Evidence map›Paper›PMID 33797737›Full record

ArticleCellular oncology (Dordrecht, Netherlands)2021

Long non-coding RNA LINC01137 contributes to oral squamous cell carcinoma development and is negatively regulated by miR-22-3p.

Yong Du, Haiyan Yang, Yue Li, Wenli Guo, Yufeng Zhang, Haitao Shen, Lingxiao Xing, Yuehong Li, Wenxin Wu, Xianghong Zhang

Abstract read
In one paragraph

Article in Cellular oncology (Dordrecht, Netherlands), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Yong Du *Department of Stomatology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Haiyan Yang *Laboratory of Pathology, Hebei Medical University, Shijiazhuang, China.
Yue LiDepartment of Pathology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Wenli GuoDepartment of Pathology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Yufeng ZhangDepartment of Radiotherapy, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Haitao ShenDepartment of Pathology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Lingxiao XingDepartment of Pathology, The Second Hospital of Hebei Medical University, Shijiazhuang, China.
Yuehong LiLaboratory of Pathology, Hebei Medical University, Shijiazhuang, China.
Wenxin WuLaboratory of Pathology, Hebei Medical University, Shijiazhuang, China.
Xianghong ZhangDepartment of Pathology, The Second Hospital of Hebei Medical University, Shijiazhuang, China. zhangxianghong@hb2h.com.ORCID http://orcid.org/0000-0001-5331-9590
Hebei Medical University · CN

Funding

China National Funds for Distinguished Young Scientists 81702299Natural Science Foundation of Hebei Province H2017206022
6 · The paper itself

Abstract

purposeLong noncoding RNAs (lncRNAs) are emerging as key regulators in cancer initiation and progression. LINC01137 is a recently identified lncRNA of which the functional role in the development of oral squamous cell carcinoma (OSCC) has not been determined yet.

methodsWe analyzed the expression of LINC01137 using a microarray-based OSCC gene expression dataset (GSE31056), and validated the results obtained using RT-qPCR in 26 pairs of primary OSCC tumor tissues and adjacent non-tumor tissues. The proliferative and invasive effects of LINC01137 on OSCC cells were determined using CCK-8, colony formation and transwell assays, respectively. Targeted binding between miR-22-3p and LINC01137 was verified using a dual luciferase reporter assay.

resultsWe found that LINC01137 was significantly upregulated in primary OSCCs. LINC01137 knockdown inhibited OSCC cell proliferation, migration and invasion, whereas LINC01137 overexpression induced opposite effects. LINC01137 upregulation along with p53 inhibition enhanced the malignant transformation of oral cells. In addition, we found that miR-22-3p can directly target LINC01137 through interaction with a putative miR-22-3p-binding site present within the LINC01137 sequence. A significant negative correlation was observed between LINC01137 and miR-22-3p expression in primary OSCC specimens. Exogenous overexpression of miR-22-3p markedly reduced the endogenous expression level of LINC01137 in OSCC cells. Additional functional assays showed that miR-22-3p overexpression enhanced the inhibitory effect of siRNA-mediated LINC01137 silencing on OSCC cell proliferation, migration and invasion, whereas miR-22-3p inhibition had the opposite effect.

conclusionsOur results indicate that LINC01137 functions as an oncogenic lncRNA in OSCC. miR-22-3p can directly target LINC01137 and negatively regulate its expression and function.

Indexed as

Gene Expression Regulation, NeoplasticHumansMicroRNAsMouth NeoplasmsRNA, Long NoncodingSquamous Cell Carcinoma of Head and NeckMicroRNAsMIRN22 microRNA, humanRNA, Long NoncodingInvasionlncRNA LINC01137miR-22-3pOral squamous cell carcinomaProliferation Migration

Identifiers

PMID33797737
PMCPMC12980792
OpenAlexW3148106428

What OpenQuestion holds

Textmetadata
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.