DOI: 10.66106/mzabb7.20250101 ISSN: 3105-6636

咽癌发生进展机制研究基于YY1靶向KDM1A信号通路研究鼻咽癌发生进展机制（Study on the Mechanism of Nasopharyngeal Carcinoma Progression Based on YY1 Targeting KDM1A Signal Pathway）

戴珊 Shan Dai
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Abstract：Objective To investigate the mechanism of nasopharyngeal carcinoma (NPC) progression based on YY1 targeting theKDM1A signaling pathway. Methods A total of 100 archived NPC paraffin-embedded tissue specimens (including cancerous tissue,adjacent normal tissue, primary lesions, recurrent lesions, and metastatic lesions) and 30 corresponding fresh frozen tissue sampleswere collected from the pathology department of Danyang People’s Hospital. All patients were pathologically confirmed, and com-plete clinical-pathological data (age, gender, TNM staging, histological grade, lymph node metastasis status, etc.) were obtained. Bioinformatics analysis was conducted to predict the regulatory relationship between YY1 and KDM1A. In NPC cell lines (HNE2,CNE2), YY1 expression was modulated using siRNA interference and overexpression techniques. Western blot, RT-PCR, chromatinimmunoprecipitation (ChIP), flow cytometry, scratch assay, and Transwell experiments were employed to detect the effects of YY1on KDM1A expression and its downstream signaling pathways (such as H3K4me2, H3K9me, EMT-related proteins, p53, ERK/JNK),as well as its impact on cell proliferation, apoptosis, cycle, migration, and invasive capacity. Additionally, the expression correlationbetween YY1 and KDM1A and its clinical significance were validated in clinical NPC tissue samples. Results YY1 expression wasdownregulated in nasopharyngeal carcinoma (NPC) tissues and negatively correlated with KDM1A expression. YY1 directly bindsto the KDM1A promoter region to inhibit its transcription. Interfering with YY1 expression promotes KDM1A expression, enhancesNPC cell proliferation, migration, and invasion, inhibits apoptosis, and induces S-phase cell cycle arrest. Conclusion YY1 negative-ly regulates KDM1A expression, contributing to the pathogenesis of NPC. Its mechanism involves cell cycle regulation, apoptosis,and epithelial-mesenchymal transition (EMT), providing a new theoretical basis for molecular targeted therapy of NPC.

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