Evidence map›Paper›PMID 32190006›Full record

ArticleCancer cell international2020

MiR-26a/miR-26b represses tongue squamous cell carcinoma progression by targeting PAK1.

Zhenxing Wei, Kunpeng Chang, Chongsheng Fan, Yang Zhang

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

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  11. The Functional Mechanism of MicroRNA in Oral Lichen Planus.Journal of inflammation research · 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.

Zhenxing WeiDepartment of Otorhinolaryngology-Head and Neck Surgery, The Luoyang Central Hospital Affiliated to Zhengzhou University, No. 288 Middle Zhongzhou Road, Xigong District, Luoyang, 471000 Henan China.ORCID 0000-0003-1696-8801
Kunpeng ChangDepartment of Otorhinolaryngology-Head and Neck Surgery, The Luoyang Central Hospital Affiliated to Zhengzhou University, No. 288 Middle Zhongzhou Road, Xigong District, Luoyang, 471000 Henan China.
Chongsheng FanDepartment of Otorhinolaryngology-Head and Neck Surgery, The Luoyang Central Hospital Affiliated to Zhengzhou University, No. 288 Middle Zhongzhou Road, Xigong District, Luoyang, 471000 Henan China.
Yang ZhangDepartment of Otorhinolaryngology-Head and Neck Surgery, The Luoyang Central Hospital Affiliated to Zhengzhou University, No. 288 Middle Zhongzhou Road, Xigong District, Luoyang, 471000 Henan China.
Luoyang Central Hospital Affiliated to Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTongue squamous cell carcinoma (TSCC) is the most common oral malignancy. Previous studies found that microRNA (miR)-26a and miR-26b were downregulated in TSCC tissues. The current study was designed to explore the effects of miR-26a/miR-26b on TSCC progression and the potential mechanism.

methodsExpression of miR-26a, miR-26b and p21 Activated Kinase 1 (PAK1) in TSCC tissues and cell lines was detected by reverse transcription- quantitative polymerase chain reaction (RT-qPCR). Flow cytometry analysis was performed to examine cell cycle and apoptosis. Transwell assay was conducted to evaluate the migrated and invasive abilities of SCC4 and Cal27 cells. In addition, western blot assay was employed to analyze the protein level. Glucose assay kit and lactate assay kit were utilized to analyze glycolysis. Dual-luciferase reporter and RNA immunoprecipitation (RIP) assays were applied to explore the relationship between miR-26a/miR-26b and PAK1. Xenograft tumor model was constructed to explore the role of miR-26a/miR-26b in vivo.

resultsBoth miR-26a and miR-26b were underexpressed, while PAK1 was highly enriched in TSCC. Overexpression of miR-26a and miR-26b inhibited TSCC cell cycle, migration invasion and glycolysis, while promoted cell apoptosis. Both miR-26a and miR-26b directly targeted and negatively regulated PAK1 expression. Introduction of PAK1 partially reversed miR-26a/miR-26b upregulation-mediated cellular behaviors in TSCC cells. Gain of miR-26a/miR-26b blocked TSCC tumor growth in vivo.

conclusionMiR-26a/miR-26b repressed TSCC progression via targeting PAK1 in vitro and in vivo, which enriched our understanding about TSCC development and provided new insights into the its treatment.

Indexed as

GlycolysismicroRNA-26amicroRNA-26bPAK1TSCC

Identifiers

PMID32190006
PMCPMC7071636
OpenAlexW3012646224

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.