Evidence map›Paper›PMID 36631800›Full record

ArticleJournal of translational medicine2023

AFAP1L1 promotes gastric cancer progression by interacting with VAV2 to facilitate CDC42-mediated activation of ITGA5 signaling pathway.

Bo Sun, Bai Ding, Yu Chen, Chuang Peng, Xu Chen

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 16 citations in OpenAlex.

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  8. MultiZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
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  16. Aldo-keto Reductase 1B10 Restrains Cell Migration, Invasion, and Adhesion of Gastric Cancer via Regulating Integrin Subunit Alpha 5.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 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

5 authors at 1 institution in 1 country.

Bo SunDepartment of Hepatobiliary Surgery, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, No. 61 Jiefang West Road, Changsha, 410005, Hunan, China.
Bai DingDepartment of Hepatobiliary Surgery, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, No. 61 Jiefang West Road, Changsha, 410005, Hunan, China.
Yu ChenDepartment of Hepatobiliary Surgery, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, No. 61 Jiefang West Road, Changsha, 410005, Hunan, China.
Chuang PengDepartment of Hepatobiliary Surgery, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, No. 61 Jiefang West Road, Changsha, 410005, Hunan, China. pengchuangcn@163.com.
Xu ChenDepartment of Hepatobiliary Surgery, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, No. 61 Jiefang West Road, Changsha, 410005, Hunan, China. chenxu941218@163.com.ORCID 0000-0003-3743-5043
Hunan Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe actin filament-associated protein (AFAP) family genes include AFAP1/AFAP-110, AFAP1L1 and AFAP1L2/XB130. Increasing evidence indicates these three AFAP family members participate in tumor progression, but their clinical significance and molecular mechanisms in gastric cancer (GC) remain unclear.

methodsWe first analyzed expression of AFAP family genes using public datasets and verified the results. The clinical significance of AFAP family genes in GC patients was also analyzed. In vitro and in vivo experiments were applied to explore the function of AFAP1L1. Enrichment analysis was used to explore potential molecular mechanisms. We then performed additional experiments, such as cell adhesion assay, co-immunoprecipitation and so on to confirm the downstream molecular mechanisms of AFAP1L1.

resultsPublic data analyses and our verification both showed AFAP1L1 was the only AFAP family members that was significantly upregulated in GC compared with normal gastric tissues. Besides, only AFAP1L1 could predict poor prognosis and act as an independent risk factor for GC patients. In addition, AFAP1L1 promotes GC cells proliferation, migration, invasion in vitro and tumor growth, metastasis in vivo by inducing epithelial-to-mesenchymal transition (EMT). In terms of mechanism, AFAP1L1 interacts with VAV guanine nucleotide exchange factor 2 (VAV2) to activate Rho family GTPases CDC42, which finally promotes expression of integrin subunit alpha 5 (ITGA5) and activation of integrin signaling pathway.

conclusionAFAP1L1 promotes GC progression by inducing EMT through VAV2-mediated activation of CDC42 and ITGA5 signaling pathway, indicating AFAP1L1 may be a promising prognostic biomarker and therapeutic target for GC patients.

Indexed as

Stomach NeoplasmsAdaptor Proteins, Signal Transducingcdc42 GTP-Binding ProteinCell Line, TumorCell MovementCell ProliferationEpithelial-Mesenchymal TransitionHumansIntegrinsMicrofilament ProteinsNeoplasm InvasivenessProto-Oncogene Proteins c-vavSignal TransductionAdaptor Proteins, Signal TransducingAFAP1L1 protein, humancdc42 GTP-Binding ProteinCDC42 protein, humanIntegrinsITGA5 protein, humanMicrofilament ProteinsProto-Oncogene Proteins c-vavVAV2 protein, humanActin filament associated protein 1 like 1Epithelial-mesenchymal transitionGastric cancerIntegrin subunit alpha 5

Identifiers

PMID36631800
PMCPMC9835296
OpenAlexW4315645571

What Socratic 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 Socratic graph.