{"title":"sirt7介导的MVP去琥珀酰化通过激活JAK2/STAT3通路促进舌鳞状细胞癌进展。","authors":"Zhuo Zhang, Tingting Guo, Xiangyu Zhao","doi":"10.1002/cbin.70048","DOIUrl":null,"url":null,"abstract":"<p><p>Major vault protein (MVP) plays a contributing role in multifarious cancers, and then its role in Tongue squamous cell carcinoma (TSCC) is uncomprehending. This study aimed to investigate the regulatory effect of MVP on malignant behavior of TSCC cells and its mechanism. We first pointed out the abnormal upregulation of MVP in tumor tissues by immunohistochemistry, western blot, and reverse transcription-quantitative polymerase chain reaction assays. Depletion of MVP hindered TSCC cell viability, migration, and invasion and accelerated apoptosis. Mechanistically, depletion of MVP inactivated Janus Kinase 2 (JAK2)/Signal Transducer and Activator of Transcription 3 (STAT3) pathway. Coumermycin A1 (CA1), a JAK2 agonist, was used to trigger JAK2/STAT3 signaling. Functional experiments demonstrated that CA1 significantly counteracted the inhibitory effects of MVP silencing on cell proliferation, invasion, and migration, as well as the stimulatory effects of MVP silencing on cell apoptosis. Moreover, we discovered that MVP undergoes succinylation and identified Sirtuin 7 (SIRT7) as the desuccinylase for MVP. Addition of SIRT7 promoted the protein stability of MVP in TSCC cells. Further, addition of MVP expedited the viability, migration, and invasion and suppressed apoptosis of TSCC cells, which was partly neutralized following depleted SIRT7. Our findings revealed that MVP desuccinylated by SIRT7 accelerated TSCC progression via regulating JAK2/STAT3 signaling.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3000,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"SIRT7-Mediated MVP Desuccinylation Facilitates Tongue Squamous Cell Carcinoma Progression by Activating JAK2/STAT3 Pathway.\",\"authors\":\"Zhuo Zhang, Tingting Guo, Xiangyu Zhao\",\"doi\":\"10.1002/cbin.70048\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Major vault protein (MVP) plays a contributing role in multifarious cancers, and then its role in Tongue squamous cell carcinoma (TSCC) is uncomprehending. This study aimed to investigate the regulatory effect of MVP on malignant behavior of TSCC cells and its mechanism. We first pointed out the abnormal upregulation of MVP in tumor tissues by immunohistochemistry, western blot, and reverse transcription-quantitative polymerase chain reaction assays. Depletion of MVP hindered TSCC cell viability, migration, and invasion and accelerated apoptosis. Mechanistically, depletion of MVP inactivated Janus Kinase 2 (JAK2)/Signal Transducer and Activator of Transcription 3 (STAT3) pathway. Coumermycin A1 (CA1), a JAK2 agonist, was used to trigger JAK2/STAT3 signaling. Functional experiments demonstrated that CA1 significantly counteracted the inhibitory effects of MVP silencing on cell proliferation, invasion, and migration, as well as the stimulatory effects of MVP silencing on cell apoptosis. Moreover, we discovered that MVP undergoes succinylation and identified Sirtuin 7 (SIRT7) as the desuccinylase for MVP. Addition of SIRT7 promoted the protein stability of MVP in TSCC cells. Further, addition of MVP expedited the viability, migration, and invasion and suppressed apoptosis of TSCC cells, which was partly neutralized following depleted SIRT7. Our findings revealed that MVP desuccinylated by SIRT7 accelerated TSCC progression via regulating JAK2/STAT3 signaling.</p>\",\"PeriodicalId\":9806,\"journal\":{\"name\":\"Cell Biology International\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":3.3000,\"publicationDate\":\"2025-06-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cell Biology International\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1002/cbin.70048\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cell Biology International","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1002/cbin.70048","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
主要拱顶蛋白(MVP)在多种癌症中发挥重要作用,但在舌鳞癌(TSCC)中的作用尚不清楚。本研究旨在探讨MVP对TSCC细胞恶性行为的调控作用及其机制。我们首先通过免疫组化、western blot和逆转录-定量聚合酶链反应分析指出了肿瘤组织中MVP的异常上调。MVP的缺失阻碍了TSCC细胞的活力、迁移和侵袭,加速了细胞凋亡。在机制上,MVP的缺失使Janus Kinase 2 (JAK2)/Signal transducator and Activator of Transcription 3 (STAT3)通路失活。Coumermycin A1 (CA1)是一种JAK2激动剂,用于触发JAK2/STAT3信号传导。功能实验表明,CA1显著抵消了MVP沉默对细胞增殖、侵袭和迁移的抑制作用,以及MVP沉默对细胞凋亡的刺激作用。此外,我们发现MVP经历琥珀酰化,并确定Sirtuin 7 (SIRT7)是MVP的去琥珀酰化酶。SIRT7的加入促进了TSCC细胞中MVP蛋白的稳定性。此外,添加MVP加速了TSCC细胞的活力、迁移和侵袭,并抑制了TSCC细胞的凋亡,这在SIRT7耗尽后部分被中和。我们的研究结果表明,SIRT7介导的MVP去乙酰化通过调节JAK2/STAT3信号通路加速TSCC的进展。
Major vault protein (MVP) plays a contributing role in multifarious cancers, and then its role in Tongue squamous cell carcinoma (TSCC) is uncomprehending. This study aimed to investigate the regulatory effect of MVP on malignant behavior of TSCC cells and its mechanism. We first pointed out the abnormal upregulation of MVP in tumor tissues by immunohistochemistry, western blot, and reverse transcription-quantitative polymerase chain reaction assays. Depletion of MVP hindered TSCC cell viability, migration, and invasion and accelerated apoptosis. Mechanistically, depletion of MVP inactivated Janus Kinase 2 (JAK2)/Signal Transducer and Activator of Transcription 3 (STAT3) pathway. Coumermycin A1 (CA1), a JAK2 agonist, was used to trigger JAK2/STAT3 signaling. Functional experiments demonstrated that CA1 significantly counteracted the inhibitory effects of MVP silencing on cell proliferation, invasion, and migration, as well as the stimulatory effects of MVP silencing on cell apoptosis. Moreover, we discovered that MVP undergoes succinylation and identified Sirtuin 7 (SIRT7) as the desuccinylase for MVP. Addition of SIRT7 promoted the protein stability of MVP in TSCC cells. Further, addition of MVP expedited the viability, migration, and invasion and suppressed apoptosis of TSCC cells, which was partly neutralized following depleted SIRT7. Our findings revealed that MVP desuccinylated by SIRT7 accelerated TSCC progression via regulating JAK2/STAT3 signaling.
期刊介绍:
Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect.
These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.