, Tianjin Key Laboratory of Inflammation Biology, Collaborative Innovation Center of Tianjin for Medical Epigenetics, Department of Pathogen Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, People's Republic of China.ORCID 0000-0002-7230-6063
Zhe HanTianjin Life Science Research Center, Tianjin Key Laboratory of Inflammation Biology, Collaborative Innovation Center of Tianjin for Medical Epigenetics, Department of Pathogen Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, People's Republic of China.
Hua TangTianjin Life Science Research Center, Tianjin Key Laboratory of Inflammation Biology, Collaborative Innovation Center of Tianjin for Medical Epigenetics, Department of Pathogen Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, People's Republic of China.ORCID 0000-0002-6202-9656
Tianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimTo explore the role and potential mechanism of circSND1 in cervical cancer (CC). MAIN

methodsqRT-PCR was used to determine the expression of circSND1 in tumor necrosis factor-α (TNF-α)-treated HeLa cells. CircSND1 overexpression and knockdown were performed to indicate the functional role of circSND1 in vitro and in vivo. Luciferase assay was used to analyze promoter activity. The expression and regulation of circSND1, miR-125a-3p and FUT6 were evaluated using EGFP fluorescent reporter assay and rescue experiments. Immunofluorescence and Western blot assays were used to analyze the activation of nuclear factor-κB (NF-κB).

resultsIn HeLa cells, TNF-α up-regulated the expression of circSND1 by activating the NF-κB signaling pathway. Overexpression of circSND1 significantly increased the migration and invasion and the epithelial-mesenchymal transition (EMT) process of CC cells, and promoted tumor metastasis in xenograft nude mouse model, whereas down-regulation of circSND1 exerted opposite effects. Furthermore, circSND1 enhanced the expression of FUT6 via sponging miR-125a-3p, and FUT6 activated NF-κB signaling pathway.

conclusionWe found that circSND1 promoted the expression of FUT6 and the malignant behavior of cervical cancer through the ceRNA mechanism, and there was a TNF-α/NF-κB/circSND1/miR-125a-3p/FUT6/NF-κB positive feedback pathway between them, which suggests that circSND1 can be a promising prognostic marker and therapeutical target for cervical cancer.

Indexed as

ceRNAcervical cancercircSND1FUT6miR-125a-3pNF-κB

Identifiers

PMID33469369
PMCPMC7811455
OpenAlexW3120091701

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.