Evidence map›Paper›PMID 32086297›Full record

ArticleDrug metabolism and disposition: the biological fate of chemicals2020

Coordinated Regulation of UGT2B15 Expression by Long Noncoding RNA LINC00574 and hsa-miR-129-5p in HepaRG Cells.

Dianke Yu, Jing Chen, Si Chen, Lin Xu, Leihong Wu, Dongying Li, Jiao Luo, Yuan Jin, Yanjie Zhao, Bridgett Knox and 5 more

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Drug metabolism and disposition: the biological fate of chemicals, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 42% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
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  5. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 3 institutions in 2 countries.

Dianke YuSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas dianke.yu@qdu.edu.cn.
Jing ChenSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas.
Si ChenSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas.
Lin XuSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas.
Leihong WuSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas.
Dongying LiSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas dianke.yu@qdu.edu.cn.
Jiao LuoSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas.
Yuan JinSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas.
Yanjie ZhaoSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas.
Bridgett KnoxSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas.
William H TollesonSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas.
Xubing WangSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas.
Lei GuoSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas.
Weida TongSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas.
Baitang NingSchool of Public Health, Qingdao University, Qingdao, China; National Center for Toxicological Research (NCTR), US Food and Drug Administration, Jefferson, Arkansas.
United States Food and Drug Administration · USQingdao University · CNNational Center for Toxicological Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have shown that microRNAs and long noncoding RNAs (lncRNAs) regulate the expression of drug metabolizing enzymes (DMEs) in human hepatic cells and that a set of DMEs, including UDP glucuronosyltransferase (UGT) 2B15, is down-regulated dramatically in liver cells by toxic acetaminophen (APAP) concentrations. In this study we analyzed mRNA, microRNA, and lncRNA expression profiles in APAP-treated HepaRG cells to explore noncoding RNA-dependent regulation of DME expression. The expression of UGT2B15 and lncRNA LINC00574 was decreased in APAP-treated HepaRG cells. UGT2B15 levels were diminished by LINC00574 suppression using antisense oligonucleotides or small interfering RNA. Furthermore, we found that hsa-miR-129-5p suppressed LINC00574 and decreased UGT2B15 expression via LINC00574 in HepaRG cells. In conclusion, our results indicate that LINC00574 acts as an important regulator of UGT2B15 expression in human hepatic cells, providing experimental evidence and new clues to understand the role of cross-talk between noncoding RNAs. SIGNIFICANCE STATEMENT: We showed a molecular network that displays the cross-talk and consequences among mRNA, micro RNA, long noncoding RNA, and proteins in acetaminophen (APAP)-treated HepaRG cells. APAP treatment increased the level of hsa-miR-129-5p and decreased that of LINC00574, ultimately decreasing the production of UDP glucuronosyltransferase (UGT) 2B15. The proposed regulatory network suppresses UGT2B15 expression through interaction of hsa-miR-129-5p and LINC00574, which may be achieved potentially by recruiting RNA binding proteins.

Indexed as

Gene Expression Regulation, EnzymologicGlucuronosyltransferaseHep G2 CellsHumansMicroRNAsRNA, Long NoncodingGlucuronosyltransferaseMicroRNAsMirn129 microRNA, humanRNA, Long NoncodingUDP-glucuronosyltransferase 2B15, human

Identifiers

PMID32086297
PMCPMC7153565
OpenAlexW3008174967

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.