Evidence map›Paper›PMID 41407812›Full record

ArticleScientific reports2025

Clinical significance and potential molecular mechanisms of SYT15 expression in lung adenocarcinoma.

Mei Tian, Lili Deng, Lele Jin, Xiaoyu Qiang, Yiming Li, Xiaotian Liu, Huanhuan Wang, Xiaojing Wang, Nan Wu

Abstract read
In one paragraph

Article in Scientific reports, 2025. 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

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Mei Tian *Anhui Province Key Laboratory of Respiratory Tumor and Infectious Disease, The Department of Pulmonary Critical Care Medicine, First Affiliated Hospital of Bengbu Medical University, Bengbu, 233004, China.
Lili Deng *Anhui Province Key Laboratory of Respiratory Tumor and Infectious Disease, The Department of Pulmonary Critical Care Medicine, First Affiliated Hospital of Bengbu Medical University, Bengbu, 233004, China.
Lele JinAnhui Province Key Laboratory of Respiratory Tumor and Infectious Disease, The Department of Pulmonary Critical Care Medicine, First Affiliated Hospital of Bengbu Medical University, Bengbu, 233004, China.
Xiaoyu QiangShanghan Teaching and Research Section, School of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, 201203, China.
Yiming LiCollege of Laboratory Medicine, Bengbu Medical University, Bengbu, 233004, China.
Xiaotian LiuCollege of Laboratory Medicine, Bengbu Medical University, Bengbu, 233004, China.
Huanhuan WangAnhui Province Key Laboratory of Respiratory Tumor and Infectious Disease, The Department of Pulmonary Critical Care Medicine, First Affiliated Hospital of Bengbu Medical University, Bengbu, 233004, China.
Xiaojing WangAnhui Province Key Laboratory of Respiratory Tumor and Infectious Disease, The Department of Pulmonary Critical Care Medicine, First Affiliated Hospital of Bengbu Medical University, Bengbu, 233004, China. wangxiaojing8888@163.com.
Nan WuAnhui Province Key Laboratory of Respiratory Tumor and Infectious Disease, The Department of Pulmonary Critical Care Medicine, First Affiliated Hospital of Bengbu Medical University, Bengbu, 233004, China. bbmcwunan@163.com.

Funding

Anhui Provincial Major Science and Technology Project for Key Laboratory S202305a12020038National Natural Science Foundation of China 82373329Research Funds of Joint Research Center for Regional Diseases of Institute of Health and Medicine (IHM), Hefei Comprehensive National Science Center 2024bydjk007, 2024bydjk008Scientific Research Project of Colleges and Universities in Anhui Province 2024AH051254
6 · The paper itself

Abstract

Increasing evidence suggests that the synaptotagmin (SYT) family is associated with the development of multiple types of cancer, yet research on SYT15 remains limited. The aim of this study was to elucidate the clinical significance and possible molecular mechanisms of SYT15 expression in lung adenocarcinoma (LUAD). The expression, clinical value, cellular function and possible molecular mechanisms of SYT15 in LUAD were evaluated by using bioinformatics analysis combined with cellular experiments. In LUAD, SYT15 expression was downregulated. Notably, this reduced expression was negatively associated with patient survival but positively correlated with immune cell infiltration in the tumor microenvironment. Furthermore, SYT15 expression correlated with three key aspects: sensitivity to 20 distinct drugs, the expression of immune checkpoint genes (ICGs), and the efficacy of immunotherapy. SYT15 was most highly expressed in Mono/Macro, CD8Tex, and CD8T cells within LUAD tissues. Cellular experiments confirmed that SYT15 overexpression reduced the malignant phenotype of A549 and H1975 cells. RNA sequencing results showed that the PI3K/AKT signaling pathway was significantly enriched after overexpression of SYT15 in A549 cells, and qPCR and WB experiments confirmed significant downregulation of genes related to this pathway.. Further experiments confirmed that PI3K agonist 740Y-P reversed the regulatory effects of SYT15 overexpression on A549 cell malignant phenotype and the PI3K/Akt signaling pathway. In LUAD, SYT15 acts as a tumor suppressor by potentially regulating immune cell infiltration in the tumor microenvironment and inhibiting the expression of key PI3K/AKT pathway genes in A549 cells. Consequently, it holds promise as a novel prognostic marker and potential therapeutic target..

Indexed as

Adenocarcinoma of LungGene Expression Regulation, NeoplasticLung NeoplasmsSynaptotagminsA549 CellsBiomarkers, TumorCell Line, TumorClinical RelevanceFemaleHumansMaleMiddle AgedPhosphatidylinositol 3-KinasesPrognosisProto-Oncogene Proteins c-aktSignal TransductionBiomarkers, TumorPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSynaptotagminsDrug sensitivityLUADPI3K/AKTSYT15TME

Identifiers

PMID41407812
PMCPMC12820372

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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.