核蛋白 1 (NUPR1)（也称为 p8）是与转录因子相关的基因之一，参与癌症发生和发展的各个方面。然而，NUPR1 在膀胱癌（BLCA）中的分子机制仍不清楚。我们使用基因表达综合（GEO）在线数据库对 NUPR1 表达与相关基因之间的相关性进行了分析。我们采用慢病毒介导的小干扰 RNA (siRNA) 来敲低两种人 BLCA 细胞系中 NUPR1 的表达。通过体外实验验证NUPR1干扰BLCA的影响以及NUPR1对趋化因子受体2（CCR2）转录的影响。此外，使用 PROMO 数据库预测了 CCR2 的转录因子。采用免疫共沉淀（Co-IP）和免疫荧光双染色检测NUPR1与CCAAT/增强子结合蛋白γ（CEBPG）之间的结合。进行体内和体外实验验证NUPR1通过CEBPG调节CCR2转录。体外实验表明，抑制 NUPR1 可抑制 BLCA 生长。 GEO数据库分析显示NUPR1和CCR2的表达呈正相关。荧光素酶实验证实 NUPR1 影响 CCR2 的转录。在线数据表明CEBPG是CCR2的转录因子。 Co-IP 和免疫荧光双染色证实了 NUPR1 和 CEBPG 之间的结合。荧光素酶检测和染色质免疫沉淀 (ChIP) 证明 CEBPG 调节 CCR2 的转录。此外，细胞水平的救援实验和动物实验也验证了上述机制。 NUPR1对BLCA有促进作用，干扰NUPR1可以抑制BLCA的增殖和侵袭能力。 NUPR1和CCR2的表达存在相关性，并且NUPR1在细胞核中与CEBPG结合。 NUPR1 对 CCR2 的转录调控可以通过 CEBPG 的参与来实现。© 2024 Wiley periodicals LLC。

Nuclear protein-1 (NUPR1) (also known as p8) is one of the genes associated with transcription factors that participate in various aspects of cancer initiation and development. However, the molecular mechanisms of NUPR1 in bladder cancer (BLCA) remain unclear. We conducted an analysis of the correlation between NUPR1 expression and related genes using the Gene Expression Omnibus (GEO) online database. We employed lentivirus-mediated small interfering RNA (siRNA) to knockdown the expression of NUPR1 in two human BLCA cell lines. In vitro experiments were conducted to validate the impact of NUPR1 interference on BLCA and the influence of NUPR1 on the transcription of chemokine receptor-2 (CCR2). Furthermore, transcription factors for CCR2 were predicted using the PROMO database. Co-immunoprecipitation (Co-IP) and immunofluorescence double staining were used to detect the binding between NUPR1 and CCAAT/enhancer binding protein γ (CEBPG). In vivo and in vitro experiments were conducted to validate that NUPR1 regulates CCR2 transcription through CEBPG. In vitro experiments indicate that the suppression of NUPR1 inhibited BLCA growth. Analysis of the GEO database revealed a positive correlation between the expression of NUPR1 and CCR2. Luciferase experiments confirmed that NUPR1 influences the transcription of CCR2. Online data indicates that CEBPG is a transcription factor for CCR2. Co-IP and immunofluorescence double staining confirmed binding between NUPR1 and CEBPG. Luciferase assays and chromatin immunoprecipitation (ChIP) demonstrate that CEBPG regulates the transcription of CCR2. Additionally, rescue experiments at the cellular level and animal experiments validated the aforementioned mechanism. NUPR1 promotes a promotional role in BLCA, and interference with NUPR1 can inhibit the proliferation and invasive abilities of BLCA. There was a correlation between the expressions of NUPR1 and CCR2, and NUPR1 binds with CEBPG in the cell nucleus. Transcriptional regulation of CCR2 by NUPR1 may be achieved through the involvement of CEBPG.© 2024 Wiley Periodicals LLC.