Evidence map›Paper›PMID 30785086›Full record

ArticleRedox biology2019

miR-125b suppresses oral oncogenicity by targeting the anti-oxidative gene PRXL2A.

Yi-Fen Chen, Yun-Yen Wei, Cheng-Chieh Yang, Chung-Ji Liu, Li-Yin Yeh, Chung-Hsien Chou, Kuo-Wei Chang, Shu-Chun Lin

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.4field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
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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

8 authors at 3 institutions in 1 country.

Yi-Fen ChenInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan.
Yun-Yen WeiInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan.
Cheng-Chieh YangInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan; Department of Dentistry, National Yang-Ming University, Taipei, Taiwan; Department of Stomatology, Taipei Veterans General Hospital, Taipei, Taiwan.
Chung-Ji LiuDepartment of Dentistry, National Yang-Ming University, Taipei, Taiwan; Department of Dentistry, MacKay Memorial Hospital, Taipei, Taiwan.
Li-Yin YehInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan.
Chung-Hsien ChouInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan.
Kuo-Wei ChangInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan; Department of Dentistry, National Yang-Ming University, Taipei, Taiwan; Department of Stomatology, Taipei Veterans General Hospital, Taipei, Taiwan. Electronic address: ckcw@ym.edu.tw.
Shu-Chun LinInstitute of Oral Biology, National Yang-Ming University, Taipei, Taiwan; Department of Dentistry, National Yang-Ming University, Taipei, Taiwan; Department of Stomatology, Taipei Veterans General Hospital, Taipei, Taiwan. Electronic address: sclin@ym.edu.tw.
National Yang Ming Chiao Tung University · TWNational Yang Ming Chiao Tung University · TWMackay Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oral squamous cell carcinoma (OSCC) is a globally prevalent malignancy. The molecular mechanisms of this cancer are not well understood and acquire elucidation. Peroxiredoxin like 2A (PRXL2A) has been reported to be an antioxidant protein that protects cells from oxidative stress. Our previous study identified an association between PRXL2A upregulation in OSCC and a worse patient prognosis. MicroRNAs (miRNAs) are small non-coding RNAs that are involved in the modulation of biological/pathological properties. The miR-125 family of genes drive pluripotent regulation across a wide variety of cancers. In this study, we identify the oncogenic eligibility of PRXL2A and clarify miR-125b as its upstream regulator. Downregulation of miR-125b can be observed in OSCC tumors. Lower miR-125b expression in tumors results in a worse patient prognosis at the relatively early stage. Reporter assays are able to validate that PRXL2A is a direct target of miR-125b. Exogenous miR-125b expression in OSCC cells results in increased oxidative stress, increased drug sensitivity, and suppressor activity that is paralleled by the knockout of PRXL2A gene. The suppressor activity of miR-125b is able to be rescued by PRXL2A, which suggests the existence of a miR-125b-PRXL2A regulatory axis that is part of OSCC pathogenesis. Nuclear factor-erythroid 2-related factor 2 (NRF2) was found to be a downstream effector of the miR-125b-PRXL2A cascade. As a whole, this study has pinpointed novel clues demonstrating that downregulation of miR-125b suppressor underlies upregulation of PRXL2A in OSCC, and this then protects the affected tumor cells from oxidative stress.

Indexed as

CarcinogenesisCell Line, TumorCell ProliferationCisplatinGene Expression Regulation, NeoplasticGene Knockdown TechniquesGenes, ReporterHumansMicroRNAsMouth NeoplasmsOxidative StressPeroxiredoxinsPhenotypeReactive Oxygen SpeciesROC CurveCisplatinMicroRNAsMIRN125 microRNA, humanPeroxiredoxinsPRDX2 protein, humanReactive Oxygen SpeciesHNSCCmiR-125NRF2OxidationPeroxiredoxin like 2A

Identifiers

PMID30785086
PMCPMC6383183
OpenAlexW2911841653

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.