富含半胱氨酸的分泌蛋白 3 (CRISP3) 成为许多癌症研究中的潜在生物标志物，包括宫颈癌 (CC)。本研究旨在分析用表观遗传药物曲古抑菌素 A (TSA) 和 5-aza-2'-脱氧胞苷 (5-aza) 治疗后 CC 患者和 CC 细胞谱系中 CRISP3 的表达模式。 GSE63514中的蛋白质被用来构建蛋白质-蛋白质相互作用网络。选择CRISP3进行后续分析。我们利用 TCGA 和 GENT2 项目的数据来评估 CRISP3 的表达谱和临床行为。此外，我们还进行了细胞培养实验来分析细胞中 CRISP3 的表达谱。在鳞状细胞癌 (SCC) 和人乳头瘤病毒 (HPV)16 中观察到 CRISP3 水平较低，并且与较差的总生存期 (OS) 相关。分析了 MIR-1229-3p，其高表达与较差的预后结果相关。在 CC 衍生细胞系中，我们在 SiHa 中观察到 CRISP3 水平较低，其次是 SW756、C33A、HeLa，在 CaSki 中观察到较高水平。所有细胞均用 TSA、5-aza 或两者处理。在所有细胞系中，TSA 处理都会导致 CRISP3 转录增加。我们发现 CC 中 CRISP3 显着下调，特别是在 HPV16 感染和 SCC 的病例中，这与 OS 较差有关。初步研究结果表明，TSA 和 5-aza 的表观遗传治疗可能会调节 CRISP3 表达，需要进一步研究以阐明其调节机制和作为预后生物标志物的潜力。© 作者 2024。由牛津大学出版社代表西方出版中国医学院

Cysteine-rich secretory protein 3 (CRISP3) emerges as a potential biomarker in the study of many cancers, including cervical cancer (CC). This study aimed to analyze the expression pattern of CRISP3 in CC patients and CC cell lineages, following treatment with the epigenetic drugs: trichostatin A (TSA) and 5-aza-2'-deoxycytidine (5-aza).The differentially expressed genes identified in GSE63514 were used to construct a protein-protein interaction network. CRISP3 was selected for subsequent analyses. We utilized data from the TCGA and GENT2 projects to evaluate the expression profile and clinical behavior of CRISP3. Additionally, we conducted cell culture experiments to analyze the expression profile of CRISP3 in cells.Low levels of CRISP3 were observed in squamous cell carcinoma (SCC) and human papillomavirus (HPV)16+, along with being associated with worse overall survival (OS). MIR-1229-3p was analyzed, and its high expression was associated with worse prognostic outcomes. In CC-derived cell lines, we observed low levels of CRISP3 in SiHa, followed by SW756, C33A, HeLa, and higher levels in CaSki. All cells were treated with TSA, 5-aza, or both. In all cell lines, treatment with TSA resulted in increased transcription of CRISP3.We identified a significant downregulation of CRISP3 in CC, particularly in cases with HPV16 infection and SCC, which was associated with poorer OS. Preliminary findings suggest that epigenetic treatments with TSA and 5-aza may modulate CRISP3 expression, warranting further research to elucidate its regulatory mechanisms and potential as a prognostic biomarker.© The Author(s) 2024. Published by Oxford University Press on behalf of the West China School of Medicine & West China Hospital of Sichuan University.