Cellular signalling最新文献

筛选
英文 中文
Lipopolysaccharide-regulated RNF31/NRF2 axis in colonic epithelial cells mediates homeostasis of the intestinal barrier in ulcerative colitis 结肠上皮细胞中受脂多糖调控的 RNF31/NRF2 轴介导了溃疡性结肠炎肠屏障的平衡。
IF 4.4 2区 生物学
Cellular signalling Pub Date : 2024-10-20 DOI: 10.1016/j.cellsig.2024.111480
Chao-Tao Tang , Zi-de Liu , Peng Wang , Chun-Yan Zeng , You-Xiang Chen
{"title":"Lipopolysaccharide-regulated RNF31/NRF2 axis in colonic epithelial cells mediates homeostasis of the intestinal barrier in ulcerative colitis","authors":"Chao-Tao Tang ,&nbsp;Zi-de Liu ,&nbsp;Peng Wang ,&nbsp;Chun-Yan Zeng ,&nbsp;You-Xiang Chen","doi":"10.1016/j.cellsig.2024.111480","DOIUrl":"10.1016/j.cellsig.2024.111480","url":null,"abstract":"<div><h3>Background</h3><div>Although previous studies have shown that the Ring Finger Protein 31 (RNF31) gene confers susceptibility to inflammatory disease and colorectal cancer, the exact function of this protein in ulcerative colitis (UC) has not been determined.</div></div><div><h3>Methods</h3><div>A mouse dextran sulfate sodium (DSS)-induced experimental colitis model was used to study RNF31 and NRF2 in colitis. RNF31 silencing or overexpression in vitro was applied to address the role of RNF31 in colonic mucosal barrier damage. Immunohistochemistry and silico analysis was performed to investigate the expression of RNF31 via taking advantage of UC tissue samples and Gene Expression Omnibus (GEO) data, respectively. The cycloheximide (CHX)-chase experiment and Co-Immunoprecipitation (Co-IP) assays were conducted to explore the association of RNF31 protein with NRF2 and P62.</div></div><div><h3>Results</h3><div>RNF31 is highly expressed in UC patients, in inflamed murine colon induced DSS and Lipopolysaccharide (LPS)-treated epithelial cells, while the express of NRF2 was Tabdecreased. RNF31-knockdown mice in the DSS-induced colitis model had a less severe phenotype, which was associated with a more integrated barrier of colon epithelial cells. While depletion of NRF2 in colitis model exacerbated intestinal inflammation. Mechanistically, RNF31 promoted the degradation of NRF2 by regulating its ubiquitination. Upon stimulation by RNF31, NRF2 is K63 ubiquitinated, which is associated with the C871 residue of RNF31. Moreover, downregulated NRF2 mediates inflammation by promoting the secretion of IL1β and IL18, leading to damage of the intestinal barrier. Upon LPS stimulation, the interaction of the PUB domain of RNF31 with the UBA domain of P62 increased, resulting in decreased degradation of the RNF31 protein via autophagy.</div></div><div><h3>Conclusion</h3><div>Overall, depletion of RNF31 effectively relieves DSS-induced colitis in mice by inhibiting NRF2 degradation, suggesting that RNF31 may be a potential therapy for human ulcerative colitis.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"124 ","pages":"Article 111480"},"PeriodicalIF":4.4,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495987","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Sirt1-mediated deacetylation of PGC-1α alleviated hepatic steatosis in type 2 diabetes mellitus via improving mitochondrial fatty acid oxidation Sirt1 介导的 PGC-1α 去乙酰化可通过改善线粒体脂肪酸氧化减轻 2 型糖尿病患者的肝脂肪变性。
IF 4.4 2区 生物学
Cellular signalling Pub Date : 2024-10-18 DOI: 10.1016/j.cellsig.2024.111478
Jiale Pang , Longxiang Yin , Wenjie Jiang , Haiyan Wang , Qian Cheng , Zhenzhou Jiang , Yanjuan Cao , Xia Zhu , Baojing Li , Sitong Qian , Xiaoxing Yin , Tao Wang , Qian Lu , Tingting Yang
{"title":"Sirt1-mediated deacetylation of PGC-1α alleviated hepatic steatosis in type 2 diabetes mellitus via improving mitochondrial fatty acid oxidation","authors":"Jiale Pang ,&nbsp;Longxiang Yin ,&nbsp;Wenjie Jiang ,&nbsp;Haiyan Wang ,&nbsp;Qian Cheng ,&nbsp;Zhenzhou Jiang ,&nbsp;Yanjuan Cao ,&nbsp;Xia Zhu ,&nbsp;Baojing Li ,&nbsp;Sitong Qian ,&nbsp;Xiaoxing Yin ,&nbsp;Tao Wang ,&nbsp;Qian Lu ,&nbsp;Tingting Yang","doi":"10.1016/j.cellsig.2024.111478","DOIUrl":"10.1016/j.cellsig.2024.111478","url":null,"abstract":"<div><div>Being activated by deacetylation, peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) has become an important regulator of metabolic-related diseases. The activation of Sirtuin 1 (Sirt1) by resveratrol was likely to deacetylate PGC-1α. However, the role of deacetylated PGC-1α in the alleviation of activated Sirt1 on type 2 diabetes mellitus (T2DM)-related fatty liver disease (FLD) remained unexplored. The aim of this study was to investigate the potential impact of Sirt1-mediated deacetylation of PGC-1α on T2DM-associated FLD and its underlying mechanisms. Our findings revealed that, along with the decreased Sirt1, the levels of acetylated PGC-1α were up-regulated in hepatocytes co-stimulated with high glucose (HG) and free fatty acids (FFA). Down-regulated Sirt1 inactivated PGC-1α by inhibiting its deacetylation, while activating Sirt1 improved hepatic injury by reducing lipid droplet accumulation through the deacetylation of PGC-1α. However, the beneficial effects of Sirt1 activation on hepatic steatosis were inhibited by PGC-1α antagonist in vitro. Mechanistically, activating Sirt1 enhanced mitochondrial function by promoting PGC-1α activity, thereby facilitating hepatic fatty acid oxidation (FAO). In conclusion, Sirt1-mediated deacetylation of PGC-1α mitigated hepatic lipotoxicity by enhancing mitochondrial FAO, which contributed to the restoration of mitochondrial function in T2DM. The activation of Sirt1-mediated PGC-1α deacetylation might represent a promising therapeutic approach for T2DM-associated FLD.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"124 ","pages":"Article 111478"},"PeriodicalIF":4.4,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
GALNT14-mediated O-glycosylation drives lung adenocarcinoma progression by reducing endogenous reactive oxygen species generation GALNT14 介导的 O 型糖基化通过减少内源性活性氧的生成来推动肺腺癌的发展。
IF 4.4 2区 生物学
Cellular signalling Pub Date : 2024-10-18 DOI: 10.1016/j.cellsig.2024.111477
Bingbing Tang , Kelong Wang , Qiulei Ren , Junshuo Zhou , Yuewen Xu , Liaoyuan Liu , Bin Yin , Yaling Zhang , Qian Huang , Ruiqi Lv , Zhiguo Luo , Hongyan Zhao , Li Shen
{"title":"GALNT14-mediated O-glycosylation drives lung adenocarcinoma progression by reducing endogenous reactive oxygen species generation","authors":"Bingbing Tang ,&nbsp;Kelong Wang ,&nbsp;Qiulei Ren ,&nbsp;Junshuo Zhou ,&nbsp;Yuewen Xu ,&nbsp;Liaoyuan Liu ,&nbsp;Bin Yin ,&nbsp;Yaling Zhang ,&nbsp;Qian Huang ,&nbsp;Ruiqi Lv ,&nbsp;Zhiguo Luo ,&nbsp;Hongyan Zhao ,&nbsp;Li Shen","doi":"10.1016/j.cellsig.2024.111477","DOIUrl":"10.1016/j.cellsig.2024.111477","url":null,"abstract":"<div><div>Aberrant glycosylation, resulting from dysregulated expression of glycosyltransferases, is a prevalent feature of cancer cells. <em>N</em>-acetylgalactosaminyltransferase-14 (GALNT14) serves as a pivotal enzyme responsible for initiating O-GalNAcylation. It remains unclear whether and how GALNT14 affects lung adenocarcinoma (LUAD). Here, GALNT14 expression in LUAD was analyzed by searching public databases and verified by examining clinical samples. Bioinformatics, LC-MS/MS, RNA-seq, and RIP-seq analyses were used to uncover the mechanism underlying GALNT14. We observed that GALNT14 was frequently overexpressed in LUAD tissues. High GALNT14 expression was positively associated with advanced TNM stage, larger tumor size, and unfavorable prognosis. Functionally, GALNT14 facilitated LUAD cell proliferation, migration, and invasion in vitro and accelerated tumor growth in vivo. Mechanistically, GALNT14 reduced the accumulation of endogenous reactive oxygen species (ROS) to exert its oncogenic function via O-glycosylating hnRNPUL1 to upregulate AKR1C2 expression. Meanwhile, GALNT14 expression was directly modulated by miR-125a.These findings indicated that GALNT14-mediated O-GalNAcylation could drive LUAD progression via eliminating ROS and might be a valuable therapeutic target.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"124 ","pages":"Article 111477"},"PeriodicalIF":4.4,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Foxd3/SLC5A6 axis regulates apoptosis in LUAD cells by controlling mitochondrial biotin uptake Foxd3/SLC5A6轴通过控制线粒体生物素摄取调节LUAD细胞的凋亡。
IF 4.4 2区 生物学
Cellular signalling Pub Date : 2024-10-18 DOI: 10.1016/j.cellsig.2024.111473
Chong Zheng , Wenxuan Hu , Danni Wu , Ruiheng Chen , Chun Xu , Risheng Huang
{"title":"Foxd3/SLC5A6 axis regulates apoptosis in LUAD cells by controlling mitochondrial biotin uptake","authors":"Chong Zheng ,&nbsp;Wenxuan Hu ,&nbsp;Danni Wu ,&nbsp;Ruiheng Chen ,&nbsp;Chun Xu ,&nbsp;Risheng Huang","doi":"10.1016/j.cellsig.2024.111473","DOIUrl":"10.1016/j.cellsig.2024.111473","url":null,"abstract":"<div><div>Lung cancer remains one of the leading causes of cancer-related mortality worldwide, with non-small cell lung cancer (NSCLC) accounting for over 85 % of cases. Lung adenocarcinoma (LUAD) is the most common subtype of NSCLC, and while targeted therapies and immune checkpoint inhibitors have improved outcomes, many patients exhibit resistance, necessitating the development of novel treatments. This study explores the role of the SLC5A6 gene, which encodes a sodium-dependent multivitamin transporter critical for mitochondrial function, in LUAD progression. We found that SLC5A6 is significantly upregulated in LUAD tissues and is associated with poor prognosis. Overexpression of SLC5A6 enhanced cell proliferation and migration, while knockout of SLC5A6 impaired these processes and induced apoptosis by disrupting mitochondrial function. Additionally, we identified Foxd3 as a key transcription factor regulating SLC5A6 expression. In vivo experiments demonstrated that SLC5A6 knockout effectively inhibited tumor growth. These findings suggest that SLC5A6 is a potential therapeutic target for LUAD, offering a new avenue for treatment strategies.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"125 ","pages":"Article 111473"},"PeriodicalIF":4.4,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459259","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
NSUN5 promotes tumorigenic phenotypes through the WNT signaling pathway and immunosuppression of CD8+ T cells in gastric cancer NSUN5 通过 WNT 信号通路和 CD8+ T 细胞的免疫抑制促进胃癌的致瘤表型。
IF 4.4 2区 生物学
Cellular signalling Pub Date : 2024-10-18 DOI: 10.1016/j.cellsig.2024.111475
Shuhao Liu , Yong Liu , Yijun Zhou , Gaoshui Xia , Haibo Liu , Yu Zeng , Zhihui Pei , Jing Cao , Guifang Jing , Hailin Zou , Chuanwen Liao
{"title":"NSUN5 promotes tumorigenic phenotypes through the WNT signaling pathway and immunosuppression of CD8+ T cells in gastric cancer","authors":"Shuhao Liu ,&nbsp;Yong Liu ,&nbsp;Yijun Zhou ,&nbsp;Gaoshui Xia ,&nbsp;Haibo Liu ,&nbsp;Yu Zeng ,&nbsp;Zhihui Pei ,&nbsp;Jing Cao ,&nbsp;Guifang Jing ,&nbsp;Hailin Zou ,&nbsp;Chuanwen Liao","doi":"10.1016/j.cellsig.2024.111475","DOIUrl":"10.1016/j.cellsig.2024.111475","url":null,"abstract":"<div><div>NSUN5, a key member of the M5C methylation family, plays a significant role in fundamental biological processes like cell proliferation and differentiation. However, its specific function and mechanisms in gastric cancer remain insufficiently understood. Initially, we examined NSUN5's differential expression in gastric cancer versus normal tissues, along with survival trends, associated signaling pathways, and immune infiltration using the TCGA database. Subsequently, we conducted immunohistochemistry experiments to assess NSUN5 expression in gastric cancer tissues. Gain-and loss-of-function experiments were carried out to investigate NSUN5's impact on the proliferation, stemness, and migratory capabilities of gastric cancer cells, as well as the expression of vital proteins in pertinent signaling pathways. Our findings demonstrate that NSUN5 is not only overexpressed in gastric cancer tissues, but also positively associated with tumor stage and inversely linked with patient prognosis. NSUN5 promotes the in vitro proliferation, stemness, and migration of gastric cancer cells, and the in vivo growth of these cells, chiefly through the activation of the WNT/β-catenin signaling pathway. Additionally, NSUN5 appears to diminish the infiltration of CD8+ T cells in gastric cancer, contributing to immune evasion. In conclusion, NSUN5 functions as a proto-oncogene in the progression of gastric cancer and may serve as a potential therapeutic target.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"124 ","pages":"Article 111475"},"PeriodicalIF":4.4,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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
Notch signaling in digestive system cancers: Roles and therapeutic prospects 消化系统癌症中的 Notch 信号:作用和治疗前景
IF 4.4 2区 生物学
Cellular signalling Pub Date : 2024-10-18 DOI: 10.1016/j.cellsig.2024.111476
Yingru Liu , Xinyu Gu , Mengjuan Xuan , Na Lou , Leiya Fu , Juan Li , Chen Xue
{"title":"Notch signaling in digestive system cancers: Roles and therapeutic prospects","authors":"Yingru Liu ,&nbsp;Xinyu Gu ,&nbsp;Mengjuan Xuan ,&nbsp;Na Lou ,&nbsp;Leiya Fu ,&nbsp;Juan Li ,&nbsp;Chen Xue","doi":"10.1016/j.cellsig.2024.111476","DOIUrl":"10.1016/j.cellsig.2024.111476","url":null,"abstract":"<div><div>Digestive system cancers rank among the most prevalent malignant tumors, maintaining persistently high incidence and mortality rates. Notch signaling activity, often aberrant in esophageal, gastric, hepatic, pancreatic, and colorectal cancers, plays a pivotal role in the initiation, progression, and therapy resistance of these malignancies. As a highly conserved pathway, Notch signaling is integral to cell differentiation, survival, proliferation, stem cell renewal, development, and morphogenesis. Its dysregulation has been increasingly linked to various diseases, particularly digestive system cancers. In these malignancies, altered Notch signaling influences multiple biological processes, including cell proliferation, invasion, cell cycle progression, immune evasion, drug resistance, and stemness maintenance. Understanding the mechanisms of Notch signaling in digestive system cancers is essential for the development of novel targeted therapies. Numerous Notch pathway-targeting drugs are currently in preclinical studies, demonstrating promising efficacy both as monotherapies and in combination with conventional anti-cancer treatments. This review summarizes recent high-quality findings on the involvement of Notch signaling in digestive system cancers, focusing on the expression changes and pathological mechanisms of its dysregulated components. Special emphasis is placed on the potential of translating Notch-targeted approaches into therapeutic strategies, which hold promise for overcoming the limitations of existing treatments and improving the poor prognosis associated with these cancers.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"124 ","pages":"Article 111476"},"PeriodicalIF":4.4,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459261","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
HKDC1 promotes autophagy and proliferation in pancreatic adenocarcinoma through interaction with PARP1 and poly(ADP-ribosyl)ation HKDC1 通过与 PARP1 和聚(ADP-核糖基)的相互作用促进胰腺癌的自噬和增殖。
IF 4.4 2区 生物学
Cellular signalling Pub Date : 2024-10-16 DOI: 10.1016/j.cellsig.2024.111474
Qiang Pang , Shansong Huang , Huiying Wang , Jiaqing Cao
{"title":"HKDC1 promotes autophagy and proliferation in pancreatic adenocarcinoma through interaction with PARP1 and poly(ADP-ribosyl)ation","authors":"Qiang Pang ,&nbsp;Shansong Huang ,&nbsp;Huiying Wang ,&nbsp;Jiaqing Cao","doi":"10.1016/j.cellsig.2024.111474","DOIUrl":"10.1016/j.cellsig.2024.111474","url":null,"abstract":"<div><h3>Background</h3><div>HKDC1 has been shown to play an important role in promoting malignant progression of pancreatic adenocarcinoma (PAAD), but the exact mechanism is unclear. This study aimed to investigate the function of HKDC1 in autophagy activation and cell proliferation.</div></div><div><h3>Methods</h3><div>By GSEA analysis of TCGA data of PAAD, we found that HKDC1 was closely associated with autophagy. We evaluated the effects of HKDC1 knockdown and overexpression on the expression of LC3B, an autophagy marker, and Cyclin D1 and PCNA, cell proliferation-associated proteins, by Western blotting (WB) and transmission electron microscopy (TEM) analysis.</div></div><div><h3>Results</h3><div>Knockdown of HKDC1 decreased LC3B expression and led to a decrease in the accumulation of autophagic vesicles and autophagic lysosomes, while overexpression of HKDC1 produced the opposite effect. Meanwhile, HKDC1 overexpression significantly promoted the proliferation of PAAD cells and increased the expression levels of Cyclin D1 and PCNA. Further studies showed that HKDC1 enhanced PARP1's own poly ADP-ribosylation (PARylation) activity by interacting with PARP1, which in turn promoted autophagy. In vivo experiments showed that knockdown of HKDC1 significantly inhibited the growth of pancreatic cancer cells in nude mice in vivo, reduced tumor volume and weight, and down-regulated the expression of PARP1, LC3, Cyclin D1 and PCNA.</div></div><div><h3>Conclusion</h3><div>HKDC1 plays a critical role in the malignant progression of PAAD by activating autophagy and promoting cell proliferation. Our findings suggest that targeting HKDC1 and its downstream signaling pathways may provide novel strategies for PAAD treatment.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"124 ","pages":"Article 111474"},"PeriodicalIF":4.4,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459270","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Glycolytic reprogramming in microglia: A potential therapeutic target for ischemic stroke 小胶质细胞中的糖酵解重编程:缺血性中风的潜在治疗靶点
IF 4.4 2区 生物学
Cellular signalling Pub Date : 2024-10-15 DOI: 10.1016/j.cellsig.2024.111466
Guangming Zhang , Anliu Zhao , Xiaolu Zhang , Miao Zeng , Huayuan Wei , Xu Yan , Jie Wang , Xijuan Jiang , Yongna Dai
{"title":"Glycolytic reprogramming in microglia: A potential therapeutic target for ischemic stroke","authors":"Guangming Zhang ,&nbsp;Anliu Zhao ,&nbsp;Xiaolu Zhang ,&nbsp;Miao Zeng ,&nbsp;Huayuan Wei ,&nbsp;Xu Yan ,&nbsp;Jie Wang ,&nbsp;Xijuan Jiang ,&nbsp;Yongna Dai","doi":"10.1016/j.cellsig.2024.111466","DOIUrl":"10.1016/j.cellsig.2024.111466","url":null,"abstract":"<div><div>Ischemic stroke is currently the second leading cause of mortality worldwide, with limited treatment options available. As resident immune cells, microglia promptly respond to cerebral ischemic injury, influencing neuroinflammatory damage and neurorepair. Studies suggest that microglia undergo metabolic reprogramming from mitochondrial oxidative phosphorylation to glycolysis in response to ischemia, significantly impacting their function during ischemic stroke. Therefore, this study aims to investigate the roles and regulatory mechanisms involved in this process, aiming to identify a new therapeutic target or potential drug candidate.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"124 ","pages":"Article 111466"},"PeriodicalIF":4.4,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
ARL8B promotes hepatocellular carcinoma progression and inhibits antitumor activity of lenvatinib via MAPK/ERK signaling by interacting with RAB2A ARL8B 与 RAB2A 相互作用,通过 MAPK/ERK 信号转导促进肝细胞癌的进展并抑制来伐替尼的抗肿瘤活性。
IF 4.4 2区 生物学
Cellular signalling Pub Date : 2024-10-15 DOI: 10.1016/j.cellsig.2024.111470
Mo-Mo Cao , Yi-Ming Li , Xiang Ding , Feng Fang , Lian-Yue Yang
{"title":"ARL8B promotes hepatocellular carcinoma progression and inhibits antitumor activity of lenvatinib via MAPK/ERK signaling by interacting with RAB2A","authors":"Mo-Mo Cao ,&nbsp;Yi-Ming Li ,&nbsp;Xiang Ding ,&nbsp;Feng Fang ,&nbsp;Lian-Yue Yang","doi":"10.1016/j.cellsig.2024.111470","DOIUrl":"10.1016/j.cellsig.2024.111470","url":null,"abstract":"<div><div>Tumor recurrence and metastasis are important factors affecting postoperative survival in hepatocellular carcinoma (HCC) patients. ADP Ribosylation factor-like GTPase 8B (ARL8B) plays a crucial role in many biological processes, including lysosomal function, immune response, and cellular communication, all of which are related to the occurrence and development of tumors. However, its role in HCC remains unclear. Herein, we revealed that ARL8B is consistently elevated in HCC tissues compared to normal liver tissues, suggesting an unfavorable outcome in HCC patients. Increased ARL8B levels promoted the malignant phenotype of HCC <em>in vitro</em> and <em>in vivo</em>. Notably, ARL8B also induced epithelial-to-mesenchymal transition (EMT) in HCC cells. Mechanistically, the results of bioinformatics analysis combined with mass spectrometry revealed the potential downstream target molecule RAB2A of ARL8B. ARL8B directly interacted with RAB2A and increased the levels of GTP-bound RAB2A, thereby contributing to the activation of the extracellular signal-regulated kinase (ERK) signaling pathway. Interestingly, knockout of ARL8B in Hep3B cells enhanced the antitumor activity of lenvatinib <em>in vitro</em> and <em>in vivo</em>. Furthermore, AAV-shARL8B enhanced the inhibition of HCC growth through lenvatinib, providing new insights into its mechanism of action in lenvatinib-insensitive patients. In conclusion, ARL8B promotes the malignant phenotype of HCC and EMT <em>via</em> RAB2A mediated activation of the MAPK/ERK signaling pathway and is expected to be a valuable prognostic indicator and therapeutic target for HCC patients.</div></div>","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"124 ","pages":"Article 111470"},"PeriodicalIF":4.4,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Retraction notice to “Tumor-secreted GRP78 facilitates the migration of macrophages into tumors by promoting cytoskeleton remodeling” [Cellular Signalling volume (60) August 2019, 1–16] 肿瘤分泌的GRP78通过促进细胞骨架重塑促进巨噬细胞向肿瘤迁移》的撤稿通知[《细胞信号》2019年8月卷(60),1-16]。
IF 4.4 2区 生物学
Cellular signalling Pub Date : 2024-10-15 DOI: 10.1016/j.cellsig.2024.111460
Xiaoqin La , Lichao Zhang , Yufei Yang , Hanqing Li , Guisheng Song , Zhuoyu Li
{"title":"Retraction notice to “Tumor-secreted GRP78 facilitates the migration of macrophages into tumors by promoting cytoskeleton remodeling” [Cellular Signalling volume (60) August 2019, 1–16]","authors":"Xiaoqin La ,&nbsp;Lichao Zhang ,&nbsp;Yufei Yang ,&nbsp;Hanqing Li ,&nbsp;Guisheng Song ,&nbsp;Zhuoyu Li","doi":"10.1016/j.cellsig.2024.111460","DOIUrl":"10.1016/j.cellsig.2024.111460","url":null,"abstract":"","PeriodicalId":9902,"journal":{"name":"Cellular signalling","volume":"124 ","pages":"Article 111460"},"PeriodicalIF":4.4,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142459263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信