Evidence map›Paper›PMID 30938030›Full record

ArticleCell proliferation2019

Suppression of long non-coding RNA TNRC6C-AS1 protects against thyroid carcinoma through DNA demethylation of STK4 via the Hippo signalling pathway.

Liu-Xue Yang, Ji Wu, Man-Li Guo, Yong Zhang, Shao-Gang Ma

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 40 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

5 authors at 4 institutions in 1 country.

Liu-Xue YangDepartment of Endocrinology and Metabolism, The Second Affiliated Hospital of Guilin Medical University, Guilin, China.
Ji WuDepartment of Thyroid and Breast Surgery, Suqian Hospital Affiliated to Xuzhou Medical University, Suqian, China.
Man-Li GuoDepartment of Endocrinology and Metabolism, Suqian People's Hospital, Nanjing Drum Tower Hospital, Suqian, China.
Yong ZhangDepartment of Endocrinology and Metabolism, Huai'an Hospital Affiliated to Xuzhou Medical College and Huai'an Second People's Hospital, Huai'an, China.
Shao-Gang MaDepartment of Endocrinology and Metabolism, Suqian First Hospital, Suqian, China.ORCID https://orcid.org/0000-0002-6355-6415
Xuzhou Medical College · CNGuilin Medical University · CNNanjing Drum Tower Hospital · CNThe First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine · CN

Funding

Basic Professional Ability Improvement Project for Young and Middle-aged Teachers of Colleges and Universities in Guangxi (2016) KY2016YB322Science and Technology Program of Guilin 2016012705-8
6 · The paper itself

Abstract

objectivesThyroid carcinoma (TC) represents a malignant neoplasm affecting the thyroid. Current treatment strategies include the removal of part of the thyroid; however, this approach is associated with a significant risk of developing hypothyroidism. In order to adequately understand the expression profiles of TNRC6C-AS1 and STK4 and their potential functions in TC, an investigation into their involvement with Hippo signalling pathway and the mechanism by which they influence TC apoptosis and autophagy were conducted.

methodsA microarray analysis was performed to screen differentially expressed lncRNAs associated with TC. TC cells were employed to evaluate the role of TNRC6C-AS1 by over-expression or silencing means. The interaction of TNRC6C-AS1 with methylation of STK4 promoter was evaluated to elucidate its ability to elicit autophagy, proliferation and apoptosis.

resultsTNRC6C-AS1 was up-regulated while STK4 was down-regulated, where methylation level was elevated. STK4 was verified as a target gene of TNRC6C-AS1, which was enriched by methyltransferase. Methyltransferase's binding to STK4 increased expression of its promoter. Over-expressed TNRC6C-AS1 inhibited STK4 by promoting STK4 methylation and reducing the total protein levels of MST1 and LATS1/2. The phosphorylation of YAP1 phosphorylation was decreased, which resulted in the promotion of SW579 cell proliferation and tumorigenicity.

conclusionBased on our observations, we subsequently confirmed the anti-proliferative, pro-apoptotic and pro-autophagy capabilities of TNRC6C-AS1 through STK4 methylation via the Hippo signalling pathway in TC.

Indexed as

AnimalsApoptosisAutophagyBase SequenceCell Line, TumorCell ProliferationDNA DemethylationDown-RegulationHeterograftsHippo KinasesHippo Signaling PathwayHumansIntracellular Signaling Peptides and ProteinsMiceMice, Inbred BALB CMice, NudeHippo KinasesIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesRNA, AntisenseRNA-Binding ProteinsRNA, Long NoncodingSTK4 protein, humanTNRC6C protein, humanHippo signalling pathwaylong noncoding RNAproliferationserine/threonine kinase 4thyroid carcinomaTNRC6C-AS1

Identifiers

PMID30938030
PMCPMC6536409
OpenAlexW2934622391

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.