Evidence map›Paper›PMID 37277890›Full record

ArticleThoracic cancer2023

FOXA1-induced LINC00621 promotes lung adenocarcinoma progression via activating the TGF-β signaling pathway.

Jingjing Wei, Haiyang Yu, Tan Liu, Ziming Wang, Chuandong Lang, Yueyin Pan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Thoracic cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Observational
  2. Review
  3. 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

6 authors at 2 institutions in 1 country.

Jingjing WeiDepartment of Tumor Chemotherapy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Haiyang YuDepartment of Tumor Chemotherapy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0002-4085-9472
Tan LiuDepartment of Medical Oncology, 901 Hospital of Joint Logistics Support Force of People Liberation Army, Hefei, China.ORCID 0000-0002-9620-7166
Ziming WangDepartment of Tumor Chemotherapy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Chuandong LangDepartment of Orthopedics, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Yueyin PanDepartment of Tumor Chemotherapy, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0003-0532-5368
University of Science and Technology of China · CN117th Hospital of People's Liberation Army · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLung adenocarcinoma (LUAD) is highly malignant and associated with poor prognoses in patients worldwide. There has been widespread recognition that lncRNAs are tightly linked to LUAD tumorigenesis and development. Here, we identified that the LINC00621 level was increased in LUAD tissues and concerned with the poor prognoses in LUAD patients.

methodsBioinformatical analysis and RT-qPCR determined the level of LINC00621 in LUAD tissues and cell lines. The admeasurement of the proliferation, migration, and invasion abilities of LUAD cells was utilized in the CCK8 and Transwell formulas. Luciferase reporter assay was used to corroborate the downstream target genes of LINC00621. The phosphorylated SMAD3 protein was tested by Western blotting assay. The impression of LINC00621 knockdown on LUAD tumor growth and metastasis put into effect by murine models. ChIP-qPCR assay was carried out to verify the transcriptional regulation by FOXA1 on LINC00621.

resultsIn vitro, the knockdown of LINC00621 significantly reduced the proliferative, migrating, and invasive abilities, the same was true for tumorigenesis and metastasis in vivo. MiR-34a-5p as a straight target of LINC00621 was ascertained, and LUAD patients with inferior miR-34a-5p levels had undesirable prognoses. Furthermore, TGFBR1 is an immediate and functional connection site of miR-34a-5p. Collectively, LINC00621 can sponge miR-34a-5p and upregulate TGFBR1 levels, which further sensitized TGF-β signaling pathway. Finally, it was revealed that FOXA1 transcriptionally upregulated LINC00621.

conclusionThis study uncovered that FOXA1-induced LINC00621 promotes LUAD progression via the miR-34a-5p/TGFBR1/TGF-β axis, and is one novel therapeutic target that may be used in LUAD treatment.

Indexed as

AdenocarcinomaLung NeoplasmsMicroRNAsRNA, Long NoncodingAnimalsCarcinogenesisCell Line, TumorCell MovementCell ProliferationCell Transformation, NeoplasticGene Expression Regulation, NeoplasticHepatocyte Nuclear Factor 3-alphaHumansLungMiceReceptor, Transforming Growth Factor-beta Type IFOXA1 protein, humanHepatocyte Nuclear Factor 3-alphaMicroRNAsReceptor, Transforming Growth Factor-beta Type IRNA, Long NoncodingTransforming Growth Factor betaFOXA1LINC00621lung adenocarcinomaMiR-34a-5pTGF-β

Identifiers

PMID37277890
PMCPMC10363846
OpenAlexW4379508550

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

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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.