Evidence map›Paper›PMID 38622149›Full record

ArticleScientific reports2024

RACGAP1 promotes lung cancer cell proliferation through the PI3K/AKT signaling pathway.

Zhiyang Xu, Shaohang Wu, Jiahua Tu, Mingyang Wang, Weicheng Liang, Jiangdong Cheng, Jun Guan, Jianxin Xu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
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  4. 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

8 authors at 2 institutions in 1 country.

Zhiyang XuDepartment of Thoracic Surgery, The First Hospital of Putian, The School of Clinical Medicine, Fujian Medical University Putian, Fujian, 351100, China.
Shaohang WuDepartment of Thoracic Surgery, The First Hospital of Putian, The School of Clinical Medicine, Fujian Medical University Putian, Fujian, 351100, China.
Jiahua TuDepartment of Thoracic Surgery, The First Hospital of Putian, The School of Clinical Medicine, Fujian Medical University Putian, Fujian, 351100, China.
Mingyang WangDepartment of Thoracic Surgery, The First Hospital of Putian, The School of Clinical Medicine, Fujian Medical University Putian, Fujian, 351100, China.
Weicheng LiangDepartment of Thoracic Surgery, The First Hospital of Putian, The School of Clinical Medicine, Fujian Medical University Putian, Fujian, 351100, China.
Jiangdong ChengDepartment of Thoracic Surgery, The First Hospital of Putian, The School of Clinical Medicine, Fujian Medical University Putian, Fujian, 351100, China.
Jun GuanDepartment of Thoracic Surgery, The First Hospital of Putian, The School of Clinical Medicine, Fujian Medical University Putian, Fujian, 351100, China. guanjun69888@126.com.
Jianxin XuDepartment of Thoracic Surgery, The First Hospital of Putian, The School of Clinical Medicine, Fujian Medical University Putian, Fujian, 351100, China. xujianxin8210@126.com.
Putian University · CNFujian Medical University · CN

Funding

Fujian Provincial Health Commission for Young and Middle-aged training Program 2020GGB050
6 · The paper itself

Abstract

We aimed to investigate the expression and clinic significance of Rac GTPase Activating Protein 1 (RACGAP1) in human lung adenocarcinoma (LUAD). Online database analysis revealed a significant increase in RACGAP1 mRNA expression among 26 types of tumor tissues, including LUAD tissues. Online database and tissue microarray analyses indicated that RACGAP1 expression was significantly upregulated in LUAD tissues. Genetic variation analysis identified four different genetic variations of RACGAPs in LUAD. Moreover, online database analysis showed that RACGAP1 upregulation was correlated with shorter survival in patients with LUAD. After silencing RACGAP1 expression in A549 cells using siRNA and assessing its protein levels via Western blotting, we found that RACGAP1 knockdown inhibited cell growth and induced apoptosis determined using the Cell Counting Kit-8 assay, colony formation assay, and flow cytometry. Mechanistically, western blot analysis indicated that Bax expression increased, whereas Bcl-2 expression decreased. Moreover, RACGAP1 knockdown attenuated PI3K/AKT pathway activation in lung cancer cells. Taken together, our findings showed that RACGAP1 was overexpressed in LUAD tissues and played an important role in lung cancer by increasing cell growth through the PI3K/AKT signaling pathway. This study suggests recommends evaluating RACGAP1 in clinical settings as a novel biomarker and potential therapeutic target for lung cancer.

Indexed as

Adenocarcinoma of LungLung NeoplasmsCell Line, TumorCell MovementCell ProliferationGene Expression Regulation, NeoplasticHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktApoptosisLung adenocarcinomaProliferationRACGAP1Survival

Identifiers

PMID38622149
PMCPMC11018837
OpenAlexW4394821538

What OpenQuestion holds

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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.