Evidence map›Paper›PMID 32934732›Full record

ArticleOncology letters2020

lncRNA MALAT1 promotes cell proliferation and invasion by regulating the miR-101/EZH2 axis in oral squamous cell carcinoma.

Lei Xiao, Weiping Wang, Jingjing Zhao, Hongyan Xu, Shaozhen Li, Xiuhua Yang

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Epigenetic regulation of EZH2 by ncRNAs: mechanisms and oncogenic implications.Naunyn-Schmiedeberg's archives of pharmacology · 2026
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  7. Advanced biomedical research · 2025
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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 at 4 institutions in 1 country.

Lei XiaoDepartment of Stomatology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong 264000, P.R. China.
Weiping WangDepartment of Stomatology, Yantaishan Hospital, Yantai, Shandong 264000, P.R. China.
Jingjing ZhaoDepartment of Surgery, The People's Hospital of Zhangqiu Area, Jinan, Shandong 250200, P.R. China.
Hongyan XuDepartment of Stomatology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710000, P.R. China.
Shaozhen LiDepartment of Imaging, The People's Hospital of Zhangqiu Area, Jinan, Shandong 250200, P.R. China.
Xiuhua YangDepartment of Pharmacy, The People's Hospital of Zhangqiu Area, Jinan, Shandong 250200, P.R. China.
Zhangqiu City People's Hospital · CNShaanxi Provincial People's Hospital · CNYantaishan Hospital · CNYuhuangding Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oral squamous cell carcinoma (OSCC) is the most common malignant tumor of the oral cavity. Emerging evidence indicates that long non-coding (lnc)RNAs play a key role in the cellular processes of tumor cells, including glycolysis, growth and movement. Here, the purpose of this study was to explore the biological functions and potential mechanism of lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in OSCC. OSCC tissues and adjacent matched paraneoplastic normal tissues were collected from 20 OSCC patients. The expression of MALAT1 and miR-101 in OSCC tissues and cell lines (HSC3, SCC9, SCC15 and SCC25) were determined by real-time-polymerase chain reaction (qPCR). Caspase-3, xaspase-8 and EZH2 protein levels were determined by western blot analysis. MALAT1-mediated miRNAs were verified by bioinformatics analysis of StarBase and Luciferase reporter assay. Cell Counting Kit-8 (CCK-8) and Transwell assays were used for investigating MALAT1 effect on cell proliferation and invasion in the OSCC cells. qPCR analysis indicated that MALAT1 expression was obviously increased, and miR-101 was decreased in the OSCC tissues and cell lines. Functional studies revealed that overexpression of MALAT1 promoted OSCC cell proliferation and invasion. Further experiments revealed that miR-101 was a target of MALAT1 and that the miR-101 inhibitor abolished the effect of MALAT1 on OSCC cell proliferation and invasion. Enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) acted as a downstream effecter of MALAT1 in the OSCC cells. Collectively, these findings revealed that upregulation of MALAT1 facilitated OSCC proliferation and invasion by targeting the miR-101/EZH2 axis.

Indexed as

EZH2long non-coding RNAMALAT1microRNA-101oral squamous cell carcinoma

Identifiers

PMID32934732
PMCPMC7471703
OpenAlexW3080954967

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.