Evidence map›Paper›PMID 35313900›Full record

ArticleJournal of cardiothoracic surgery2022

CTHRC1 targeted by miR-30a-5p regulates cell adhesion, invasion and migration in lung adenocarcinoma.

Chaomian Yang, Tianxia Huang, Yue Liang, Yanlong Xue, Ying Liang, Xianqin Wei, Fangchan Meng, Qiu Wei

Open access · goldAbstract read
In one paragraph

Article in Journal of cardiothoracic surgery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Tumor-suppressive action of miR-30a-5p in lung adenocarcinoma correlates with ABL2 inhibition and PI3K/AKT pathway inactivation.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2024
    Article
  6. 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.

Chaomian YangDepartment of Respiratory Medicine, The First People's Hospital of Nanning, No. 89 Qixing Road, Nanning, 530022, China.
Tianxia HuangDepartment of Respiratory Medicine, The First People's Hospital of Nanning, No. 89 Qixing Road, Nanning, 530022, China.
Yue LiangDepartment of Respiratory Medicine, The First People's Hospital of Nanning, No. 89 Qixing Road, Nanning, 530022, China.
Yanlong XueDepartment of Respiratory Medicine, The First People's Hospital of Nanning, No. 89 Qixing Road, Nanning, 530022, China.
Ying LiangDepartment of Respiratory Medicine, The First People's Hospital of Nanning, No. 89 Qixing Road, Nanning, 530022, China.
Xianqin WeiDepartment of Respiratory Medicine, The First People's Hospital of Nanning, No. 89 Qixing Road, Nanning, 530022, China.
Fangchan MengDepartment of Respiratory Medicine, The First People's Hospital of Nanning, No. 89 Qixing Road, Nanning, 530022, China.
Qiu WeiDepartment of Respiratory Medicine, The First People's Hospital of Nanning, No. 89 Qixing Road, Nanning, 530022, China. drweiqiu@163.com.
First People's Hospital of Nanning · CN

Funding

Respiratory medicine is a key discipline of Guangxi medical and health care 2021QZD01
6 · The paper itself

Abstract

The morbidity of lung cancer ranks first among all cancers. Lung adenocarcinoma (LUAD) is a classification of lung cancer, and cell invasion and migration of LUAD are the main causes for its high mortality. Therefore, further exploring the potential mechanism of LUAD metastasis may provide bases for following targeted drug development and treatment of LUAD. In this study, clinical data as well as gene expression profiles were obtained from TCGA-LUAD and GEO to analyze CTHRC1 expression. The result found that CTHRC1 was significantly high in LUAD. Similar results were also discovered in 4 cancer cell lines. Moreover, overexpressed/knock-down CTHRC1 cell lines were constructed. It was uncovered that overexpressing CTHRC1 promoted LUAD cell migration and invasion, and inhibited cell adhesion, while knocked down CTHRC1 had the opposite effect. Afterward, the upstream miRNAs that regulated CTHRC1 were predicted by several bioinformatics websites. It was testified by dual-luciferase method that CTHRC1 was negatively mediated by miR-30a-5p. Overexpressed miR-30a-5p suppressed cell invasion/migration, and increased cell adhesion, while overexpressing CTHRC1 as well reversed such impacts. In conclusion, it was disclosed in this study that CTHRC1 worked as a cancer promoter in LUAD, and miR-30a-5p could target and downregulate CTHRC1 to regulate cell adhesion, and inhibited LUAD cell invasion and migration. These results elucidated at cellular level that upregulated CTHRC1 may be a marker protein for LUAD metastasis.

Indexed as

Adenocarcinoma of LungExtracellular Matrix ProteinsLung NeoplasmsMicroRNAsCell AdhesionCell ProliferationGene Expression Regulation, NeoplasticHumansCTHRC1 protein, humanExtracellular Matrix ProteinsMicroRNAsMIRN30a microRNA, humanCell adhesionCTHRC1Invasion and migrationLUADmiR-30a-5p

Identifiers

PMID35313900
PMCPMC8935819
OpenAlexW4221108626

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.