Evidence map›Paper›PMID 34811354›Full record

ArticleCell death & disease2021

LncRNA-MIAT promotes thyroid cancer progression and function as ceRNA to target EZH2 by sponging miR-150-5p.

Kai Guo, Kai Qian, Yuan Shi, Tuanqi Sun, Zhuoying Wang

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
8.6field-weighted citation impact, top 1% 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

88 citing papers in PubMed, 131 citations in OpenAlex.

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  17. Epigenetic regulation of cancer stemness.Signal transduction and targeted therapy · 2025
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28 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Kai Guo *Department of Head and Neck Surgery, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, 200001, Shanghai, China.
Kai Qian *Department of Head and Neck Surgery, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, 200001, Shanghai, China.
Yuan ShiDepartment of Head and Neck Surgery, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, 200001, Shanghai, China.
Tuanqi SunDepartment of Head and Neck Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
Zhuoying WangDepartment of Head and Neck Surgery, Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital, 200001, Shanghai, China. zhuoyingwang@hotmail.com.ORCID http://orcid.org/0000-0002-8121-5286
Shanghai Jiao Tong University · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While long noncoding RNAs (lncRNAs) have been reported to play an important role in human cancer types, they remain poorly understood in papillary thyroid carcinoma (PTC). The aim of this study was to use genome-wide expression profiling to identify lncRNAs acting as competing endogenous RNAs (ceRNAs) in PTC. We constructed a ceRNA network based on our lncRNA microarray data and validated the correlation between myocardial infarction-associated transcript lncRNA (MIAT), miRNA-150-5p, and EZH2 in vitro and in vivo. We found 15 lncRNAs, 28 miRNAs, and hundreds of mRNAs involved in this ceRNA network. Splendid positive correlations were found between the MIAT and EZH2 expression in types of cancer in TCGA data. Besides, significant differences in MIAT/EZH2 expression were found among various clinicopathological features. Gain- and loss-of-function experiments revealed that MIAT inhibited cell proliferation and migration in vitro. Moreover, EZH2 was identified as a direct downstream target of miR-150-5p in PTC cells. Restoration of EZH2 expression partially abolished the biological effects of miR-150-5p. Furthermore, overexpression of MIAT was inversely correlated with miR-150-5p expression. Knockdown of MIAT produced significant behavioral alter maybe partly due to the function of the MIAT-150-5p-EZH2 network. Our findings suggest MIAT may inhibit EZH2 expression and promote PTC cell invasion via the miR-150/EZH2 pathway. Therefore, MIAT may serve as a valuable prognostic biomarker and therapeutic target for PTC.

Indexed as

AnimalsBiomarkers, TumorCell ProliferationDisease ProgressionEnhancer of Zeste Homolog 2 ProteinFemaleHeterograftsHumansMiceMice, Inbred BALB CMicroRNAsRNA, Long NoncodingThyroid NeoplasmsTransfectionBiomarkers, TumorEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanMiat long non-coding RNAMicroRNAsMIR150, humanRNA, Long Noncoding

Identifiers

PMID34811354
PMCPMC8608816
OpenAlexW3216692713

What OpenQuestion holds

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LicenceCC BY
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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.