Evidence map›Paper›PMID 39976859›Full record

ArticleMolecular biotechnology2026

The Role of Yes-Associated Protein in Autophagy and Tumor Progression in Gastric Cancer.

Yanzhao Jin, Hua Cheng, Xiaoyun Hu, Jiaqing Cao

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Article in Molecular biotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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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

4 authors.

Yanzhao JinDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, No.1 Minde Road, Nanchang, 330006, Jiangxi, China. 15979031916@sohu.com.ORCID http://orcid.org/0009-0003-7945-1487
Hua ChengDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, No.1 Minde Road, Nanchang, 330006, Jiangxi, China.
Xiaoyun HuDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, No.1 Minde Road, Nanchang, 330006, Jiangxi, China.
Jiaqing CaoDepartment of General Surgery, The Second Affiliated Hospital of Nanchang University, No.1 Minde Road, Nanchang, 330006, Jiangxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Yes-associated protein (YAP) is a key regulator in the pathogenesis of gastric cancer (GC), yet its role in modulating autophagy remains unclear. This study investigated the effects of YAP modulation on autophagy and tumor progression using the SNU-484 and MKN-74 gastric cancer cell lines. YAP overexpression led to increased B-cell lymphoma-2 (BCL-2) transcription, reducing autophagy and enhancing cell survival, while YAP knockdown resulted in elevated autophagic activity. In vivo experiments with nude mice confirmed that YAP overexpression promotes tumor growth, whereas YAP silencing inhibits it. Further analysis revealed that YAP directly binds to the BCL-2 promoter, driving its transcription and thereby inhibiting autophagy-induced cell death. Importantly, silencing BCL-2 mitigated the autophagy inhibition caused by YAP without affecting YAP expression itself. These findings indicate that YAP, by upregulating BCL-2, suppresses autophagy and contributes to gastric cancer progression, suggesting a potential therapeutic strategy targeting the YAP-BCL-2 axis in GC treatment.

Indexed as

Adaptor Proteins, Signal TransducingAutophagyStomach NeoplasmsTranscription FactorsAnimalsCell Cycle ProteinsCell Line, TumorCell ProliferationDisease ProgressionGene Expression Regulation, NeoplasticHumansMiceMice, NudePromoter Regions, GeneticProto-Oncogene Proteins c-bcl-2YAP-Signaling ProteinsAdaptor Proteins, Signal TransducingCell Cycle ProteinsProto-Oncogene Proteins c-bcl-2Transcription FactorsYAP1 protein, humanYAP-Signaling ProteinsAutophagyBCL2Gastric cancerYAP

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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.