Evidence map›Paper›PMID 31984860›Full record

ArticleTechnology in cancer research & treatment

miR-331-3p Inhibits Proliferation and Promotes Apoptosis of Nasopharyngeal Carcinoma Cells by Targeting elf4B-PI3K-AKT Pathway.

Zhang Xuefang, Zheng Ruinian, Jiang Liji, Zhang Chun, Zheng Qiaolan, Jia Jun, Chen Yuming, Huang Junrong

RetractedErratum issuedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Technology in cancer research & treatment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
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  10. METTL14-mediated mMolecular cancer · 2022
    Article
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  16. AFrontiers in genetics · 2021
    Article
  17. Article
  18. Article
  19. Regulatory Mechanism of MicroRNA Expression in Cancer.International journal of molecular sciences · 2020
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Zhang XuefangDepartment of Radiotherapy, Dongguan People' Hospital, Dongguan, China.
Zheng RuinianDepartment of Medical Oncology, Dongguan People' Hospital, Dongguan, Guangdong, China.
Jiang LijiDepartment of Radiotherapy, Dongguan People' Hospital, Dongguan, China.
Zhang ChunDepartment of Radiotherapy, Dongguan People' Hospital, Dongguan, China.ORCID 0000-0001-8249-6545
Zheng QiaolanDepartment of Journal Center, Third Affiliated Hospital of SUN YAT-SEN University, Guangzhou, China.
Jia JunDepartment of Medical Oncology, Dongguan People' Hospital, Dongguan, Guangdong, China.
Chen YumingDepartment of Radiotherapy, Dongguan People' Hospital, Dongguan, China.
Huang JunrongDepartment of Radiotherapy, Dongguan People' Hospital, Dongguan, China.
Dongguan People’s Hospital · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe incidence of nasopharyngeal carcinoma is increasing gradually, but the pathogenesis is not completely clear. MicroRNA, a highly conserved endogenous noncoding small molecule RNA, plays an essential role in the regulation of gene expression and is a hotspot in cancer research worldwide.

objectivesAlthough previous studies have confirmed that the abnormal expression of microRNAs is closely related to the progression of nasopharyngeal carcinoma, the role of miRNA-331-3p in nasopharyngeal carcinoma has not been studied. The purpose of this study was to explore the role and mechanism of miRNA-331-3p in the progression of nasopharyngeal carcinoma. MATERIALS AND

methodsReal-time quantitative reverse transcription polymerase chain reaction was performed to detect the expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cell lines (CNE-1 and 5-8F cells). After overexpression of miRNA-331-3p in CNE-1 cells, cell proliferation was measured by Cell Counting Kit-8 assay, cell invasion was detected by Transwell assay, and apoptosis was tested by flow cytometry. In addition, the dual-luciferase reporter assay was used to identify the target gene of miRNA-331-3p and Western blotting was performed to measure the relative protein expression.

resultsThe expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cells was decreased significantly. Overexpression of miRNA-331-3p markedly inhibited the proliferation and invasion of CNE-1 cells and promoted cell apoptosis. Moreover, overexpression of miRNA-331-3p reduced the expression of target gene elF4B, leading to inhibition of the phosphorylation of Phosphoinositide 3-kinase (PI3K) and Serine/ threonine kinase (AKT).

conclusionmiRNA-331-3p inhibited cell proliferation and induced cell apoptosis in nasopharyngeal carcinoma by targeting SIGNIFICANCE: The role of miRNA-331-3p in the development of NPC and its mechanism provide new ideas for the treatment of nasopharyngeal carcinoma.

Indexed as

ApoptosisCell ProliferationCell Line, TumorCell MovementClass I Phosphatidylinositol 3-KinasesEukaryotic Initiation FactorsGene Expression Regulation, NeoplasticHumansMicroRNAsNasopharyngeal CarcinomaNasopharyngeal NeoplasmsProto-Oncogene Proteins c-aktSignal TransductionAKT1 protein, humanClass I Phosphatidylinositol 3-KinaseseIF-4BEukaryotic Initiation FactorsMicroRNAsMIRN331 microRNA, humanPIK3CA protein, humanProto-Oncogene Proteins c-aktelF4BmiRNA-331-3pnasopharyngeal carcinomaPI3K–AKT signaling pathway

Identifiers

PMID31984860
PMCPMC6985969
OpenAlexW3004123776

What OpenQuestion holds

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LicenceCC BY
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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.