Evidence map›Paper›PMID 38151913›Full record

ArticleThoracic cancer2024

GIMAP7 inhibits epithelial-mesenchymal transition and glycolysis in lung adenocarcinoma cells via regulating the Smo/AMPK signaling pathway.

Liyuan Cui, Yumei Shen, Shanzhou Duan, Qifeng Ding, Yifei Wang, Wentao Yang, Yongbing Chen

Open access · goldAbstract read
In one paragraph

Article in Thoracic cancer, 2024. 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
0.7field-weighted citation impact, top 22% 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

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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, 3 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Liyuan CuiDepartment of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0009-0008-7792-3715
Yumei ShenOperation Room Department, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Shanzhou DuanDepartment of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Qifeng DingDepartment of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Yifei WangDepartment of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Wentao YangDepartment of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0003-1957-3661
Yongbing ChenDepartment of Thoracic Surgery, The Second Affiliated Hospital of Soochow University, Suzhou, China.ORCID 0000-0002-7595-092X
Soochow University · CN

Funding

Discipline construction project of the Second Affiliated Hospital of Soochow University XKTJ-XK202004Gusu Health Leading Talent Program of Suzhou GSWS2021020Jiangsu Key Research and Development Plan (Social Development) Project BE2020653Key Scientific Program of Jiangsu Provincial Health Commission ZD2021033National Natural Science Foundation of China 82172076Scientific Program of Suzhou Municipal Health and Health Committee LCZX202004
6 · The paper itself

Abstract

backgroundGTPase immunity-associated protein 7 (GIMAP7) has been previously recognized as a prognostic marker in pan-cancer. Our objective was to explore the function of GIMAP7 in the progression of lung adenocarcinoma (LUAD).

methodsGIMAP7 was overexpressed by transfection with GIMAP7 plasmid, and knocked down using siRNAs. The biological functions of GIMAP7 were examined by employing CCK-8, EdU, colony formation, flow cytometry, wound healing, and transwell assays. The effects of GIMAP7 on the extracellular acidification rate (ECAR), oxygen consumption rate (OCR), lactate production, and glucose uptake were evaluated. In addition, the related mRNA and protein expression was detected employing immunohistochemical, western blot, and qRT-PCR. A xenograft tumor model was established in nude mice to evaluate the effects of GIMAP7 on tumor growth.

resultsGIMAP7 was lowly expressed in LUAD tissues and cells. GIMAP7 inhibited the proliferation, mobility, EMT, glycolysis, but promoted apoptosis in LUAD cells. Moreover, we also confirmed that GIMAP7 suppressed Smo/AMPK signaling in LUAD cells. By adding the Smo agonist SAG and AMPK agonist GSK621, the results of rescue experiments further verified that GIMAP7 played a role in LUAD inhibition through inhibition of the Smo/AMPK signaling pathway. Furthermore, the role of GIMAP7 in inhibiting tumor growth was verified in vivo.

conclusionsThese results demonstrate that GIMAP7 could inhibit cell proliferation, mobility and glycolysis, but accelerate apoptosis via repressing the Smo/AMPK signaling pathway in LUAD.

Indexed as

Adenocarcinoma of LungLung NeoplasmsAMP-Activated Protein KinasesAnimalsCell Line, TumorCell ProliferationDisease Models, AnimalEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticGlycolysisGTP-Binding ProteinsGTP PhosphohydrolasesHumansMiceMice, NudeSignal TransductionAMP-Activated Protein KinasesGIMAP7 protein, humanGTP-Binding ProteinsGTP Phosphohydrolasesepithelial-mesenchymal transitionGIMAP7glycolysislung adenocarcinomaSmo/AMPK signaling

Identifiers

PMID38151913
PMCPMC10834198
OpenAlexW4390341499

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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.