Evidence map›Paper›PMID 34174897›Full record

ArticleCancer cell international2021

ARHGAP10 inhibits the epithelial-mesenchymal transition of non-small cell lung cancer by inactivating PI3K/Akt/GSK3β signaling pathway.

Lan-Lan Lin, Fan Yang, Dong-Huan Zhang, Cong Hu, Sheng Yang, Xiang-Qi Chen

Open access · goldAbstract read
In one paragraph

Article in Cancer cell international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 11 citations in OpenAlex.

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  7. ATM-Inhibitor AZD1390 Is a Radiosensitizer for Breast Cancer CNS Metastasis.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023
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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 1 institution in 1 country.

Lan-Lan LinDepartment of Respiratory Medicine, Fujian Medical University Union Hospital, Fuzhou, 350001, Fujian, People's Republic of China.
Fan YangDepartment of Respiratory Medicine, Fujian Medical University Union Hospital, Fuzhou, 350001, Fujian, People's Republic of China.
Dong-Huan ZhangDepartment of Oncology, Fujian Medical University Union Hospital, Fuzhou, 350001, Fujian, People's Republic of China.
Cong HuDepartment of Respiratory Medicine, Fujian Medical University Union Hospital, Fuzhou, 350001, Fujian, People's Republic of China.
Sheng YangDepartment of Oncology, Fujian Medical University Union Hospital, Fuzhou, 350001, Fujian, People's Republic of China. dryangxh@126.com.
Xiang-Qi ChenDepartment of Respiratory Medicine, Fujian Medical University Union Hospital, Fuzhou, 350001, Fujian, People's Republic of China. chxqq@fjmu.edu.cn.ORCID http://orcid.org/0000-0002-8054-3800
Fujian Medical University · CN

Funding

Fujian Medical Innovation Grant 2020CXB016the Science Technology Innovation Joint Project Foundation of Fujian Province 2017Y9003the Science Technology Innovation Joint Project Foundation of Fujian Province 2018Y9038
6 · The paper itself

Abstract

backgroundRho GTPase activating protein 10 (ARHGAP10) has been implicated as an essential element in multiple cellular process, including cell migration, adhesion and actin cytoskeleton dynamic reorganization. However, the correlation of ARHGAP10 expression with epithelial-mesenchymal transition (EMT) in lung cancer cells is unclear and remains to be elucidated. Herein, we investigated the relationship between the trait of ARHGAP10 and non-small cell lung cancer (NSCLC) pathological process.

methodsImmunohistochemistry was conducted to evaluate the expression of ARHGAP10 in NSCLC tissues. CCK-8 assays, Transwell assays, scratch assays were applied to assess cell proliferation, invasion and migration. The expression levels of EMT biomarkers and active molecules involved in PI3K/Akt/GSK3β signaling pathway were examined through immunofluorescence and Western blot.

resultsARHGAP10 was detected to be lower expression in NSCLC tissues compared with normal tissues from individuals. Moreover, overexpression of ARHGAP10 inhibited migratory and invasive potentials of A549 and NCI-H1299 cells. In addition, ARHGAP10 directly mediated the process of EMT via PI3K/Akt/GSK3β pathway. Meanwhile, activation of the signaling pathway of insulin-like growth factors-1 (IGF-1) reversed ARHGAP10 overexpression regulated EMT in NSCLC cells.

conclusionARHGAP10 inhibits the epithelial-mesenchymal transition in NSCLC via PI3K/Akt/GSK3β signaling pathway, suggesting agonist of ARHGAP10 may be an optional remedy for NSCLC patients than traditional opioids.

Indexed as

ARHGAP10Epithelial–mesenchymal transitionNon-small cell lung cancerPI3K/Akt/GSK3β

Identifiers

PMID34174897
PMCPMC8236192
OpenAlexW3177063564

What OpenQuestion holds

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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.