Evidence map›Paper›PMID 36347827›Full record

ArticleJournal of clinical laboratory analysis2022

Silencing of lncRNA MIR31HG promotes nasopharyngeal carcinoma cell proliferation and inhibits apoptosis through suppressing the PI3K/AKT signaling pathway.

Bo Feng, Ke Chen, Weiwei Zhang, Qi Zheng, Yong He

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

9 citing papers in PubMed, 11 citations in OpenAlex.

  1. MIR31HG Modulates IL-4 Secretion by Keratinocytes and M2-Like Macrophage Polarization to Promote Local Immunosuppression in Condyloma Acuminata.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2026
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  7. Host gene and its guest: short story about relation of long-noncodingReports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation Oncology · 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

5 authors at 1 institution in 1 country.

Bo FengDepartment of Otorhinolaryngology, The Affiliated Hospital of Medical School of Ningbo University, Ningbo City, China.
Ke ChenDepartment of Radiochemotherapy, Yinzhou Hospital Affiliated to Medical School of Ningbo University, Ningbo City, China.
Weiwei ZhangDepartment of Otorhinolaryngology, The Affiliated Hospital of Medical School of Ningbo University, Ningbo City, China.
Qi ZhengDepartment of Otorhinolaryngology, The Affiliated Hospital of Medical School of Ningbo University, Ningbo City, China.
Yong HeDepartment of Otorhinolaryngology, The Affiliated Hospital of Medical School of Ningbo University, Ningbo City, China.ORCID https://orcid.org/0000-0003-3601-5274
Ningbo University · CN

Funding

Medical Health Science and Technology Project of Zhejiang Provincial Health Commission 2020KY847
6 · The paper itself

Abstract

backgroundMIR31HG has been affirmed to regulate the tumorigenesis of head-neck squamous cell carcinoma (HNSC). This study aims to reveal the function of MIR31HG in nasopharyngeal carcinoma (NPC), which falls into the category of HNSC.

methodsMIR31HG expression pattern in HNSC tissues was predicted by starBase. FISH and qRT-PCR were employed to detect MIR31HG expression in NPC tissues and to analyze the association between MIR31HG and clinicopathological features. NPC cell viability, colony formation, and apoptosis were measured by MTT assay, colony formation assay, and flow cytometry. The expressions of protein kinase B (AKT), phosphorylated (p)-AKT, phosphoinositide 3-kinases (PI3K) and p-PI3K in NPC cells were analyzed by Western blot. The correlation between MIR31HG expression and AKT1 mRNA expression was analyzed by The Cancer Genome Atlas and starBase.

resultsMIR31HG was highly expressed in HNSC tissues and NPC tissues. Meanwhile, the association between high MIR31HG expression and aggressive clinicopathological traits was significant in NPC patients at tumor stage III-IV (T3-T4) and in those with lymph node metastasis 1-2 (N1-N2). Silencing of MIR31HG suppressed NPC cell viability and colony formation, promoted apoptosis, and decreased the expressions of p-PI3K, and p-AKT. 740Y-P reversed the above effects of si-MIR31HG on NPC cells. Besides, MIR31HG expression was positively correlated with AKT1 mRNA expression in HNSC patients.

conclusionMIR31HG silencing promotes NPC cell proliferation and inhibits apoptosis through suppressing the PI3K/AKT signaling pathway.

Indexed as

MicroRNAsNasopharyngeal NeoplasmsRNA, Long NoncodingApoptosisCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansNasopharyngeal CarcinomaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, MessengerSignal TransductionMicroRNAsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long NoncodingRNA, MessengerapoptosisMIR31HGnasopharyngeal carcinomaPI3K/AKT signaling pathwayproliferation

Identifiers

PMID36347827
PMCPMC9757018
OpenAlexW4308564880

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.