Zhi-ming Chen, Lei Mou, Yi-heng Pan, Chi Feng, Jun Liu, Jing-jing Zhang, Chang-Xiang Yan
{"title":"NIBAN2通过调控JAK2/STAT3/c-Myc通路刺激胶质瘤生长","authors":"Zhi-ming Chen, Lei Mou, Yi-heng Pan, Chi Feng, Jun Liu, Jing-jing Zhang, Chang-Xiang Yan","doi":"10.1002/cam4.71239","DOIUrl":null,"url":null,"abstract":"<div>\n \n \n <section>\n \n <h3> Background</h3>\n \n <p>Niban-like protein 2 (NIBAN2) has recently been linked to various neurological diseases; however, its exact role in glioma development remains unclear.</p>\n </section>\n \n <section>\n \n <h3> Methods</h3>\n \n <p>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.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p>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.</p>\n </section>\n \n <section>\n \n <h3> Conclusion</h3>\n \n <p>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.</p>\n </section>\n </div>","PeriodicalId":139,"journal":{"name":"Cancer Medicine","volume":"14 18","pages":""},"PeriodicalIF":3.1000,"publicationDate":"2025-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.71239","citationCount":"0","resultStr":"{\"title\":\"NIBAN2 Stimulates Glioma Growth by Regulating the JAK2/STAT3/c-Myc Pathway\",\"authors\":\"Zhi-ming Chen, Lei Mou, Yi-heng Pan, Chi Feng, Jun Liu, Jing-jing Zhang, Chang-Xiang Yan\",\"doi\":\"10.1002/cam4.71239\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Background</h3>\\n \\n <p>Niban-like protein 2 (NIBAN2) has recently been linked to various neurological diseases; however, its exact role in glioma development remains unclear.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Methods</h3>\\n \\n <p>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.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p>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.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Conclusion</h3>\\n \\n <p>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.</p>\\n </section>\\n </div>\",\"PeriodicalId\":139,\"journal\":{\"name\":\"Cancer Medicine\",\"volume\":\"14 18\",\"pages\":\"\"},\"PeriodicalIF\":3.1000,\"publicationDate\":\"2025-09-13\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cam4.71239\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cancer Medicine\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1002/cam4.71239\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Medicine","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/cam4.71239","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
niban样蛋白2 (NIBAN2)最近被发现与多种神经系统疾病有关;然而,它在胶质瘤发展中的确切作用尚不清楚。方法采用定量逆转录聚合酶链反应、免疫印迹法和免疫组化法检测NIBAN2在胶质瘤组织中的表达。此外,我们在各种功能试验中检查了NIBAN2对胶质瘤进展的影响。动物模型被用来阐明NIBAN2的作用,特别是它对Janus kinase 2/signal transducer and activator of transcription 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,其表达水平与肿瘤分级和临床结局密切相关。功能分析显示,NIBAN2通过激活JAK2/STAT3信号通路增强胶质瘤细胞的侵袭性,并通过阻止细胞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,提示其是一个潜在的治疗靶点。
NIBAN2 Stimulates Glioma Growth by Regulating the JAK2/STAT3/c-Myc Pathway
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.
期刊介绍:
Cancer Medicine is a peer-reviewed, open access, interdisciplinary journal providing rapid publication of research from global biomedical researchers across the cancer sciences. The journal will consider submissions from all oncologic specialties, including, but not limited to, the following areas:
Clinical Cancer Research
Translational research ∙ clinical trials ∙ chemotherapy ∙ radiation therapy ∙ surgical therapy ∙ clinical observations ∙ clinical guidelines ∙ genetic consultation ∙ ethical considerations
Cancer Biology:
Molecular biology ∙ cellular biology ∙ molecular genetics ∙ genomics ∙ immunology ∙ epigenetics ∙ metabolic studies ∙ proteomics ∙ cytopathology ∙ carcinogenesis ∙ drug discovery and delivery.
Cancer Prevention:
Behavioral science ∙ psychosocial studies ∙ screening ∙ nutrition ∙ epidemiology and prevention ∙ community outreach.
Bioinformatics:
Gene expressions profiles ∙ gene regulation networks ∙ genome bioinformatics ∙ pathwayanalysis ∙ prognostic biomarkers.
Cancer Medicine publishes original research articles, systematic reviews, meta-analyses, and research methods papers, along with invited editorials and commentaries. Original research papers must report well-conducted research with conclusions supported by the data presented in the paper.