N-钙黏附素（cadherin-2 [CDH2]）广为人知作为前列腺癌（PCa）侵袭和阉割抵抗的促进剂。然而，N-钙黏附素在PCa进展中的生物学机制尚不清楚。本研究中，我们通过慢病毒转导在LNCaP细胞中过表达了N-钙黏附素，并在PC3细胞中通过慢病毒转导抑制了N-钙黏附素。然后，通过RNA测序（RNA-seq）分析研究了差异表达基因（DEGs）和失调的生物学功能。我们发现13个长非编码RNA（lncRNA）转录本，72个信使RNA（mRNA）转录本和3个整合基因被N-钙黏附素失调。在疾病富集中，骨癌和神经退行性疾病与N-钙黏附素在环状RNA（circRNA；PC3对比LNCaP）和DEG分析（LNCaP_oe_CDH2对比LNCaP_oe_NC）中相关。基因本体论（GO）分析中富集了表观遗传重编程，如核酸结合，染色质和组蛋白修饰（LNCaP_oe_CDH2/NC和PC3_sh_NC/CDH2中的DEGs以及PC3/LNCaP中circRNA的宿主基因）。在通路富集分析中，转录调控失调的癌症，翻译后蛋白修饰，基因表达和通用转录途径在PC3/LNCaP中circRNA的宿主基因以及LNCaP_oe_CDH2/NC和PC3_sh_NC/CDH2中DEGs中被失调。通过TCGA-PRAD数据集验证DEGs揭示了六个癌基因（ARHGEF1，GRAMD1A，GTF2H4，MAPK8IP3，POLD1和PTBP1）同时被N-钙黏附素上调和高级PCa阶段上调。总之，我们在PCa细胞中鉴定了与N-钙黏附素表达相关的多个癌基因和生物学功能。N-钙黏附素可能触发PCa细胞中的表观遗传重编程以促进肿瘤进展。

N-cadherin (cadherin-2 [CDH2]) is widely known as the promoter of prostate cancer (PCa) invasion and castration resistance. However, the biological mechanism of N-cadherin in PCa progression is unclear. In this study, we overexpressed N-cadherin in LNCaP cells and downregulated N-cadherin in PC3 cells by lentiviral transduction. Then, differentially expressed genes (DEGs) and dysregulated biological functions were investigated through RNA sequencing (RNA-seq) analyses. We found 13 long noncoding RNA (lncRNA) transcripts, 72 messenger RNA (mRNA) transcripts, and 3 integrated genes were dysregulated by N-cadherin. In the disease enrichment, bone cancer, and neurodegenerative and nervous system diseases were associated with N-cadherin in the circular RNA (circRNA; PC3 versus [vs.,/] LNCaP [PC3/LNCaP] comparison) and DEG analysis (LNCaP_oe_CDH2 vs. LNCaP_oe_NC [LNCaP_oe_CDH2/NC] comparison). Epigenetic reprogramming, such as nucleic acid binding, and chromatin and histone modifications, was enriched in Gene Ontology (GO) analysis (DEGs in LNCaP_oe_CDH2/NC and PC3_sh_NC/CDH2, and host genes of circRNA in PC3/LNCaP). Transcriptional misregulation in cancer, post-translational protein modification, gene expression, and generic transcription pathways were dysregulated in the pathway enrichment analysis (host genes of circRNA in PC3/LNCaP, and DEGs in LNCaP_oe_CDH2/NC and PC3_sh_NC/CDH2). Verifying DEGs through TCGA-PRAD dataset revealed six oncogenes (ARHGEF1, GRAMD1A, GTF2H4, MAPK8IP3, POLD1, and PTBP1) that were commonly upregulated by N-cadherin and in advanced PCa stages. In summary, we identified several oncogenes and biological functions associated with N-cadherin expression in PCa cells. N-cadherin may trigger epigenetic reprogramming in PCa cells to promote tumor progression.