Evidence map›Paper›PMID 33603394›Full record

ArticleOncoTargets and therapy2021

LncRNA WT1-AS/miR-494-3p Regulates Cell Proliferation, Apoptosis, Migration and Invasion via PTEN/PI3K/AKT Signaling Pathway in Non-Small Cell Lung Cancer.

Chaohui Wu, Jiansheng Yang, Rongbin Li, Xianbin Lin, Jiayun Wu, Jingyang Wu

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in OncoTargets and therapy, 2021. 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 It has been retracted, and should not be counted.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 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.1field-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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
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  7. Review
  8. RAS‑stimulated release of exosomalInternational journal of molecular medicine · 2023
    Article
  9. Review
  10. Role of microRNA-494 in tumor progression.American journal of translational research · 2023
    Review
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  12. Review
  13. Article
  14. Extracellular Polysaccharide fromJournal of clinical and translational hepatology · 2022
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Chaohui WuDepartment of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, 362000, People's Republic of China.
Jiansheng YangDepartment of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, 362000, People's Republic of China.
Rongbin LiDepartment of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, 362000, People's Republic of China.
Xianbin LinDepartment of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, 362000, People's Republic of China.
Jiayun WuDepartment of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, 362000, People's Republic of China.
Jingyang WuDepartment of Thoracic and Cardiovascular Surgery, The Second Affiliated Hospital of Fujian Medical University, Quanzhou, Fujian Province, 362000, People's Republic of China.
Fujian Medical University · CNSecond Affiliated Hospital of Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNon-small cell lung cancer (NSCLC) is one of the most common malignancies with the highest morbidity and mortality worldwide. Long non-coding RNAs (lncRNAs) are recently recognized as noteworthy regulators of different tumors, counting NSCLC. However, the biological functions and regulatory mechanism of lncRNA WT1-AS in NSCLC progression still stay uninvestigated.

methodsWT1-AS and miR-494-3p levels in NSCLC cell lines were detected by real-time quantitative polymerase chain reaction (RT-qPCR). In the current study, the regulatory effects of WT1-AS/miR-494-3p axis on cellular behaviors of NSCLC cell lines (A549 and NCI-H1975) were evaluated by a variety of methods. Cell counting kit-8 (CCK-8) and EDU assays were adopted to assess NSCLC cell proliferation. Tunnel staining and flow cytometry assay were applied to determine cell apoptosis and cell cycle distribution. Besides, cell migration and invasion abilities were analyzed by performing wound healing and transwell assays. Meanwhile, the levels of key proteins related to NSCLC cell apoptosis and PTEN/PI3K/AKT pathway were examined using Western blot assay. In addition, luciferase reporter assays were used to determine the interaction between WT1-AS and miR-494-3p or miR-494-3p and PTEN.

resultsVisibly downregulated WT1-AS in NSCLC cell lines was obtained from Broad Institute Cancer Cell Line Encyclopedia (CCLE) database and further verified by performing RT-qPCR. Besides, miR-494-3p was the downstream target gene of WT1-AS and obviously upregulated miR-494-3p in NSCLC cell lines was confirmed. WT1-AS overexpression suppressed cell proliferation, migration and invasion abilities while enhanced cell apoptosis of A549 and NCI-H1975 cells. Furthermore, upregulation of miR-494-3p distinctly reversed these inhibitory effects of WT1-AS overexpression on the tumorigenesis and progression of NSCLC. In addition, WT1-AS promoted PTEN expression and thereby inhibited activation of PI3K/AKT pathway by sponging miR-494-3p.

conclusionTo conclude, lncRNA WT1-AS impeded cell proliferation, migration, invasion but accelerated cell apoptosis via negatively regulating miR-494-3p to mediate PTEN/PI3K/AKT pathway in NSCLC.

Indexed as

lncRNA WT1-ASmiR-494-3pnon-small cell lung cancer; NSCLCPTEN/PI3K/AKTtumor progression

Identifiers

PMID33603394
PMCPMC7881945
OpenAlexW3127536043

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.