NUPR1 imparts oncogenic potential in bladder cancer.
NUPR1 imparts oncogenic potential in bladder cancer.
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NUPR1 赋予膀胱癌致癌潜力
DOI：
10.1002/cam4.5518
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发表时间：
2023-03
期刊：
影响因子：
4
通讯作者：
Qi, Chunjian
中科院分区：
文献类型：
--
作者：
Zhang, Lifeng;Gao, Shenglin;Shi, Xiaokai;Chen, Yin;Wei, Shuzhang;Mi, Yuanyuan;Zuo, Li;Qi, Chunjian
NUPR1（或 p8）是一种小染色质蛋白，在癌症治疗抵抗和进展中发挥着核心作用。然而，NUPR1在膀胱癌（BLCA）中的分子机制仍不清楚。我们使用在线数据库和免疫组织化学 (IHC) 来探索 BLCA 组织和对照中 NUPR1 的表达。慢病毒介导的小干扰核糖核酸 (siRNA) 用于敲低两种人 BLCA 细胞系中 NUPR1 的表达。我们使用体内实验来研究 NUPR1 敲低对 BLCA 生长的影响。此外，还进行了计算机分析以评估 NUPR1 干扰后的差异表达谱。利用 CIBERSORT 算法评估肿瘤浸润免疫细胞对 BLCA 患者的影响。 BLCA组织中NUPR1的表达显着高于对照。 NUPR1表达也与BLCA分期呈正相关。经过慢病毒介导的干扰后，BLCA细胞系中NUPR1的表达显着下调。两种细胞系的细胞周期均被阻断在G1期，S期细胞比例均下降。此外，体内实验表明，BLCA可以通过抑制NUPR1的表达来延缓肿瘤生长。计算机分析和功能实验均表明 NUPR1 与上皮间质转化 (EMT) 相关。我们还发现巨噬细胞是与 BLCA 中 NUPR1 表达最相关的免疫细胞。这项研究表明 NUPR1 在 BLCA 中发挥致癌作用。 NUPR1 慢病毒介导的干扰可能干扰 BLCA 细胞的周期进程，导致细胞周期停滞在 G1 期。 BLCA 中 NUPR1 的致癌作用很可能是通过 EMT 实现的。 NUPR1 与 M0 型巨噬细胞标记物 CD68 和 CD11b 整合素相关。我们使用体内和体外实验来研究 NUPR1 敲低对 BLCA 生长的影响。我们发现 NUPR1 慢病毒介导的干扰可以干扰 BLCA 细胞的周期进程，导致细胞周期停滞在 G1 期。 BLCA 中 NUPR1 的致癌作用很可能是通过 EMT 实现的。
NUPR1, or p8, is a small chromatin protein that plays a central role in the resistance to treatment and progression of cancer. Nevertheless, the molecular mechanism of NUPR1 in bladder cancer (BLCA) remains unclear. We used online databases and immunohistochemistry (IHC) to explore the expression of NUPR1 in BLCA tissues and controls. Lentivirus‐mediated small interfering ribonucleic acid (siRNA) was used to knockdown the expression of NUPR1 in two human BLCA cell lines. We used an in vivo experiment to investigate the effect of NUPR1 knockdown on the growth of BLCA. Moreover, an in silico analysis was conducted to assess the differential expression profile after NUPR1 interference. The CIBERSORT algorithm was utilized to evaluate the effects of tumor‐infiltrating immune cells among BLCA patients. The expression of NUPR1 in BLCA tissues was significantly higher than in the control. NUPR1 expression was also positively correlated with the stage of BLCA. After lentivirus‐mediated interference, the expression of NUPR1 was significantly down‐regulated in BLCA cell lines. The cell cycle was blocked in G1 phase and the cell proportion of S phase was decreased in both two cell lines. Moreover, in vivo experiment revealed that the tumor growth of BLCA can be delayed by inhibiting the expression of NUPR1. Both in silico analysis and functional experiments revealed that NUPR1 was correlated with epithelial–mesenchymal transition (EMT). We also revealed that macrophages were the most related immune cells associated with the expression of NUPR1 in BLCA. This study suggests that NUPR1 plays a carcinogenic role in BLCA. NUPR1 lentivirus‐mediated interference could interfere with cycle progression of the BLCA cell, resulting in cell cycle arrest in the G1‐phase. The carcinogenic effect of NUPR1 in BLCA is likely achieved through EMT. NUPR1 is correlated with the M0‐type macrophage markers CD68 and CD11b‐integrin. We used an in vivo and in vitro experiment to investigate the effect of NUPR1 knockdown on the growth of BLCA. We revealed that NUPR1 lentivirus‐mediated interference could interfere with cycle progression of the BLCA cell, resulting in cell cycle arrest in the G1‐phase. The carcinogenic effect of NUPR1 in BLCA is likely achieved through EMT.
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影响因子：
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作者：
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影响因子：
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