Evidence map›Paper›PMID 28822783›Full record

ArticleBiochemical pharmacology2017

The expression, induction and pharmacological activity of CYP1A2 are post-transcriptionally regulated by microRNA hsa-miR-132-5p.

Yinting Chen, Linjuan Zeng, Yong Wang, William H Tolleson, Bridgett Knox, Si Chen, Zhen Ren, Lei Guo, Nan Mei, Feng Qian and 5 more

Open access · greenAbstract read
In one paragraph

Article in Biochemical pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Synthesis and Antitumor Potency of 2International journal of molecular sciences · 2026
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  11. Novel Approaches to Characterize Individual Drug Metabolism and Advance Precision Medicine.Drug metabolism and disposition: the biological fate of chemicals · 2023
    Review
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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

15 authors at 5 institutions in 2 countries.

Yinting ChenDepartment of Gastroenterology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China; Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China; National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
Linjuan ZengNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA; Department of Oncology, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai 519000, China.
Yong WangNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
William H TollesonNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
Bridgett KnoxNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
Si ChenNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
Zhen RenNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
Lei GuoNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
Nan MeiNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
Feng QianNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
Kaihong HuangDepartment of Gastroenterology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China; Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China.
David LiuLongevity Center of CHI St. Vincent Hospital, Little Rock, AR 72205, USA.
Weida TongNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA.
Dianke YuNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA; School of Public Health, Qingdao University, Qingdao 266071, China. Electronic address: dianke.yu@fda.hhs.gov.
Baitang NingNational Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA. Electronic address: baitang.ning@fda.hhs.gov.
National Center for Toxicological Research · USUnited States Food and Drug Administration · USCHI St. Vincent · USQingdao University · CNSun Yat-sen Memorial Hospital · CN

Funding

Intramural FDA HHS FD999999
6 · The paper itself

Abstract

Cytochrome P450 1A2 (CYP1A2) is one of the most abundant and important drug metabolizing enzymes in human liver. However, little is known about the post-transcriptional regulation of CYP1A2, especially the mechanisms involving microRNAs (miRNAs). This study applied a systematic approach to investigate the post-transcriptional regulation of CYP1A2 by miRNAs. Candidate miRNAs targeting the 3'-untranslated region (3'-UTR) of CYP1A2 were screened in silico, resulting in the selection of sixty-two potential miRNAs for further analysis. The levels of two miRNAs, hsa-miR-132-5p and hsa-miR-221-5p, were inversely correlated with the expression of CYP1A2 mRNA transcripts in normal human liver tissue samples represented in The Cancer Genome Atlas (TCGA) dataset. The interactions between these miRNAs and cognate CYP1A2 mRNA sequences were evaluated using luciferase reporter gene studies and electrophoretic mobility shift assays, by which a direct interaction was confirmed involving hsa-miR-132-5p and a cognate binding site present in the CYP1A2 3'-UTR. Experiments by which hsa-miR-132-5p or random miRNA controls were introduced into HepG2, Huh-7 and HepaRG hepatic cell lines showed that only hsa-miR-132-5p suppressed the endogenous and lansoprazole-induced expression of CYP1A2, at biological activity, protein production, and mRNA transcript levels. Furthermore, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), and lactate dehydrogenase (LDH) assays showed that hsa-miR-132-5p attenuates CYP1A2-mediated, lansoprazole-enhanced, flutamide-induced hepatic cell toxicity. Results from multilayer experiments demonstrate that hsa-miR-132-5p suppresses the expression of CYP1A2 and that this suppression is able to decrease the extent of an adverse drug-drug interaction involving lansoprazole and flutamide.

Indexed as

Antineoplastic Agents, HormonalCell LineCell ProliferationComputer SimulationCytochrome P-450 CYP1A2FlutamideGene Expression Regulation, EnzymologicHumansLansoprazoleMicroRNAsProton Pump InhibitorsRNA, MessengerRNA Processing, Post-TranscriptionalAntineoplastic Agents, HormonalCYP1A2 protein, humanCytochrome P-450 CYP1A2FlutamideLansoprazoleMicroRNAsProton Pump InhibitorsRNA, MessengerCYP1A2Drug metabolizing enzymeshsa-miR-132-5pMicroRNAToxicity

Identifiers

PMID28822783
PMCPMC5712447
OpenAlexW2747572211

What OpenQuestion holds

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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.