NIBAN2通过调节JAK2/STAT3/c-Myc信号通路促进胶质瘤生长。
NIBAN2 Stimulates Glioma Growth by Regulating the JAK2/STAT3/c-Myc Pathway.
作者信息
Chen Zhi-Ming, Mou Lei, Pan Yi-Heng, Feng Chi, Liu Jun, Zhang Jing-Jing, Yan Chang-Xiang
机构信息
Department of Neurosurgery, Sanbo Brain Hospital, Capital Medical University, Beijing, China.
Department of Neurosurgery, Hubei Provincial Clinical Research Center of Central Nervous System Repair and Functional Reconstruction, Taihe Hospital, Hubei University of Medicine, Shiyan, Hubei, China.
出版信息
Cancer Med. 2025 Sep;14(18):e71239. doi: 10.1002/cam4.71239.
BACKGROUND
Niban-like protein 2 (NIBAN2) has recently been linked to various neurological diseases; however, its exact role in glioma development remains unclear.
METHODS
Quantitative reverse transcription-polymerase chain reaction, western blotting, and immunohistochemistry were used to evaluate NIBAN2 expression in glioma tissues. In addition, we examined the effects of NIBAN2 on glioma progression in various functional trials. Animal models were used to clarify the role of NIBAN2, especially its impact on the Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway.
RESULTS
The research outcomes revealed that NIBAN2 was highly upregulated in gliomas and its levels were strongly correlated with tumor grade and clinical outcomes. Functional assays showed that NIBAN2 enhanced glioma cell aggressiveness by activating JAK2/STAT3 signaling and promoted tumor growth by preventing apoptosis and accelerating the cell cycle.
CONCLUSION
The findings of this study show that NIBAN2 plays a key role in glioma aggression and poor prognosis, suggesting that it is a potential therapeutic target.
背景
Niban样蛋白2（NIBAN2）最近与多种神经系统疾病有关；然而，其在胶质瘤发生发展中的确切作用仍不清楚。
方法
采用定量逆转录-聚合酶链反应、蛋白质印迹法和免疫组织化学法评估NIBAN2在胶质瘤组织中的表达。此外，我们在各种功能试验中研究了NIBAN2对胶质瘤进展的影响。使用动物模型来阐明NIBAN2的作用，特别是其对Janus激酶2/信号转导和转录激活因子3（JAK2/STAT3）信号通路的影响。
结果
研究结果显示，NIBAN2在胶质瘤中高度上调，其水平与肿瘤分级和临床结果密切相关。功能分析表明，NIBAN2通过激活JAK2/STAT3信号增强胶质瘤细胞的侵袭性，并通过抑制凋亡和加速细胞周期促进肿瘤生长。
结论
本研究结果表明，NIBAN2在胶质瘤侵袭和不良预后中起关键作用，提示它是一个潜在的治疗靶点。
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