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<p>Autophagy has a context-dependent role in cervical cancer (CC). This study aimed to identify and functionally validate autophagy-related genes contributing to cervical cancer progression.</p><p>Transcriptome data were analyzed to screen DEGs, followed by Gene Ontology, Kyoto Encyclopedia of Genes and Genome, and protein-protein interaction network analysis. Candidate autophagy-associated DEGs were validated using GEPIA and ENCORI databases. Expression levels were further examined in clinical CC specimens. Functional assays were performed in SiHa cells transfected with overexpression or silencing vectors for PEG3, SYNPO2, and DCN. Cellular phenotypes (proliferation, colony formation, invasion, apoptosis, and cell cycle) were assessed, and the expression of autophagy- and ferroptosis-associated proteins was examined. Reactive oxygen species (ROS) and intracellular Fe²⁺ were detected by fluorescence probes. Finally, a xenograft model was established to evaluate tumor growth and cells proliferation. </p><p>Two thousand, seven hundred forty DEGs were identified (1,109 upregulated, 1,631 downregulated), of which PEG3, SYNPO2, and DCN were selected as autophagy-associated candidates. Database analyses and patient samples confirmed their reduced expression in CC. In vitro, overexpression of PEG3, SYNPO2, or DCN suppressed colony formation and invasion and increased apoptosis and G0/G1 arrest, while silencing produced the opposite effects. Autophagosome markers (LC3-II, Beclin-1) were lower in overexpression groups and ferroptosis-related profiles (GPX4, FTH, ACSL4, ROS, Fe²⁺) were consistent with reduced lipid/iron-stress propensity. In vivo, overexpression reduced tumor growth and Ki-67/p16 staining.</p><p>PEG3, SYNPO2, and DCN act as cytostatic tumor suppressors that modulate cellular stress in CC and represent potential therapeutic targets pending further validation.</p>

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Integrated analysis and functional validation of PEG3, SYNPO2, and DCN as regulators of tumor suppression and cellular stress in cervical cancer

  • 期刊论文

  • 发表日期：

    2026年3月25日

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  • Caiyun Han,
  • Yan Zhao,
  • Xiaoyan Yang,
  • Fengtao Sun

摘要

Autophagy has a context-dependent role in cervical cancer (CC). This study aimed to identify and functionally validate autophagy-related genes contributing to cervical cancer progression.

Transcriptome data were analyzed to screen DEGs, followed by Gene Ontology, Kyoto Encyclopedia of Genes and Genome, and protein-protein interaction network analysis. Candidate autophagy-associated DEGs were validated using GEPIA and ENCORI databases. Expression levels were further examined in clinical CC specimens. Functional assays were performed in SiHa cells transfected with overexpression or silencing vectors for PEG3, SYNPO2, and DCN. Cellular phenotypes (proliferation, colony formation, invasion, apoptosis, and cell cycle) were assessed, and the expression of autophagy- and ferroptosis-associated proteins was examined. Reactive oxygen species (ROS) and intracellular Fe²⁺ were detected by fluorescence probes. Finally, a xenograft model was established to evaluate tumor growth and cells proliferation.

Two thousand, seven hundred forty DEGs were identified (1,109 upregulated, 1,631 downregulated), of which PEG3, SYNPO2, and DCN were selected as autophagy-associated candidates. Database analyses and patient samples confirmed their reduced expression in CC. In vitro, overexpression of PEG3, SYNPO2, or DCN suppressed colony formation and invasion and increased apoptosis and G0/G1 arrest, while silencing produced the opposite effects. Autophagosome markers (LC3-II, Beclin-1) were lower in overexpression groups and ferroptosis-related profiles (GPX4, FTH, ACSL4, ROS, Fe²⁺) were consistent with reduced lipid/iron-stress propensity. In vivo, overexpression reduced tumor growth and Ki-67/p16 staining.

PEG3, SYNPO2, and DCN act as cytostatic tumor suppressors that modulate cellular stress in CC and represent potential therapeutic targets pending further validation.