Evidence map›Paper›PMID 31157169›Full record

ArticleFrontiers in oncology2019

The Oncogene IARS2 Promotes Non-small Cell Lung Cancer Tumorigenesis by Activating the AKT/MTOR Pathway.

Xin Di, Xin Jin, He Ma, Ruimin Wang, Shan Cong, Chang Tian, Jiaying Liu, Min Zhao, Ranwei Li, Ke Wang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

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  6. [Expression of YARS1 in hepatocellular carcinoma and its prognostic effect].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Article
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  17. tRNA Metabolism and Lung Cancer: Beyond Translation.Frontiers in molecular biosciences · 2021
    Review
  18. Article
  19. 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

10 authors at 1 institution in 1 country.

Xin DiDepartment of Respiratory Medicine, The Second Hospital of Jilin University, Changchun, China.
Xin JinDepartment of Respiratory Medicine, The Second Hospital of Jilin University, Changchun, China.
He MaDepartment of Anesthesiology, The Second Hospital of Jilin University, Changchun, China.
Ruimin WangDepartment of Operation Room, The Second Hospital of Jilin University, Changchun, China.
Shan CongDepartment of Respiratory Medicine, The Second Hospital of Jilin University, Changchun, China.
Chang TianDepartment of Respiratory Medicine, The Second Hospital of Jilin University, Changchun, China.
Jiaying LiuDepartment of Respiratory Medicine, The Second Hospital of Jilin University, Changchun, China.
Min ZhaoDepartment of Respiratory Medicine, The Second Hospital of Jilin University, Changchun, China.
Ranwei LiDepartment of Urinary Surgery, The Second Hospital of Jilin University, Changchun, China.
Ke WangDepartment of Respiratory Medicine, The Second Hospital of Jilin University, Changchun, China.
Second Affiliated Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A limited number of studies have indicated an association between isoleucyl-tRNA synthetase 2 (IARS2) and tumorigenesis. We evaluated IARS2 protein expression in lung tumor tissues and paired non-tumor tissues. We found higher IARS2 expression in the tumor tissues, which was associated with the late Tumor and Node stages of the Tumor, Node, Metastasis staging system. Silencing IARS2 inhibited the activity of A549 and H1299 cells, resulting in G0/G1 stasis of A549 cells and mitochondrial apoptosis. IARS2 silencing was also found to inhibit NSCLC tumor growth in nude mice. Complementary DNA microarray analysis revealed 742 differentially expressed genes (507 upregulated and 235 downregulated) in IARS2-silenced A549 cells compared to controls. Ingenuity Pathway Analysis of the differential expression data suggested that multiple pathways are associated with IARS2 silencing in NSCLC cells; upstream analysis predicted the activation or inhibition of transcriptional regulators. Correlation analysis revealed that AKT and MTOR activities were significantly inhibited in IARS2-silenced cells, but were partially restored by the AKT-stimulating agent SC79. IARS2 appears to regulate lung cancer cell proliferation via the AKT/MTOR pathway. Our results help clarify the complex roles of IARS2 in tumorigenesis and suggest that it may be a novel regulator of lung cancer development.

Indexed as

AKTcDNA microarrayingenuity pathway analysisisoleucyl-tRNA synthetase 2lung cancermammalian target of rapamycintumorigenesis

Identifiers

PMID31157169
PMCPMC6528107
OpenAlexW2945826391

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.