Evidence map›Paper›PMID 34143366›Full record

ArticleJournal of endocrinological investigation2022

microRNA-181a promotes the oncogene S100A2 and enhances papillary thyroid carcinoma growth by mediating the expression of histone demethylase KDM5C.

Y Wang, H Ye, Y Yang, J Li, A Cen, L Zhao

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of endocrinological investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 35% 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

12 citing papers in PubMed, 14 citations in OpenAlex.

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  8. Role of miR‑181a‑5p in cancer (Review).International journal of oncology · 2023
    Review
  9. Review
  10. Article
  11. Influence of S100A2 in Human Diseases.Diagnostics (Basel, Switzerland) · 2022
    Review
  12. Review
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.

Y WangDepartment of Endocrinology, the First Affiliated Hospital of Jinan University, No. 613, West Huangpu Avenue, Tianhe District, Guangzhou, 510630, Guangdong Province, People's Republic of China. smeea@126.com.
H YeGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Hepatopancreatobiliary Surgery, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China.
Y YangDepartment of Radiation Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
J LiDepartment of Endocrinology, the First Affiliated Hospital of Jinan University, No. 613, West Huangpu Avenue, Tianhe District, Guangzhou, 510630, Guangdong Province, People's Republic of China.
A CenDepartment of Endocrinology, the First Affiliated Hospital of Jinan University, No. 613, West Huangpu Avenue, Tianhe District, Guangzhou, 510630, Guangdong Province, People's Republic of China.
L ZhaoDepartment of Radiation Oncology, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, People's Republic of China.
First Affiliated Hospital of Jinan University · CNSun Yat-sen Memorial Hospital · CNSun Yat-sen University · CNSun Yat-sen University Cancer Center · CN

Funding

Characteristic Innovation Projects of General Colleges and Universities in Guangdong Province Grant No. 2019KTSCX009Guangdong Basic and Applied Basic Research Foundation Grant No. 2020A151501030the National Natural Science Foundation of China Grant No. 81402213the National Natural Science Foundation of China Grant No. 81874220
6 · The paper itself

Abstract

background and purposePapillary thyroid carcinoma (PTC) is an endocrine malignancy. Increasing evidence highlights microRNAs (miRNAs) as important participants in PTC. Here, we investigated the role of miR-181a in PTC.

methodsA microarray-based analysis was performed to identify the differential expression of miR-181a in PTC, which was validated with RT-qPCR. Protein expression of the proliferation-related factor Ki-67 and apoptosis- and migration-related factors in PTC was assessed with immunoblot analysis. A dual-luciferase reporter gene assay was adopted to verify the relationship between miR-181a and lysine demethylase 5C (KDM5C). Chromatin immunoprecipitation (ChIP) was used to detect the level of the H3K4me3 modification on S100 calcium-binding protein A2 (S100A2). Cell viability, apoptosis, and invasion and migration abilities were evaluated by Cell Counting Kit-8 (CCK-8), flow cytometry, and transwell assays, respectively. The in vitro results were verified in in vivo nude mouse models.

resultsmiR-181a was highly expressed in PTC tissues and cell lines. Silencing miR-181a repressed the proliferation and migration of PTC cells. KDM5C was identified as the target gene of miR-181a and represses S100A2 expression through histone demethylation to diminish the migration and proliferation of PTC cells. miR-181a depletion suppressed tumor growth.

conclusionCollectively, these results suggest that highly expressed miR-181a promotes the proliferation of PTC cells by increasing the expression of the oncogene S100A2. This study contributes to the advancement of miR-181a-targeted therapeutics.

Indexed as

Thyroid Cancer, PapillaryAdultAnimalsApoptosisCell MovementCell ProliferationChemotactic FactorsDrug DiscoveryFemaleGene Expression ProfilingGene Expression Regulation, NeoplasticHistone DemethylasesHumansMaleMiceMicroRNAsChemotactic FactorsHistone DemethylasesKDM5C protein, humanKdm5c protein, mouseMicroRNAsMIrn181 microRNA, humanmirn181 microRNA, mouseS100A2 protein, humanS100A2 protein, mouseS100 ProteinsCell proliferationLysine demethylase 5CmicroRNA-181aPapillary thyroid carcinomaS100 calcium-binding protein A2

Identifiers

PMID34143366
OpenAlexW3169762249

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.