Evidence map›Paper›PMID 27571935›Full record

ArticleCell proliferation2016

MicroRNA-137 suppresses tongue squamous carcinoma cell proliferation, migration and invasion.

Lanying Sun, Jin Liang, Qibao Wang, Zhaoyuan Li, Yi Du, Xin Xu

Abstract read
In one paragraph

Article in Cell proliferation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing 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

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

35 citing papers in PubMed.

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  14. Effect of chromodomain helicase/ATPase DNA binding protein 1-like gene on the invasion and metastasis of tongue squamous cell carcinoma CAL27 cells.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 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

6 authors.

Lanying SunSchool of Stomatology, Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Shandong University, Jinan, 250012, China.
Jin LiangSchool of Stomatology, Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Shandong University, Jinan, 250012, China.
Qibao WangDepartment of Endodontics, Stomatology Hospital of Jinan, Jinan, 250001, China.
Zhaoyuan LiOral Implantology Center, Stomatology Hospital of Jinan, Jinan, 250001, China.
Yi DuDepartment of Endodontics, Stomatology Hospital of Jinan, Jinan, 250001, China.
Xin XuSchool of Stomatology, Shandong Provincial Key Laboratory of Oral Tissue Regeneration, Shandong University, Jinan, 250012, China. xinxu16@tom.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTongue squamous cell carcinoma (TSCC) is the most frequent type of oral malignancy. Increasing evidence has shown that miRNAs play key roles in many biological processes such as cell development, invasion, proliferation, differentiation, metabolism, apoptosis and migration. MATERIALS AND

methodsqRT-PCR analysis was performed to measure miR-137 expression. CCK-8 analysis, cell colony formation, wound-healing analysis and invasion were performed to detect resultant cell functions. The direct target of miR-137 was labelled and measured by luciferase assay and Western blotting.

resultsWe demonstrated that expression of miR-137 was downregulated in TSCC tissues compared to matched normal ones. miR-137 expression was downregulated in TSCC lines (SCC4, SCC1, UM1 and Cal27) compared to the immortalized NOK16B cell line and normal oral keratinocytes in culture (NHOK). In addition, we have shown that miR-137 expression was epigenetically regulated in TSCCs. Overexpression of miR-137 suppressed TSCC proliferation and colony formation. Ectopic expression of miR-137 promoted expression of the epithelial biomarker, E-cadherin, and inhibited the mesenchymal biomarker, N-cadherin, as well as vimentin and Snail expression, indicating that miR-137 suppressed TSCC epithelial-mesenchymal transition (EMT). We also showed that ectopic expression of miR-137 inhibited TSCC invasion and migration. In addition, we identified SP1 as a direct target gene of miR-137 in SCC1 cells. SP1 overexpression rescued inhibitory effects exerted by miR-137 on cell proliferation and EMT.

conclusionsThese results indicate that miR-137 acted as a tumour suppressor in TSCC by targeting SP1.

Indexed as

Gene Expression Regulation, NeoplasticCarcinoma, Squamous CellCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionHumansMicroRNAsNeoplasm InvasivenessSp1 Transcription FactorTongueTongue NeoplasmsMicroRNAsMIRN137 microRNA, humanSp1 Transcription Factor

Identifiers

PMID27571935
PMCPMC6495205

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.