Evidence map›Paper›PMID 42613558›Full record

ArticleIn vitro cellular & developmental biology. Animal2026

E3 ubiquitin ligase SYVN1 promotes the malignant phenotype of A549 cells by upregulating GATA3 expression via NRP1.

Shan Wang, Suli Lu, Zhen Wang, Guiping Xuan, Jianhua Tan

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Article in In vitro cellular & developmental biology. Animal, 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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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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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Shan WangHunan Polytechnic of Environment and Biology, Hengyang, 421000, Hunan, China.
Suli LuHunan Polytechnic of Environment and Biology, Hengyang, 421000, Hunan, China.
Zhen WangHunan Polytechnic of Environment and Biology, Hengyang, 421000, Hunan, China.
Guiping XuanHunan Polytechnic of Environment and Biology, Hengyang, 421000, Hunan, China.
Jianhua TanThe Second Affiliated Hospital, University of South China, No. 35 Jiefang Avenue, Hengyang, 421001, Hunan, China. 18774245502@163.com.

Funding

Natural Science Foundation of Hunan Province 2025JJ81037Natural Science Foundation of Hunan Province 2026JJ81762Science Popularization Special Project of Hunan Province 2023ZK4336
6 · The paper itself

Abstract

Lung cancer remains one of the most lethal and prevalent malignancies worldwide. Although E3 ubiquitin ligase SYVN1 is frequently amplified in lung cancer, its functional role has not been fully elucidated. This study investigates the mechanistic involvement of SYVN1 in regulating the GATA3/NRP1 axis in A549 cells to provide novel insights into potential therapeutic strategies for lung cancer. Expression levels of SYVN1 were assessed in BEAS-2B, A549, NCI-H647, NCI-H2170, and NCI-H520, NCI-H69 cells. Functional assays were conducted after overexpressing or silencing SYVN1, GATA3, and/or NRP1 in A549 cells to examine their interdependent roles. The cells' proliferation, wound healing, invasion and migration abilities were evaluated through CCK-8, scratch assay and Transwell assays, respectively. The results indicated that SYVN1 was upregulated in A549 cells and significantly promoted cell proliferation, invasion, and migration. Mechanistically, SYVN1 interacted with GATA3 and regulated its ubiquitination. Knockdown of SYVN1 suppressed A549 cell proliferation, wound healing, invasion, and migration, and these effects could be reversed by overexpressing GATA3. Similarly, silencing GATA3 reduced these malignant characteristics, but these effects could be restored by overexpressing NRP1, and the knockdown of NRP1 could abrogate the tumor-promoting effects of SYVN1 overexpression. SYVN1 overexpression counteracted the inhibitory effects of NRP1 silencing on A549 tumor progression. Taken together, all these findings prove that SYVN1 could promote the malignant characteristics of A549 cells by modulating the GATA3/NRP1 axis. Thus, targeting SYVN1 could represent a promising therapeutic approach for treating lung cancer.

Indexed as

GATA3Lung cancerNRP1SYVN1Ubiquitin specific protease

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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.