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PBLD promotes IRF3 mediated the type I interferon (IFN-I) response and apoptosis to inhibit viral replication. PBLD 可促进 IRF3 介导的 I 型干扰素(IFN-I)反应和细胞凋亡,从而抑制病毒复制。
IF 8.1 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-03 DOI: 10.1038/s41419-024-07083-w
Hongchao Zhu, Peili Hou, Fengyun Chu, Xingyu Li, Wenjia Zhang, Xiaonan Sun, Yu Liu, Guimin Zhao, Yuwei Gao, Daniel Chang He, Hongmei Wang, Hongbin He

Recent studies have implicated the phenazine biosynthesis-like domain-containing protein (PBLD) in the negative regulation of the development and progression of various cancers. However, its function in viral infection remains unknown. In this study, we found that PBLD plays important roles in multiple virus infections including BPIV3, SeV, VSV, and HSV-1. Our study revealed that PBLD enhances the expression of type I interferon (IFN-I) and ISGs through interferon regulatory factor 3 (IRF3). Further study indicated that PBLD promotes transcriptional phosphorylation of IRF3 (S385/386), thereby facilitating virus-induced IFN-I production. Interestingly, PBLD mediates virus-triggered mitochondrial apoptosis through its dependence on IRF3 (K313/315). Mechanistically, PBLD facilitated virus-induced apoptosis by recruiting the Puma protein to the mitochondria via IRF3. Additionally, we performed mutational analyses of IRF3, showing that its loss of either transcriptional or apoptotic function markedly increased viral replication. Moreover, macrophages with PBLD deficiency during viral infection exhibited decreased the IFN-I and ISGs expression, exacerbating viral infection. Importantly, mice deficient in PBLD exhibited increased viral replication and susceptibility to SeV infection, leading to decreased survival. Notably, Cedrelone, a chemical activator of PBLD, has the ability to reduce SeV replication. Collectively, we first discovered the new function of PBLD in viral infection, broadening our understanding of potential therapeutic targets and offering new insights for antiviral drug development.

最近的研究表明,含吩嗪生物合成样结构域的蛋白(PBLD)与各种癌症的发生和发展的负调控有关。然而,它在病毒感染中的功能仍然未知。本研究发现,PBLD 在多种病毒感染中发挥重要作用,包括 BPIV3、SeV、VSV 和 HSV-1。我们的研究发现,PBLD 可通过干扰素调节因子 3(IRF3)增强 I 型干扰素(IFN-I)和 ISGs 的表达。进一步的研究表明,PBLD 可促进 IRF3 的转录磷酸化(S385/386),从而促进病毒诱导的 IFN-I 的产生。有趣的是,PBLD 通过依赖 IRF3(K313/315)介导病毒触发的线粒体凋亡。从机制上讲,PBLD 通过 IRF3 将 Puma 蛋白招募到线粒体,从而促进了病毒诱导的细胞凋亡。此外,我们还对 IRF3 进行了突变分析,结果表明其转录或凋亡功能的缺失会显著增加病毒复制。此外,在病毒感染过程中,缺乏 PBLD 的巨噬细胞表现出 IFN-I 和 ISGs 表达下降,从而加剧了病毒感染。重要的是,缺乏 PBLD 的小鼠表现出病毒复制增加和对 SeV 感染的易感性,导致存活率下降。值得注意的是,PBLD 的化学激活剂 Cedrelone 能够减少 SeV 的复制。总之,我们首次发现了 PBLD 在病毒感染中的新功能,拓宽了我们对潜在治疗靶点的认识,为抗病毒药物的开发提供了新的见解。
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引用次数: 0
Inhibition of poly(ADP-Ribosyl)ation reduced vascular smooth muscle cells loss and improves aortic disease in a mouse model of human accelerated aging syndrome. 在人类加速衰老综合征的小鼠模型中,抑制多聚(ADP-核糖基)生成可减少血管平滑肌细胞的损失并改善主动脉疾病。
IF 8.1 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-02 DOI: 10.1038/s41419-024-07078-7
Déborah Cardoso, Solenn Guilbert, Philippe Guigue, Aurélie Carabalona, Karim Harhouri, Cécile Peccate, Johana Tournois, Zoheir Guesmia, Lino Ferreira, Catherine Bartoli, Nicolas Levy, Laurence Colleaux, Xavier Nissan, Antoine Muchir

Hutchinson-Gilford progeria syndrome (HGPS) is an extremely rare genetic disorder associated with features of accelerated aging. HGPS is an autosomal dominant disease caused by a de novo mutation of LMNA gene, encoding A-type lamins, resulting in the truncated form of pre-lamin A called progerin. While asymptomatic at birth, patients develop symptoms within the first year of life when they begin to display accelerated aging and suffer from growth retardation, and severe cardiovascular complications including loss of vascular smooth muscle cells (VSMCs). Recent works reported the loss of VSMCs as a major factor triggering atherosclerosis in HGPS. Here, we investigated the mechanisms by which progerin expression leads to massive VSMCs loss. Using aorta tissue and primary cultures of murine VSMCs from a mouse model of HGPS, we showed increased VSMCs death associated with increased poly(ADP-Ribosyl)ation. Poly(ADP-Ribosyl)ation is recognized as a post-translational protein modification that coordinates the repair at DNA damage sites. Poly-ADP-ribose polymerase (PARP) catalyzes protein poly(ADP-Ribosyl)ation by utilizing nicotinamide adenine dinucleotide (NAD+). Our results provided the first demonstration linking progerin accumulation, augmented poly(ADP-Ribosyl)ation and decreased nicotinamide adenine dinucleotide (NAD+) level in VSMCs. Using high-throughput screening on VSMCs differentiated from iPSCs from HGPS patients, we identified a new compound, trifluridine able to increase NAD+ levels through decrease of PARP-1 activity. Lastly, we demonstrate that trifluridine treatment in vivo was able to alleviate aortic VSMCs loss and clinical sign of progeria, suggesting a novel therapeutic approach of cardiovascular disease in progeria.

哈钦森-吉尔福特早衰综合征(HGPS)是一种极其罕见的遗传性疾病,具有加速衰老的特征。HGPS 是一种常染色体显性遗传病,病因是编码 A 型片层蛋白的 LMNA 基因发生新突变,导致前片层蛋白 A 的截短形式,即早衰素。患者出生时无症状,但在出生后第一年就会出现症状,开始加速衰老、生长迟缓和严重的心血管并发症,包括血管平滑肌细胞(VSMC)的丧失。最近的研究表明,血管平滑肌细胞(VSMC)的丧失是诱发 HGPS 动脉粥样硬化的主要因素。在此,我们研究了早老素表达导致 VSMC 大量丢失的机制。通过使用 HGPS 小鼠模型的主动脉组织和小鼠 VSMCs 的原代培养物,我们发现 VSMCs 的死亡与 poly(ADP-Ribosyl)ation 的增加有关。聚(ADP-核糖基)连接被认为是一种蛋白质翻译后修饰,可协调 DNA 损伤位点的修复。聚-ADP-核糖聚合酶(PARP)利用烟酰胺腺嘌呤二核苷酸(NAD+)催化蛋白质的聚(ADP-核糖)合成。我们的研究结果首次证明,早老素的积累、聚(ADP-Ribosyl)合成的增加与 VSMC 中烟酰胺腺嘌呤二核苷酸(NAD+)水平的降低有关。通过对来自 HGPS 患者的 iPSCs 分化的 VSMCs 进行高通量筛选,我们发现了一种新化合物 trifluridine,它能通过降低 PARP-1 活性来提高 NAD+ 水平。最后,我们证明了体内曲氟尿苷治疗能够缓解主动脉VSMCs的损失和早衰症的临床表现,为早衰症心血管疾病的治疗提供了一种新方法。
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引用次数: 0
Retraction Note: Zebrafish Noxa promotes mitosis in early embryonic development and regulates apoptosis in subsequent embryogenesis. 撤回声明:斑马鱼 Noxa 在早期胚胎发育过程中促进有丝分裂,并在随后的胚胎发育过程中调节细胞凋亡。
IF 8.1 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-02 DOI: 10.1038/s41419-024-07119-1
J-X Zhong, L Zhou, Z Li, Y Wang, J-F Gui
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引用次数: 0
Dronedarone hydrochloride (DH) induces pancreatic cancer cell death by triggering mtDNA-mediated pyroptosis. 盐酸决奈达隆(DH)通过引发mtDNA介导的热解作用诱导胰腺癌细胞死亡。
IF 8.1 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-02 DOI: 10.1038/s41419-024-07102-w
Ming-Qiao Li, Yu-Qi He, Meng-Ni Zhang, Wan Tang, Ya Tan, Yue Cheng, Mei Yang, Nan Zhao, Ling Li, Si-Rui Yu, Ruo-Lan Li, Qiong Pan, Ming-Yue Wu, Jin Chai

Pancreatic cancer is one of the leading causes of cancer-associated mortality, with a poor treatment approach. Previous study has shown that inducing pyroptosis in pancreatic ductal adenocarcinoma (PDAC) slows the growth of PDACs, implying that pyroptosis inducers are potentially effective for PDAC therapy. Here, we found that Dronedarone hydrochloride (DH), an antiarrhythmic drug, induces pyroptosis in pancreatic cancer cells and inhibits PDAC development in mice. In PANC-1 cells, DH caused cell death in a dosage- and time-dependent manner, with only pyroptosis inhibitors and GSDMD silencing rescuing the cell death, indicating that DH triggered GSDMD-dependent pyroptosis. Further work revealed that DH increased mitochondrial stresses and caused mitochondrial DNA (mtDNA) leakage, activating the cytosolic STING-cGAS and pyroptosis pathways. Finally, we assessed the anti-cancer effects of DH in a pancreatic cancer mouse model and found that DH treatment suppressed pancreatic tumor development in vivo. Collectively, our investigation demonstrates that DH triggers pyroptosis in PDAC and proposes its potential effects on anti-PDAC growth.

胰腺癌是导致癌症相关死亡的主要原因之一,但治疗效果不佳。先前的研究表明,诱导胰腺导管腺癌(PDAC)的热蛋白沉着可减缓PDAC的生长,这意味着热蛋白沉着诱导剂可能对PDAC的治疗有效。在这里,我们发现抗心律失常药物盐酸决奈达隆(DH)能诱导胰腺癌细胞的热蛋白沉积,并抑制小鼠 PDAC 的发展。在 PANC-1 细胞中,DH 以剂量和时间依赖性的方式导致细胞死亡,只有热蛋白沉积抑制剂和 GSDMD 沉默能挽救细胞死亡,这表明 DH 触发了 GSDMD 依赖性热蛋白沉积。进一步的研究发现,DH增加了线粒体应激并导致线粒体DNA(mtDNA)泄漏,激活了细胞质STING-cGAS和裂解途径。最后,我们在胰腺癌小鼠模型中评估了 DH 的抗癌作用,发现 DH 治疗抑制了体内胰腺肿瘤的发展。总之,我们的研究证明了 DH 触发了 PDAC 的化脓过程,并提出了它在抗 PDAC 生长方面的潜在作用。
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引用次数: 0
Mucosa-like differentiation of head and neck cancer cells is inducible and drives the epigenetic loss of cell malignancy. 头颈癌细胞的粘膜样分化是可诱导的,并驱动细胞恶性的表观遗传缺失。
IF 8.1 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-02 DOI: 10.1038/s41419-024-07065-y
Felix Oppel, Sarah Gendreizig, Laura Martinez-Ruiz, Javier Florido, Alba López-Rodríguez, Harkiren Pabla, Lakshna Loganathan, Leonie Hose, Philipp Kühnel, Pascal Schmidt, Matthias Schürmann, Judith Martha Neumann, Flavian Viyof Ful, Lars Uwe Scholtz, Dina Ligum, Frank Brasch, Karsten Niehaus, Germaine Escames, Tobias Busche, Jörn Kalinowski, Peter Goon, Holger Sudhoff

Head and neck squamous cell carcinoma (HNSCC) is a highly malignant disease with high death rates that have remained substantially unaltered for decades. Therefore, new treatment approaches are urgently needed. Human papillomavirus-negative tumors harbor areas of terminally differentiated tissue that are characterized by cornification. Dissecting this intrinsic ability of HNSCC cells to irreversibly differentiate into non-malignant cells may have tumor-targeting potential. We modeled the cornification of HNSCC cells in a primary spheroid model and analyzed the mechanisms underlying differentiation by ATAC-seq and RNA-seq. Results were verified by immunofluorescence using human HNSCC tissue of distinct anatomical locations. HNSCC cell differentiation was accompanied by cell adhesion, proliferation stop, diminished tumor-initiating potential in immunodeficient mice, and activation of a wound-healing-associated signaling program. Small promoter accessibility increased despite overall chromatin closure. Differentiating cells upregulated KRT17 and cornification markers. Although KRT17 represents a basal stem cell marker in normal mucosa, we confirm KRT17 to represent an early differentiation marker in HNSCC tissue. Cornification was frequently found surrounding necrotic areas in human tumors, indicating an involvement of pro-inflammatory stimuli. Indeed, inflammatory mediators activated the differentiation program in primary HNSCC cells. In HNSCC tissue, distinct cell differentiation states were found to create a common tissue architecture in normal mucosa and HNSCCs. Our data demonstrate a loss of cell malignancy upon faithful HNSCC cell differentiation, indicating that targeted differentiation approaches may be therapeutically valuable. Moreover, we describe KRT17 to be a candidate biomarker for HNSCC cell differentiation and early tumor detection.

头颈部鳞状细胞癌(HNSCC)是一种恶性程度很高的疾病,死亡率很高,几十年来基本没有改变。因此,迫切需要新的治疗方法。人类乳头状瘤病毒阴性肿瘤蕴藏着以粟粒化为特征的终末分化组织区域。剖析 HNSCC 细胞不可逆地分化为非恶性细胞的这种内在能力可能具有肿瘤靶向潜力。我们在原代球形模型中模拟了HNSCC细胞的粟粒化,并通过ATAC-seq和RNA-seq分析了分化的内在机制。我们使用不同解剖位置的人类 HNSCC 组织对结果进行了免疫荧光验证。HNSCC 细胞分化伴随着细胞粘附、增殖停止、免疫缺陷小鼠肿瘤诱发潜能减弱以及伤口愈合相关信号程序的激活。尽管染色质整体封闭,但小启动子的可及性却增加了。分化细胞上调 KRT17 和粟粒化标记。虽然KRT17代表正常粘膜中的基础干细胞标记,但我们证实KRT17代表HNSCC组织中的早期分化标记。在人类肿瘤坏死区周围经常发现粟粒化现象,这表明有促炎刺激因素的参与。事实上,炎症介质激活了原发性 HNSCC 细胞的分化程序。在 HNSCC 组织中发现,不同的细胞分化状态在正常粘膜和 HNSCC 中形成了共同的组织结构。我们的数据显示,忠实的 HNSCC 细胞分化后会丧失细胞恶性,这表明靶向分化方法可能具有治疗价值。此外,我们还发现 KRT17 是 HNSCC 细胞分化和早期肿瘤检测的候选生物标记物。
{"title":"Mucosa-like differentiation of head and neck cancer cells is inducible and drives the epigenetic loss of cell malignancy.","authors":"Felix Oppel, Sarah Gendreizig, Laura Martinez-Ruiz, Javier Florido, Alba López-Rodríguez, Harkiren Pabla, Lakshna Loganathan, Leonie Hose, Philipp Kühnel, Pascal Schmidt, Matthias Schürmann, Judith Martha Neumann, Flavian Viyof Ful, Lars Uwe Scholtz, Dina Ligum, Frank Brasch, Karsten Niehaus, Germaine Escames, Tobias Busche, Jörn Kalinowski, Peter Goon, Holger Sudhoff","doi":"10.1038/s41419-024-07065-y","DOIUrl":"10.1038/s41419-024-07065-y","url":null,"abstract":"<p><p>Head and neck squamous cell carcinoma (HNSCC) is a highly malignant disease with high death rates that have remained substantially unaltered for decades. Therefore, new treatment approaches are urgently needed. Human papillomavirus-negative tumors harbor areas of terminally differentiated tissue that are characterized by cornification. Dissecting this intrinsic ability of HNSCC cells to irreversibly differentiate into non-malignant cells may have tumor-targeting potential. We modeled the cornification of HNSCC cells in a primary spheroid model and analyzed the mechanisms underlying differentiation by ATAC-seq and RNA-seq. Results were verified by immunofluorescence using human HNSCC tissue of distinct anatomical locations. HNSCC cell differentiation was accompanied by cell adhesion, proliferation stop, diminished tumor-initiating potential in immunodeficient mice, and activation of a wound-healing-associated signaling program. Small promoter accessibility increased despite overall chromatin closure. Differentiating cells upregulated KRT17 and cornification markers. Although KRT17 represents a basal stem cell marker in normal mucosa, we confirm KRT17 to represent an early differentiation marker in HNSCC tissue. Cornification was frequently found surrounding necrotic areas in human tumors, indicating an involvement of pro-inflammatory stimuli. Indeed, inflammatory mediators activated the differentiation program in primary HNSCC cells. In HNSCC tissue, distinct cell differentiation states were found to create a common tissue architecture in normal mucosa and HNSCCs. Our data demonstrate a loss of cell malignancy upon faithful HNSCC cell differentiation, indicating that targeted differentiation approaches may be therapeutically valuable. Moreover, we describe KRT17 to be a candidate biomarker for HNSCC cell differentiation and early tumor detection.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":null,"pages":null},"PeriodicalIF":8.1,"publicationDate":"2024-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11446932/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364561","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
MAT2B regulates the protein level of MAT2A to preserve RNA N6-methyladenosine. MAT2B 可调节 MAT2A 的蛋白水平,以保护 RNA N6-甲基腺苷。
IF 8.1 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-01 DOI: 10.1038/s41419-024-07093-8
Xinyi Wan, Weiwu Zeng, Haonan Fan, Chenliang Wang, Shixun Han, Zhongxing Sun, Mei Tang, Juejia Shao, Yu Liu, Yuan Fang, Junqi Jia, Yin Tang, Yanjun Zhang, Bin Zhao, Dong Fang

MAT2B works together with MAT2A to synthesize S-Adenosyl methionine (SAM) as the primary methyl donor. MAT2B, despite lacking catalytic activity, exerts regulatory control over the enzymatic activity of MAT2A. In addition to the enzymatic activity regulation, we find that, in an NADP+-dependent manner, MAT2B binds and stabilizes MAT2A. Disruption of the cellular NADP+ remodels the protein level of MAT2A. The pentose phosphatase pathway regulates the level of MAT2A protein through the interaction of NADP+ with MAT2B. Additionally, MAT2B-MAT2A interaction regulates the mRNA m6A modification and stability. In liver tumors, the Mat2a mRNA level is elevated but the protein level is decreased by the restricted NADP+. Blocking the interaction between MAT2B and MAT2A by the keto diet can suppress liver tumor growth. These findings reveal that MAT2B is essential for regulating the protein levels of MAT2A and connecting SAM synthesis to mRNA m6A.

MAT2B 与 MAT2A 共同合成作为主要甲基供体的 S-腺苷蛋氨酸(SAM)。尽管 MAT2B 缺乏催化活性,但它对 MAT2A 的酶活性具有调控作用。除了酶活性调控外,我们还发现 MAT2B 以一种依赖 NADP+ 的方式结合并稳定 MAT2A。细胞中 NADP+ 的破坏重塑了 MAT2A 的蛋白质水平。戊糖磷酸酶途径通过 NADP+ 与 MAT2B 的相互作用调节 MAT2A 蛋白水平。此外,MAT2B-MAT2A 相互作用还能调节 mRNA m6A 的修饰和稳定性。在肝脏肿瘤中,MAT2a mRNA 水平升高,但蛋白水平却因 NADP+ 的限制而降低。通过酮饮食阻断MAT2B和MAT2A之间的相互作用可以抑制肝肿瘤的生长。这些发现揭示了 MAT2B 在调节 MAT2A 蛋白水平和连接 SAM 合成与 mRNA m6A 方面的重要作用。
{"title":"MAT2B regulates the protein level of MAT2A to preserve RNA N6-methyladenosine.","authors":"Xinyi Wan, Weiwu Zeng, Haonan Fan, Chenliang Wang, Shixun Han, Zhongxing Sun, Mei Tang, Juejia Shao, Yu Liu, Yuan Fang, Junqi Jia, Yin Tang, Yanjun Zhang, Bin Zhao, Dong Fang","doi":"10.1038/s41419-024-07093-8","DOIUrl":"10.1038/s41419-024-07093-8","url":null,"abstract":"<p><p>MAT2B works together with MAT2A to synthesize S-Adenosyl methionine (SAM) as the primary methyl donor. MAT2B, despite lacking catalytic activity, exerts regulatory control over the enzymatic activity of MAT2A. In addition to the enzymatic activity regulation, we find that, in an NADP<sup>+</sup>-dependent manner, MAT2B binds and stabilizes MAT2A. Disruption of the cellular NADP<sup>+</sup> remodels the protein level of MAT2A. The pentose phosphatase pathway regulates the level of MAT2A protein through the interaction of NADP<sup>+</sup> with MAT2B. Additionally, MAT2B-MAT2A interaction regulates the mRNA m6A modification and stability. In liver tumors, the Mat2a mRNA level is elevated but the protein level is decreased by the restricted NADP<sup>+</sup>. Blocking the interaction between MAT2B and MAT2A by the keto diet can suppress liver tumor growth. These findings reveal that MAT2B is essential for regulating the protein levels of MAT2A and connecting SAM synthesis to mRNA m6A.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":null,"pages":null},"PeriodicalIF":8.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11445541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Retraction Note: LncRNA HOTAIR regulates HIF-1α/AXL signaling through inhibition of miR-217 in renal cell carcinoma. 撤稿说明:LncRNA HOTAIR通过抑制肾细胞癌中的miR-217调节HIF-1α/AXL信号传导。
IF 8.1 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-01 DOI: 10.1038/s41419-024-07111-9
Quan Hong, Ou Li, Wei Zheng, Wen-Zhen Xiao, Lu Zhang, Di Wu, Guang-Yan Cai, John Cijiang He, Xiang-Mei Chen
{"title":"Retraction Note: LncRNA HOTAIR regulates HIF-1α/AXL signaling through inhibition of miR-217 in renal cell carcinoma.","authors":"Quan Hong, Ou Li, Wei Zheng, Wen-Zhen Xiao, Lu Zhang, Di Wu, Guang-Yan Cai, John Cijiang He, Xiang-Mei Chen","doi":"10.1038/s41419-024-07111-9","DOIUrl":"10.1038/s41419-024-07111-9","url":null,"abstract":"","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":null,"pages":null},"PeriodicalIF":8.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11445251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
STAT6/LINC01637 axis regulates tumor growth via autophagy and pharmacological targeting STAT6 as a novel strategy for uveal melanoma. STAT6/LINC01637轴通过自噬调节肿瘤生长,以STAT6为药物靶点是治疗葡萄膜黑色素瘤的新策略。
IF 8.1 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-01 DOI: 10.1038/s41419-024-07115-5
Bo Liu, Xueting Yao, Qinying Huang, Yichao Fan, Bo Yu, Jing Wang, Wencan Wu, Jinhui Dai

Compelling evidence has revealed a novel function of the STAT pathway in the pathophysiology of uveal melanoma (UM); however, its regulatory mechanisms remain unclear. Here, we analyzed the clinical prognostic value of STAT family genes in UM patients using bioinformatics approaches and found that high STAT6 expression is associated with poor prognosis. Furthermore, cellular experiments and a nude mouse model demonstrated that STAT6 promotes UM progression through the autophagy pathway both in vivo and in vitro. Next, RIP-PCR revealed that STAT6 protein binds to LINC01637 mRNA, which in turn regulates STAT6 expression to promote UM growth. Finally, molecular docking indicated that STAT6 is a target of Zoledronic Acid, which can delay UM tumorigenicity by inhibiting STAT6 expression. Taken together, our results indicate that the STAT6/LINC01637 axis promotes UM progression via autophagy and may serve as a potential therapeutic target for UM.

令人信服的证据揭示了 STAT 通路在葡萄膜黑色素瘤(UM)病理生理学中的新功能;然而,其调控机制仍不清楚。在此,我们利用生物信息学方法分析了 STAT 家族基因在 UM 患者中的临床预后价值,发现 STAT6 的高表达与预后不良有关。此外,细胞实验和裸鼠模型表明,STAT6 在体内和体外都能通过自噬途径促进 UM 的进展。接着,RIP-PCR 发现 STAT6 蛋白与 LINC01637 mRNA 结合,进而调节 STAT6 的表达,促进 UM 生长。最后,分子对接表明 STAT6 是唑来膦酸的靶点,唑来膦酸可以通过抑制 STAT6 的表达来延缓 UM 的致瘤性。综上所述,我们的研究结果表明,STAT6/LINC01637轴通过自噬促进UM的进展,可作为UM的潜在治疗靶点。
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引用次数: 0
Correction to: The IL-6-STAT3 axis mediates a reciprocal crosstalk between cancer-derived mesenchymal stem cells and neutrophils to synergistically prompt gastric cancer progression. 更正为IL-6-STAT3轴介导癌症间充质干细胞和中性粒细胞之间的相互串扰,协同促进胃癌进展。
IF 8.1 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-01 DOI: 10.1038/s41419-024-07100-y
Q Zhu, X Zhang, L Zhang, W Li, H Wu, X Yuan, F Mao, M Wang, W Zhu, H Qian, W Xu
{"title":"Correction to: The IL-6-STAT3 axis mediates a reciprocal crosstalk between cancer-derived mesenchymal stem cells and neutrophils to synergistically prompt gastric cancer progression.","authors":"Q Zhu, X Zhang, L Zhang, W Li, H Wu, X Yuan, F Mao, M Wang, W Zhu, H Qian, W Xu","doi":"10.1038/s41419-024-07100-y","DOIUrl":"10.1038/s41419-024-07100-y","url":null,"abstract":"","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":null,"pages":null},"PeriodicalIF":8.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11445406/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
NOD2 reduces the chemoresistance of melanoma by inhibiting the TYMS/PLK1 signaling axis. NOD2 通过抑制 TYMS/PLK1 信号轴来降低黑色素瘤的化疗耐药性。
IF 8.1 1区 生物学 Q1 CELL BIOLOGY Pub Date : 2024-10-01 DOI: 10.1038/s41419-024-07104-8
Fang Yun, Na Wu, Xiaojia Yi, Xuedan Zhang, Yu Feng, Qinxuan Ni, Yanlong Gai, Enjiang Li, Zhe Yang, Qiao Zhang, Buqing Sai, Yingmin Kuang, Yuechun Zhu

Nucleotide-binding oligomerization domain 2 (NOD2) is an immune sensor crucial for eliciting the innate immune responses. Nevertheless, discrepancies exist regarding the effect of NOD2 on different types of cancer. This study aimed to investigate these function of NOD2 in melanoma and its underlying mechanisms. We have validated the tumor suppressor effect of NOD2 in melanoma. NOD2 inhibited the proliferation of melanoma cells, hindering their migration and invasion while promoting the onset of apoptosis. Our study showed that NOD2 expression is closely related to pyrimidine and folate metabolism. NOD2 inhibits thymidylate synthase (TYMS) expression by promoting K48-type ubiquitination modification of TYMS, thereby decreasing the resistance of melanoma cells to 5-fluorouracil (5-FU) and capecitabine (CAP). TYMS was identified to form a complex with Polo-like Kinase 1 (PLK1) and activate the PLK1 signaling pathway. Furthermore, we revealed that the combination of the PLK1 inhibitor volasertib (BI6727) with 5-FU or CAP had a synergistic effect repressing the proliferation, migration, and autophagy of melanoma cells. Overall, our research highlights the protective role of NOD2 in melanoma and suggests that targeting NOD2 and the TYMS/PLK1 signaling axis is a high-profile therapy that could be a prospect for melanoma treatment.

核苷酸结合寡聚化结构域 2(NOD2)是一种免疫传感器,对激发先天性免疫反应至关重要。然而,NOD2 对不同类型癌症的影响存在差异。本研究旨在研究 NOD2 在黑色素瘤中的功能及其内在机制。我们验证了 NOD2 在黑色素瘤中的抑瘤作用。NOD2 可抑制黑色素瘤细胞的增殖,阻碍其迁移和侵袭,同时促进细胞凋亡。我们的研究表明,NOD2的表达与嘧啶和叶酸代谢密切相关。NOD2通过促进TYMS的K48型泛素化修饰来抑制胸苷酸合成酶(TYMS)的表达,从而降低黑色素瘤细胞对5-氟尿嘧啶(5-FU)和卡培他滨(CAP)的耐药性。研究发现,TYMS能与Polo-like Kinase 1(PLK1)形成复合物,并激活PLK1信号通路。此外,我们还发现,PLK1 抑制剂 volasertib (BI6727) 与 5-FU 或 CAP 联用具有抑制黑色素瘤细胞增殖、迁移和自噬的协同作用。总之,我们的研究强调了NOD2在黑色素瘤中的保护作用,并表明靶向NOD2和TYMS/PLK1信号轴是一种备受关注的疗法,可能是黑色素瘤治疗的前景之一。
{"title":"NOD2 reduces the chemoresistance of melanoma by inhibiting the TYMS/PLK1 signaling axis.","authors":"Fang Yun, Na Wu, Xiaojia Yi, Xuedan Zhang, Yu Feng, Qinxuan Ni, Yanlong Gai, Enjiang Li, Zhe Yang, Qiao Zhang, Buqing Sai, Yingmin Kuang, Yuechun Zhu","doi":"10.1038/s41419-024-07104-8","DOIUrl":"10.1038/s41419-024-07104-8","url":null,"abstract":"<p><p>Nucleotide-binding oligomerization domain 2 (NOD2) is an immune sensor crucial for eliciting the innate immune responses. Nevertheless, discrepancies exist regarding the effect of NOD2 on different types of cancer. This study aimed to investigate these function of NOD2 in melanoma and its underlying mechanisms. We have validated the tumor suppressor effect of NOD2 in melanoma. NOD2 inhibited the proliferation of melanoma cells, hindering their migration and invasion while promoting the onset of apoptosis. Our study showed that NOD2 expression is closely related to pyrimidine and folate metabolism. NOD2 inhibits thymidylate synthase (TYMS) expression by promoting K48-type ubiquitination modification of TYMS, thereby decreasing the resistance of melanoma cells to 5-fluorouracil (5-FU) and capecitabine (CAP). TYMS was identified to form a complex with Polo-like Kinase 1 (PLK1) and activate the PLK1 signaling pathway. Furthermore, we revealed that the combination of the PLK1 inhibitor volasertib (BI6727) with 5-FU or CAP had a synergistic effect repressing the proliferation, migration, and autophagy of melanoma cells. Overall, our research highlights the protective role of NOD2 in melanoma and suggests that targeting NOD2 and the TYMS/PLK1 signaling axis is a high-profile therapy that could be a prospect for melanoma treatment.</p>","PeriodicalId":9734,"journal":{"name":"Cell Death & Disease","volume":null,"pages":null},"PeriodicalIF":8.1,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11445241/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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Cell Death & Disease
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