Evidence map›Paper›PMID 29620222›Full record

ArticleOncology reports2018

miR‑29a suppresses IL‑13‑induced cell invasion by inhibiting YY1 in the AKT pathway in lung adenocarcinoma A549 cells.

Yu Zhang, Shujin He, Renmei Mei, Yurong Kang, Jing Duan, Ran Wei, Chuqi Xiang, Yemeng Wu, Xiangtong Lu, Zhenyu Cai and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 33 citations in OpenAlex.

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  11. Basophils as a potential therapeutic target in cancer.Journal of Zhejiang University. Science. B · 2021
    Review
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  15. Alkaloid Extract ofEvidence-based complementary and alternative medicine : eCAM · 2021
    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

11 authors at 1 institution in 1 country.

Yu ZhangDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Shujin HeDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Renmei MeiDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Yurong KangDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Jing DuanDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Ran WeiDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Chuqi XiangDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Yemeng WuDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Xiangtong LuDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Zhenyu CaiDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Lixia XiongDepartment of Pathophysiology, Medical College, Nanchang University, Nanchang, Jiangxi 330006, P.R. China.
Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL‑13 is a proinflammatory cytokine associated with multiple pathological conditions and the promotion of metastasis in lung cancer. Previous studies have demonstrated that IL‑13 and YY1 are associated with PI3K/AKT signaling. In addition, miR‑29a has been found to play a critical role in cell invasion in lung cancer. However, the molecular mechanism of miR‑29a underlying its involvement in IL‑13‑induced lung cancer cell invasion remains largely unknown. In the present study, we aimed to investigate the role of miR‑29a in cell invasion mediated by IL‑13 in lung cancer. By using MTT and wound‑scratch assays, we assessed cell proliferation and migration induced by IL‑13, and identified activation of the PI3K/AKT/YY1 pathway. Inhibition of PI3K/AKT by LY294002 downregulated IL‑13‑induced YY1 expression. Furthermore, we found that miR‑29a directly targets YY1 and suppressed its expression in lung cancer. By using MTT, flow cytometry and Transwell assays, overexpression of miR‑29a restricted both YY1 and N‑cadherin expression, and inhibited IL‑13‑induced invasion of lung cancer A549 cells. Taken together, these findings demonstrate that PI3K/AKT/YY1 is involved in the regulation of lung cancer cell behavior induced by IL‑13, and miR‑29a represents a promising therapeutic target.

Indexed as

A549 CellsAdenocarcinomaAdenocarcinoma of LungCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansInterleukin-13Lung NeoplasmsMicroRNAsNeoplasm InvasivenessProto-Oncogene Proteins c-aktSignal TransductionYY1 Transcription FactorInterleukin-13MicroRNAsMIRN29a microRNA, humanProto-Oncogene Proteins c-aktYY1 protein, humanYY1 Transcription Factor

Identifiers

PMID29620222
PMCPMC5983933
OpenAlexW2796166634

What Socratic 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 Socratic graph.