International Journal of Biochemistry & Cell Biology最新文献_第3页

Integrated stress response-upregulated mitochondrial SLC1A5var enhances glucose dependency in human breast cancer cells in vitro 综合应激反应上调线粒体 SLC1A5var 可增强体外人类乳腺癌细胞对葡萄糖的依赖性。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-11-04 DOI: 10.1016/j.biocel.2024.106688

Sheng-Fan Wang , Yu-Chieh Ho , Chian-Ying Chou , Yuh-Lih Chang , Hsin-Chen Lee , Ling-Ming Tseng

{"title":"Integrated stress response-upregulated mitochondrial SLC1A5var enhances glucose dependency in human breast cancer cells in vitro","authors":"Sheng-Fan Wang , Yu-Chieh Ho , Chian-Ying Chou , Yuh-Lih Chang , Hsin-Chen Lee , Ling-Ming Tseng","doi":"10.1016/j.biocel.2024.106688","DOIUrl":"10.1016/j.biocel.2024.106688","url":null,"abstract":"<div><div>Breast cancer is the most commonly diagnosed cancer among women. The growth of triple-negative breast cancer (TNBC) cells is glucose-dependent. The integrated stress response (ISR) is a cellular stress response to glucose depletion. The ISR-solute carrier family 7 member 11 pathway is activated during glucose depletion and contributes to glucose dependence by decreasing intracellular glutamate levels. Solute carrier family 1 member 5 (SLC1A5) and the mitochondrial solute carrier family 1 member 5 variant (SLC1A5var) are glutamine transporters that play essential roles in the reprogramming of cancer metabolism. However, whether ISR can regulate mitochondrial SLC1A5var expression and further affect glucose dependence remains unclear. Glucose depletion-, oligomycin-, and salubrinal-activated activating transcription factor-4 (ATF4) induced SLC1A5var expression. ATF4 is critical for SLC1A5var regulation, as it binds to specific regulatory elements in its promoter. SLC1A5var knockdown decreases glucose depletion-induced cell death, whereas SLC1A5var overexpression increases glucose depletion-induced cell death in TNBC cells. SLC1A5var knockdown reduced cancer cell proliferation, colony formation, and migration, whereas SLC1A5var overexpression increased cell proliferation and migration. Moreover, the knockdown of SLC1A5var reduces the oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) while increasing the maximal OCR and ECAR under glucose depletion. These results suggest that activated ISR-induced increased expression of SLC1A5var may regulate mitochondrial oxidative phosphorylation and glycolytic metabolic characteristics to enhance glucose depletion-induced cell death. In conclusion, SLC1A5var plays a vital role in metabolic reprogramming and may be a potential target for breast cancer treatment.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106688"},"PeriodicalIF":3.4,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142591925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Corrigendum to “Dual blockade of the A1 and A2A adenosine receptor prevents amyloid beta toxicity in neuroblastoma cells exposed to aluminum chloride” [Int. J. Biochem. Cell Biol. 54 (2014) 122–136] 更正："双重阻断A1和A2A腺苷受体可防止暴露于氯化铝的神经母细胞瘤细胞中淀粉样β的毒性" [Int. J. Biochem. Cell Biol. 54 (2014) 122-136]。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-11-01 DOI: 10.1016/j.biocel.2024.106677

Salvatore Giunta , Violetta Andriolo , Alessandro Castorina

引用次数: 0

Corrigendum to “15-lipoxygenase-1/15-hydroxyeicosatetraenoic acid promotes hepatocellular cancer cells growth through protein kinase B and heat shock protein 90 complex activation” [Int. J. Biochem. Cell Biol. 45 (2013) 1031–41] 更正："15-脂氧合酶-1/15-羟基二十碳四烯酸通过蛋白激酶 B 和热休克蛋白 90 复合物激活促进肝癌细胞生长" [Int. J. Biochem. Cell Biol. 45 (2013) 1031-41]。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-11-01 DOI: 10.1016/j.biocel.2024.106670

Jun Ma , Lei Zhang , Jianguo Zhang , Mengmeng Liu , Liuping Wei , Tingting Shen , Cui Ma , Yanyan Wang , Yingli Chen , Daling Zhu

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Retraction notice to “Downregulation of Rab23 inhibits proliferation, invasion, and metastasis of human ovarian cancer” [Int. J. Biochem. Cell Biol. 116 (2019) 105617] 下调 Rab23 抑制人类卵巢癌的增殖、侵袭和转移》的撤稿通知 [Int. J. Biochem. Cell Biol. 116 (2019) 105617]。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-11-01 DOI: 10.1016/j.biocel.2024.106673

Lingling Gao , Mingjun Zheng , Qian Guo , Xin Nie , Xiao Li , Yingying Hao , Juanjuan Liu , Liancheng Zhu , Bei Lin

引用次数: 0

Retraction notice to “Nucleocapsid protein of SARS-CoV activates the expression of cyclooxygenase-2 by binding directly to regulatory elements for nuclear factor-kappa B and CCAAT/enhancer binding protein” [Int. J. Biochem. Cell Biol. 38 (2006) 1417–1428] 关于 "SARS-CoV的核壳蛋白通过直接与核因子-卡巴B和CCAAT/增强子结合蛋白的调控元件结合，激活环氧化酶-2的表达 "的撤稿通知[Int. J. Biochem. Cell Biol. 38 (2006) 1417-1428]。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-11-01 DOI: 10.1016/j.biocel.2024.106674

Xiaohong Yan, Qian Hao, Yongxin Mu, Khalid Amine Timani, Linbai Ye, Ying Zhu, Jianguo Wu

引用次数: 0

Aminoadipic acid aggravates atherosclerotic vascular inflammation through ROS/TXNIP/NLRP3 pathway, a harmful microbial metabolite reduced by paeonol 氨基己二酸通过 ROS/TXNIP/NLRP3 通路加重动脉粥样硬化性血管炎症，芍药酚可减少有害微生物代谢物的产生

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-10-26 DOI: 10.1016/j.biocel.2024.106678

Tian Wang , Hongfei Wu , Xiaoyan Shi , Min Dai , Yarong Liu

{"title":"Aminoadipic acid aggravates atherosclerotic vascular inflammation through ROS/TXNIP/NLRP3 pathway, a harmful microbial metabolite reduced by paeonol","authors":"Tian Wang , Hongfei Wu , Xiaoyan Shi , Min Dai , Yarong Liu","doi":"10.1016/j.biocel.2024.106678","DOIUrl":"10.1016/j.biocel.2024.106678","url":null,"abstract":"<div><h3>Aim</h3><div>Our previous study has found a differential microbial metabolite in atherosclerosis (AS) mice, aminoadipic acid (AAA), which was considered as a potential harmful metabolite. However, whether it can promote AS vascular inflammation and its mechanisms remain unclear. Paeonol (Pae) plays an anti-AS role by regulating the metabolic profile, but whether Pae exerts its antiatherogenic effect by reducing serum AAA levels is unknown.</div></div><div><h3>Results</h3><div>The clinical trial results showed that the AS patients’ serum AAA levels were higher than those healthy people’. Besides, AAA supplementation could increase aortic plaque size, serum inflammatory cytokines levels and liver malondialdehyde, superoxide dismutase levels in AS mice. Moreover, after AAA stimulation, the ROS levels and ASC, TXNIP, NLRP3 and caspase-1 proteins levels were increased in HUVECs, which could be reversed by antioxidant NAC and NLRP3 inhibitor. Pae significantly reduced the plaque size in the aorta, improved blood lipid levels and decreased serum inflammation factor levels in AS mice. Simultaneously, Pae could reduce the serum AAA levels of AS mice through the gut microbiota transmission. Finally, Pae inhibited NLRP3 inflammasome activation in aortas of AS mice. Broad-spectrum antibiotics could weaken the inhibitory effect of Pae on NLRP3 inflammasome.</div></div><div><h3>Conclusion</h3><div>Our study clarified that AAA could promote AS vascular inflammation via activating the ROS/TXNIP/NLRP3 pathway. Pae could inhibit AS development by reducing serum AAA levels in a microbiota-dependent manner. Taken together, we proposed that AAA could be served as a potential biomarker for AS clinical diagnosis and provided a new treatment strategy for AS.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"177 ","pages":"Article 106678"},"PeriodicalIF":3.4,"publicationDate":"2024-10-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142554306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

The emerging role of Never-in-Mitosis A - Related Kinases in the endothelium 内皮细胞中从未蜕变的 A 相关激酶的新作用

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-10-24 DOI: 10.1016/j.biocel.2024.106679

Nektarios Barabutis, Saikat Fakir

引用次数: 0

ASPSCR1::TFE3-mediated upregulation of insulin receptor substrate 2 (IRS-2) activates PI3K/AKT signaling and promotes malignant phenotype ASPSCR1::TFE3介导的胰岛素受体底物2（IRS-2）上调激活了PI3K/AKT信号转导，并促进了恶性表型的形成。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-10-16 DOI: 10.1016/j.biocel.2024.106676

Naoko Ishiguro, Mayumi Nakagawa

{"title":"ASPSCR1::TFE3-mediated upregulation of insulin receptor substrate 2 (IRS-2) activates PI3K/AKT signaling and promotes malignant phenotype","authors":"Naoko Ishiguro, Mayumi Nakagawa","doi":"10.1016/j.biocel.2024.106676","DOIUrl":"10.1016/j.biocel.2024.106676","url":null,"abstract":"<div><div>The <em>ASPSCR1::TFE3</em> fusion gene, resulting from chromosomal translocation, is detected in alveolar soft part sarcoma (ASPS) and a subset of renal cell carcinomas (RCC). The ASPSCR1::TFE3 oncoprotein, functioning as an aberrant transcription factor, contributes to tumor development and progression by inappropriately upregulating target genes. Here, we identified insulin receptor substrate 2 (IRS-2), a cytoplasmic adaptor protein, as a novel transcriptional target of ASPSCR1::TFE3. Ectopic expression of ASPSCR1::TFE3 led to increased IRS-2 mRNA and protein levels. Chromatin immunoprecipitation and luciferase assays demonstrated that ASPSCR1::TFE3 bound to the <em>IRS-2</em> promoter region and enhanced its transcription. Moreover, IRS-2 was highly expressed in the ASPSCR1::TFE3-positive RCC cell line FU-UR1, while small interfering RNA-mediated depletion of ASPSCR1::TFE3 markedly decreased IRS-2 mRNA and protein levels. Functionally, IRS-2 knockdown attenuated activation of the PI3K/AKT pathway and reduced proliferation, migration, invasion, adhesion, and clonogenicity in FU-UR1 cells. Pharmacological inhibition of IRS-2 also reduced AKT activation as well as cell viability, clonogenicity, migration, invasion, and adhesion. These findings suggest that IRS-2, regulated by ASPSCR1::TFE3, promotes tumor progression by activating PI3K/AKT signaling and enhancing the malignant phenotype.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106676"},"PeriodicalIF":3.4,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Paeoniflorin regulates microglia-astrocyte crosstalk, inhibits inflammatory response, and alleviates neuropathic pain through HSP90AA1/HMGB1 signaling pathway 芍药苷可通过HSP90AA1/HMGB1信号通路调节小胶质细胞与星形胶质细胞之间的串扰、抑制炎症反应并缓解神经性疼痛。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-10-11 DOI: 10.1016/j.biocel.2024.106675

Fengqin Luo , Juan Zhang , Yunfei Miao , Danhong Wu , Hongxia Shen , Man Lu

{"title":"Paeoniflorin regulates microglia-astrocyte crosstalk, inhibits inflammatory response, and alleviates neuropathic pain through HSP90AA1/HMGB1 signaling pathway","authors":"Fengqin Luo , Juan Zhang , Yunfei Miao , Danhong Wu , Hongxia Shen , Man Lu","doi":"10.1016/j.biocel.2024.106675","DOIUrl":"10.1016/j.biocel.2024.106675","url":null,"abstract":"<div><div>Given the unclear, complex pathogenesis of neuropathic pain and the potential of paeoniflorin in relieving neuropathic pain, this study aimed to further clarify the therapeutic effect of paeoniflorin on neuropathic pain and to preliminarily explore the possible protective mechanisms of paeoniflorin. Chronic constrictive injury-induced Sprague Dawley rats and lipopolysaccharide-induced BV-2 cells were used for <em>in vivo</em> and <em>in vitro</em> experiments, respectively. The exosome uptake assay of mouse astrocytes (PKH-67 fluorescent labeling) and the mechanical nociceptive assay (the von Frey fibrous filaments) were performed. The effects of paeoniflorin and its downstream mechanisms on microglial and astrocyte activation, inflammation-associated proteins and exosome marker were determined. Paeoniflorin alleviated mechanical abnormal pain, decreased levels of ionized calcium binding adapter molecule-1 (Iba-1), glial fibrillary acidic protein, Heat Shock Protein 90 Alpha Family Class A Member 1 (HSP90AA1, inflammatory factor) and High Mobility Group Box 1 (HMGB1, inflammation-related protein), and inhibited neuronal apoptosis in chronic constrictive injury rats or lipopolysaccharide-induced BV-2 cells. However, these effects were offset by HSP90AA1 overexpression in lipopolysaccharide-induced BV-2 cells. Exosomes of BV-2 cells could be absorbed by mouse astrocytes. In addition, HSP90AA1 overexpression reversed the effects of paeoniflorin on HMGB1 expression and inflammatory factors and proteins in mouse astrocytes co-cultured with exosome. Collectively, paeoniflorin alleviates neuropathic pain and inhibits inflammatory responses in chronic constrictive injury by modulating microglia-astrocyte crosstalk through HSP90AA1/HMGB1 pathways, which further evidences the potential of paeoniflorin in the treatment of neuropathic pain.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106675"},"PeriodicalIF":3.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142479640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Alteration of N-glycosylation of CDON promotes H2O2-induced DNA damage in H9c2 cardiomyocytes CDON的N-糖基化改变会促进H9c2心肌细胞中由H2O2诱导的DNA损伤。

IF 3.4 3区生物学

International Journal of Biochemistry & Cell Biology Pub Date : 2024-10-09 DOI: 10.1016/j.biocel.2024.106671

Liping Chen , Hongfei Liu , Wenxing Zhan , Changkun Long , Fang Xu , Xueer Li , Xiao-Li Tian , Shenghan Chen

{"title":"Alteration of N-glycosylation of CDON promotes H2O2-induced DNA damage in H9c2 cardiomyocytes","authors":"Liping Chen , Hongfei Liu , Wenxing Zhan , Changkun Long , Fang Xu , Xueer Li , Xiao-Li Tian , Shenghan Chen","doi":"10.1016/j.biocel.2024.106671","DOIUrl":"10.1016/j.biocel.2024.106671","url":null,"abstract":"<div><div>Protein glycosylation is involved in DNA damage. Recently, DNA damage has been connected with the pathogenesis of heart failure. Cell adhesion associated, oncogene regulated (CDON), considered as an N-linked glycoprotein, is a transmembrane receptor for modulating cardiac function. But the role of CDON and its glycosylation in DNA damage remains unknown. In this study, we found that the knockdown of CDON caused DNA double-strand breaks as indicated by an increase in phosphorylated histone H2AX (γH2AX) protein level, immunofluorescent intensity of γH2AX and tail DNA moment in H9c2 cardiomyocytes. Conversely, overexpression of CDON led to decreasing DNA damage induced by hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) and upregulating the expression of genes related to DNA repair pathways-homologous recombination (HR) and non-homologous end joining (NHEJ). Moreover, we expressed nine predicted N-glycosylation site mutants in H9c2 cells prior to treatment with H<sub>2</sub>O<sub>2</sub>. The results showed that mutation of N-glycosylation sites (N99Q, N179Q, and N870Q) increased the accumulation of DNA damage and downregulated the expression of HR-related genes, demonstrating that CDON N-glycosylation on DNA damage is site-specific and these specific N-glycan sites may regulate HR repair-related transcript abundance of genes. Our data highlight that N-glycosylation of CDON is critical to cardiomyocyte DNA lesion. It may uncover the potential strategies targeting DNA damage pathway in heart disease.</div></div>","PeriodicalId":50335,"journal":{"name":"International Journal of Biochemistry & Cell Biology","volume":"176 ","pages":"Article 106671"},"PeriodicalIF":3.4,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142401836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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