Evidence map›Paper›PMID 33687144›Full record

ArticleThoracic cancer2021

LncRNA FAM83A-AS1 promotes lung adenocarcinoma progression by enhancing the pre-mRNA stability of FAM83A.

Wenyi Wang, Zhunlin Zhao, Chun Xu, Chang Li, Cheng Ding, Jun Chen, Tengfei Chen, Jun Zhao

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2021. 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
1.9field-weighted citation impact, top 14% 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, 26 citations in OpenAlex.

  1. Metamorphosis and lncRNAs: A Close Relationship.Genesis (New York, N.Y. : 2000) · 2026
    Review
  2. Article
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  5. Review
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  7. Review
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  10. FAM83A antisense RNA 1 (Bioengineered · 2022
    Article
  11. Article
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  15. Article
  16. Natural antisense transcripts as drug targets.Frontiers in molecular biosciences · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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

8 authors at 1 institution in 1 country.

Wenyi WangDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Medical College of Soochow University, Suzhou, China.
Zhunlin ZhaoDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Medical College of Soochow University, Suzhou, China.
Chun XuDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Medical College of Soochow University, Suzhou, China.
Chang LiDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Medical College of Soochow University, Suzhou, China.
Cheng DingDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Medical College of Soochow University, Suzhou, China.
Jun ChenDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Medical College of Soochow University, Suzhou, China.
Tengfei ChenDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Medical College of Soochow University, Suzhou, China.
Jun ZhaoDepartment of Thoracic Surgery, The First Affiliated Hospital of Soochow University, Medical College of Soochow University, Suzhou, China.ORCID 0000-0003-3846-8998
Soochow University · CN

Funding

National Natural Science Foundation of China 81672934National Natural Science Foundation of China 81873417
6 · The paper itself

Abstract

backgroundLung cancer is the leading cause of cancer deaths worldwide. Long non-coding RNAs (lncRNAs) affect a series of cellular biological processes, including oncogene function promotion. In this study, we explored the functions and mechanisms of FAM83A antisense RNA 1 (FAM83A-AS1) in non-small cell lung cancer (NSCLC) progression.

methodsThe expression of FAM83A-AS1and FAM83A mRNA was analyzed using the Cancer Genome Atlas (TCGA) data. Proliferation, migration, invasion and Western blotting were measured after treatment with overexpressed or knockdown FAM83A-AS1. To determine the relationship between FAM83A-AS1 and FAM83A, RNase protection assay (RPA), amanitin treatment, RNA pulldown assay and RNA immunoprecipitation (RIP) assay were performed.

resultsHigh expression of FAM83A-AS1 in lung adenocarcinoma (LUAD) was closely associated with low overall survival (OS) and progression-free survival (PFS). Functionally, high FAM83A-AS1 expression increased LUAD cell proliferation and metastasis, indicating that FAM83A-AS1 exerted its oncogenic functions. Furthermore, FAM83A-AS1 promoted NSCLC progression via ERK signaling pathways. Mechanistically, FAM83A-AS1 post-transcriptionally increased FAM83A expression by enhancing pre-mRNA stability. FAM83A-AS1 enhanced FAM83A mRNA stability not only by forming an RNA duplex but also by binding to FBL.

conclusionsWe determined that FAM83A-AS1 increased FAM83A expression by enhancing FAM83A pre-mRNA stability and promoted the tumorigenesis of LUAD.

Indexed as

Adenocarcinoma of LungDisease ProgressionHumansLung NeoplasmsNeoplasm ProteinsRNA, Long NoncodingTransfectionFAM83A protein, humanNeoplasm ProteinsRNA, Long NoncodingFAM83AFAM83A-AS1lncRNALUAD

Identifiers

PMID33687144
PMCPMC8107032
OpenAlexW3135074908

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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.