Biochimica et biophysica acta. Molecular basis of disease最新文献_第6页

Mitochondrial classic metabolism and its often-underappreciated facets 线粒体经典代谢及其经常被低估的方面

IF 4.2 2区生物学

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-04-10 DOI: 10.1016/j.bbadis.2025.167839

João P. Moura , Paulo J. Oliveira , Ana M. Urbano

{"title":"Mitochondrial classic metabolism and its often-underappreciated facets","authors":"João P. Moura , Paulo J. Oliveira , Ana M. Urbano","doi":"10.1016/j.bbadis.2025.167839","DOIUrl":"10.1016/j.bbadis.2025.167839","url":null,"abstract":"<div><div>For many decades, mitochondria were essentially regarded as the main providers of the adenosine triphosphate (ATP) required to maintain the viability and function of eukaryotic cells, thus the widely popular metaphor “powerhouses of the cell”. Besides ATP generation – via intermediary metabolism – these intracellular organelles have also traditionally been known, albeit to a lesser degree, for their notable role in biosynthesis, both as generators of biosynthetic intermediates and/or as the sites of biosynthesis. From the 1990s onwards, the concept of mitochondria as passive organelles providing the rest of the cell, from which they were otherwise isolated, with ATP and biomolecules on an on-demand basis has been challenged by a series of paradigm-shifting discoveries. Namely, it was shown that mitochondria act as signaling effectors to upregulate ATP generation in response to growth-promoting stimuli and are actively engaged, through signaling and epigenetics, in the regulation of a plethora of cellular processes, ultimately deciding cell function and fate. With the focus of mitochondrial research increasingly placed in these “non-classical” functions, the centrality of mitochondrial intermediary metabolism to other mitochondrial functions tends to be overlooked. In this article, we revisit mitochondrial intermediary metabolism and illustrate how its intermediates, by-products and molecular machinery underpin other mitochondrial functions. A certain emphasis is given to frequently overlooked mitochondrial functions, namely the biosynthesis of iron–sulfur (Fe–S) clusters, the only known function shared by all mitochondria and mitochondrion-related organelles. The generation of reactive oxygen species (ROS) and their putative role in signaling is also discussed in detail.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 6","pages":"Article 167839"},"PeriodicalIF":4.2,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143860331","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

The function of necroptosis in liver cancer 坏死上睑下垂在肝癌中的作用

IF 4.2 2区生物学

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-04-10 DOI: 10.1016/j.bbadis.2025.167828

Mukaddas Tayir , Yan-Wen Wang , Ti Chu , Xue-Li Wang , Yong-Qi Fan , Lei Cao , Yu-Hang Chen , Dong-Dong Wu

{"title":"The function of necroptosis in liver cancer","authors":"Mukaddas Tayir , Yan-Wen Wang , Ti Chu , Xue-Li Wang , Yong-Qi Fan , Lei Cao , Yu-Hang Chen , Dong-Dong Wu","doi":"10.1016/j.bbadis.2025.167828","DOIUrl":"10.1016/j.bbadis.2025.167828","url":null,"abstract":"<div><div>Liver cancer is one of the most lethal cancers, and apoptosis resistance is a major obstacle contributing to chemotherapy failure in liver cancer treatment. Inducing cancer cell death by bypassing the apoptotic pathway is considered a promising approach to overcome this problem. Necroptosis is a non-caspase-dependent regulated mode of cell death mainly mediated by receptor-interacting protein kinase 1 (RIPK1), RIPK3, and mixed lineage kinase domain-like (MLKL) protein, and the utilization of necroptosis for treating hepatocellular carcinoma (HCC) also offers a new hope for addressing liver cancer in the clinic. In this paper, the role of necroptosis in HCC as well as the effect on differentiation of liver cancer are reviewed. We also comparatively analyze the relationship among necroptosis, apoptosis, and necrosis, as well as summarize the characteristics and functions of key proteins involved in this pathway. The bidirectional regulation of necroptosis and the mitochondrial machinery within this pathway deserve attention.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 6","pages":"Article 167828"},"PeriodicalIF":4.2,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143860332","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

Artificial intelligence-driven integration of multi-omics and radiomics: A new hope for precision cancer diagnosis and prognosis 人工智能驱动的多组学与放射组学的融合：癌症精准诊断与预后的新希望

IF 4.2 2区生物学

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-04-09 DOI: 10.1016/j.bbadis.2025.167841

Jordi Camps , Andrea Jiménez-Franco , Raquel García-Pablo , Jorge Joven , Meritxell Arenas

引用次数: 0

Implications of hippocampal excitatory amino acid transporter 2 in modulating anxiety and visceral pain in a mouse model of inflammatory bowel disease 海马兴奋性氨基酸转运蛋白2在炎症性肠病小鼠模型中调节焦虑和内脏疼痛的意义

IF 4.2 2区生物学

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-04-09 DOI: 10.1016/j.bbadis.2025.167832

Hao Jiang , Feini Zhou , Lingnan Guo , Yiyuan Gao , Ning Kong , Maosheng Xu , Fan Zhang

{"title":"Implications of hippocampal excitatory amino acid transporter 2 in modulating anxiety and visceral pain in a mouse model of inflammatory bowel disease","authors":"Hao Jiang , Feini Zhou , Lingnan Guo , Yiyuan Gao , Ning Kong , Maosheng Xu , Fan Zhang","doi":"10.1016/j.bbadis.2025.167832","DOIUrl":"10.1016/j.bbadis.2025.167832","url":null,"abstract":"<div><div>Inflammatory bowel disease (IBD) is characterized by chronic inflammation and significantly impairs quality of life through anxiety-like behaviors and visceral pain. Early evaluation of the risk of anxiety-like behaviors and visceral pain in IBD patients, along with targeted treatment, may benefit disease management. Visceral pain and anxiety-like behavior are often accompanied by neurological damage. Previous studies have shown that abnormal accumulation of glutamate can cause excitatory neurotoxic effects, leading to central nervous system (CNS) damage. Excitatory amino acid transporters (EAATs), particularly EAAT2, are known to regulate glutamate levels. The impact of hippocampal EAAT2 modulation on these clinical features in IBD is yet to be evaluated. Therefore, we designed this experiment to test this hypothesis. This study aimed to investigate the impact of altered levels of hippocampal EAAT2 on anxiety-like behaviors and visceral pain in mice with IBD. We observed reduced EAAT2 expression, increased glutamate levels, elevated <em>N</em>-methyl-<span>d</span>-aspartate receptors (NMDAR) expression, and obvious glutamate toxicity in the hippocampus of dextran sulfate sodium (DSS) induced IBD model mice. These mice exhibited significant visceral pain and anxiety-like behaviors. In summary, the reduced expression of EAAT2 in the hippocampus of individuals with IBD leads to elevated glutamate levels, resulting in neuronal damage and ultimately contributing to visceral pain and anxiety-like behaviors. These findings suggest that EAAT2 could serve as a therapeutic target for neurologically derived IBD symptoms.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 6","pages":"Article 167832"},"PeriodicalIF":4.2,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143844430","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

Study on the synthesis, characterization, and antitumor mechanism investigation of QZQ-01115 via targeting sphingosine kinase 2 以鞘氨醇激酶 2 为靶点的 QZQ-01115 的合成、表征及抗肿瘤机制研究

IF 4.2 2区生物学

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-04-09 DOI: 10.1016/j.bbadis.2025.167829

Caiyu Liu , Yaxin Guo , Yutong Dong , Zhiqiang Qu , Yanling Mu , Bo Liu , Fuwen Wang , Yan Li

{"title":"Study on the synthesis, characterization, and antitumor mechanism investigation of QZQ-01115 via targeting sphingosine kinase 2","authors":"Caiyu Liu , Yaxin Guo , Yutong Dong , Zhiqiang Qu , Yanling Mu , Bo Liu , Fuwen Wang , Yan Li","doi":"10.1016/j.bbadis.2025.167829","DOIUrl":"10.1016/j.bbadis.2025.167829","url":null,"abstract":"<div><div>Sphingosine kinase 2 (SphK2) is an oncogenic enzyme that plays an essential role in the development of oral squamous cell carcinoma (OSCC). Therefore, development of SphK2 inhibitors is of great significance for the treatment of OSCC. In this study, we synthesized a series of thiazolidinediones and screened compounds with good inhibitory activity against CAL-27 using cytotoxicity assay. The compounds were further investigated <em>in vitro</em> using a series of <em>in vitro</em> experiments such as Western blot and qPCR were used to investigate the <em>in vivo</em> anti-tumor mechanisms, and <em>in vivo</em> investigation was applied by using a nude mouse ectopic tumor model. The results showed that four new compounds were successfully synthesized, and among which the compound named QZQ-01115 showed the best inhibitory activity against CAL-27 at the concentration of 5.84 ± 0.042 μM. Further mechanistic studies showed that QZQ-01115 could inhibit the proliferation, migration and invasion of CAL-27 cells at a concentration of 4 μM–6 μM. QZQ-01115 affected the PI3K/AKT signaling pathway by influencing the levels of S1P and ceramides in CAL-27, which in turn affected the mTOR/p70S6K, resulting in the blockage of protein synthesis and the blockage of cell cycle at the G0/G0 level. Apoptosis was promoted by down-regulating Bcl-2 and up-regulating Bax. The <em>in vivo</em> results showed that QZQ-01115 reduced the volume and weight of xenograft tumors in nude mice. The induction of apoptosis by QZQ-01115 was further determined by HE staining and immunohistochemical analysis. These results suggest that QZQ-01115 may be a potential candidate for the treatment of OSCC.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 6","pages":"Article 167829"},"PeriodicalIF":4.2,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143830406","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

The role of the tumor microenvironment and inflammatory pathways in driving drug resistance in gastric cancer: A systematic review and meta-analysis 肿瘤微环境和炎症通路在胃癌耐药中的作用：系统综述和荟萃分析

IF 4.2 2区生物学

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-04-07 DOI: 10.1016/j.bbadis.2025.167821

Francesco Albano , Francesca Lospinoso Severini , Giovanni Calice , Pietro Zoppoli , Geppino Falco , Tiziana Notarangelo

引用次数: 0

Differential roles of the ADAM9/NF-κB and the ADAM9/STAT3 feedback loops in HIV-1 Tat-induced microglial inflammatory response and subsequent neuronal apoptosis ADAM9/NF-κB和ADAM9/STAT3反馈回路在HIV-1 tat诱导的小胶质细胞炎症反应和随后的神经元凋亡中的差异作用

IF 4.2 2区生物学

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-04-07 DOI: 10.1016/j.bbadis.2025.167831

Xiaoting Qiao , Hongke Wei , Weixi Sun , Cailian Ruan , Duo Cao

{"title":"Differential roles of the ADAM9/NF-κB and the ADAM9/STAT3 feedback loops in HIV-1 Tat-induced microglial inflammatory response and subsequent neuronal apoptosis","authors":"Xiaoting Qiao , Hongke Wei , Weixi Sun , Cailian Ruan , Duo Cao","doi":"10.1016/j.bbadis.2025.167831","DOIUrl":"10.1016/j.bbadis.2025.167831","url":null,"abstract":"<div><div>ADAM has been implicated in causing several neurodegenerative diseases to progress. However, the precise function they play in HIV-associated neurocognitive disorders (HAND) remains incompletely elucidated. The HIV-1 transcriptional activator (Tat) has the capacity to evoke an inflammatory reaction within the microglia of the central nervous system. This, subsequently, initiates the apoptosis of neuronal cells. In the present research, our attention was centered on the part that ADAM9 plays in the microglia's response to Tat. We discovered that the stimulation with soluble Tat remarkably enhanced the manifestation of ADAM9 by means of the NF-κB and STAT3 pathway. In contrast, inhibition of ADAM9 significantly reduced Tat-triggered NF-κB and STAT3 signaling. Moreover, both ADAM9/NF-κB and ADAM9/STAT3 feedback loops exacerbated Tat-induced microglia inflammatory responses. However, further studies showed that the ADAM9/NF-κB feedback loop more significantly promoted neuronal apoptosis mediated by conditioned medium secreted by microglia after Tat stimulation. This study offers a novel perspective on the function of diverse feedback circuits in the etiopathogenesis of HAND. It can be posited that, when considered as a collective entity, ADAM9 may represent a viable candidate for therapeutic intervention in the context of preventing neuronal injury associated with HAND by modulating the inflammatory response of microglia and influencing neuronal injury.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 6","pages":"Article 167831"},"PeriodicalIF":4.2,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143826219","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

The phosphomimetic Rab10 T73D mutation in mice leads to postnatal lethality and aberrations in neuronal development 小鼠的拟磷性Rab10 T73D突变导致出生后死亡和神经元发育异常

IF 4.2 2区生物学

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-04-07 DOI: 10.1016/j.bbadis.2025.167830

DaoBin Han , Jing Zhang , Yuan Zheng , LuWen Wang , Hui Yu , Bo Su

{"title":"The phosphomimetic Rab10 T73D mutation in mice leads to postnatal lethality and aberrations in neuronal development","authors":"DaoBin Han , Jing Zhang , Yuan Zheng , LuWen Wang , Hui Yu , Bo Su","doi":"10.1016/j.bbadis.2025.167830","DOIUrl":"10.1016/j.bbadis.2025.167830","url":null,"abstract":"<div><div>The phosphorylation of the evolutionarily conserved Thr73 residue of Rab10 has been implicated in various neurodegenerative diseases. However, its impact on neuronal physiological function remains poorly understood. In this study, we generated a novel mouse model constitutively expressing the phosphomimetic Rab10 T73D to investigate its effects. Our findings revealed that homozygous Rab10 T73D mutant mice were postnatally lethal and exhibited brain developmental defects characterized by cortical thinning and shortened neuronal processes. Further investigation demonstrated that cultured hippocampal neurons with homozygous T73D mutation displayed decreased axon development, with reduced accumulation of Rab10 at the tips of neuronal processes and increased Rab10 localization at lysosomes. Mechanistically, the T73D mutation induces a constitutively GTP-bound state and while substantially weakening interaction with GDI1, GDI2 and JIP1. These molecular alterations collectively lead to altered T73D Rab10-positive vesicle trafficking dynamics, manifesting as decreased anterograde transport and increased movement velocity. Notably, comparative localization studies in RPE cells confirmed fundamental discrepancies between T73D distribution patterns and authentic phosphorylated Rab10 dynamics, validating limitations of this phosphomimetic approach. Collectively, our study elucidates the potential physiological roles of phosphorylated Rab10 in the regulation of neuronal process outgrowth and underscores its significance in the neural system. Additionally, it highlights the limitations of the T73D mutant in fully mimicking Rab10 phosphorylation.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 6","pages":"Article 167830"},"PeriodicalIF":4.2,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143807352","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

HSPA8 and HSPA9: Two prognostic and therapeutic targets in breast, colon, and kidney cancers? HSPA8和HSPA9：乳腺癌、结肠癌和肾癌的两种预后和治疗靶点？

IF 4.2 2区生物学

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-04-04 DOI: 10.1016/j.bbadis.2025.167827

Alessia Ruzza , Elisabetta Zaltron , Federica Vianello, Ilaria Celotti, Matteo Scavezzon, Filippo Severin , Luigi Leanza

{"title":"HSPA8 and HSPA9: Two prognostic and therapeutic targets in breast, colon, and kidney cancers?","authors":"Alessia Ruzza , Elisabetta Zaltron , Federica Vianello, Ilaria Celotti, Matteo Scavezzon, Filippo Severin , Luigi Leanza","doi":"10.1016/j.bbadis.2025.167827","DOIUrl":"10.1016/j.bbadis.2025.167827","url":null,"abstract":"<div><div>The process of protein folding is important to ensure the efficient functioning of cells. The capacity of a protein to attain the three-dimensional native conformation can impact its structure and function. Errors in this process result in the accumulation of misfolded proteins, which can contribute to the development of various diseases, including cancer. To prevent the pileup of misfolded proteins, a number of control systems have been developed over the course of evolution. In this scenario, a pivotal function has been attributed to molecular chaperones and the ubiquitin-proteasome degradation system. In this paper, we concentrate on molecular chaperones, with a particular focus on a family of heat shock proteins (HSPs), to highlight any potential correlation between their expression and function and the development of cancer. Hence, we have collected data from various public databases regarding the HSP70 protein family. By employing mRNA expression signatures, prognostic value analysis, and differentially expressed gene ontology analysis, we have elucidated the tumor-specific role of two members of the HSP70 family, namely HSPA8 and HSPA9, in kidney renal clear cell carcinoma (KIRC), colon adenocarcinoma (COAD), and breast invasive carcinoma (BRCA). Our research shed light on the controversial and tumor-specific role of HSP70s. More in detail, we have identified HSPA8 and HSPA9 as potential prognostic and therapeutic targets involved in several biological processes leading to tumorigenesis, including nucleic acid maturation, cell signaling, vesicle trafficking, mitochondrial structure and function, and protein maturation.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 6","pages":"Article 167827"},"PeriodicalIF":4.2,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143797254","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

Dipeptidyl peptidase 9 (DPP9) depletion from hepatocytes in experimental primary liver cancer 实验性原发性肝癌肝细胞中二肽基肽酶9 （DPP9）的缺失

IF 4.2 2区生物学

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2025-04-04 DOI: 10.1016/j.bbadis.2025.167819

JiaLi Carrie Huang , Xinlin Linda Tong , Michelle Sui Wen Xiang , Badwi B. Boumelhem , Diarmid P. Foulis , MingChang Zhang , Catriona A. McKenzie , Geoffrey W. McCaughan , Thomas Reinheckel , Hui E. Zhang , Mark D. Gorrell

{"title":"Dipeptidyl peptidase 9 (DPP9) depletion from hepatocytes in experimental primary liver cancer","authors":"JiaLi Carrie Huang , Xinlin Linda Tong , Michelle Sui Wen Xiang , Badwi B. Boumelhem , Diarmid P. Foulis , MingChang Zhang , Catriona A. McKenzie , Geoffrey W. McCaughan , Thomas Reinheckel , Hui E. Zhang , Mark D. Gorrell","doi":"10.1016/j.bbadis.2025.167819","DOIUrl":"10.1016/j.bbadis.2025.167819","url":null,"abstract":"<div><div>Dipeptidyl peptidase 9 (DPP9) is an indispensable intracellular protease. Among its many molecular functions is suppression of the NLRP1 inflammasome. Inhibitors targeting all four proteases of the DPP4 family, including DPP9, can reduce tumour burden, including in mouse liver. To explore hepatocyte DPP9 in experimental hepatocellular carcinoma (HCC), we generated hepatocyte-specific DPP9-KO mice by crossing albumin-Cre mice with DPP9 floxed mice and treated sequentially with diethylnitrosamine, then with thioacetamide combined with an atherogenic high-fat diet until 28 weeks of age. DPP9-KO mice had less body, liver and subcutaneous adipose tissue mass, lower fasting plasma glucose and fewer small macroscopic liver nodules compared to DPP9-WT control mice. However, there were no differences in the total number of macroscopic liver nodules, or of microscopic tumour burden, inflammation, fibrosis or steatosis. Consistent with the known function of DPP9 to suppress NLRP1 activation, activated caspase-1 protein and inflammation markers <em>Nfkbib, Cxcl10</em> and <em>Ccl5</em> were elevated in DPP9-KO liver. The tumour suppressor protein p53 was increased and the autophagy proteins beclin1, LC3B and p62 were altered. In conclusion, hepatocyte-specific DPP9 gene deletion in experimental primary liver cancer improved energy metabolism and may reduce liver cancer initiation, <em>via</em> mechanisms that may include increased autophagy and tumour suppression.</div></div>","PeriodicalId":8821,"journal":{"name":"Biochimica et biophysica acta. Molecular basis of disease","volume":"1871 5","pages":"Article 167819"},"PeriodicalIF":4.2,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143768754","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