Cell Biology International最新文献

TFAP2C Affects PI3K/AKT/mTOR Pathway-Mediated EMT for Glioblastoma Development Through Transcriptional Regulation. TFAP2C通过转录调控影响PI3K/AKT/mTOR通路介导的EMT对胶质母细胞瘤的发展。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-07-16 DOI: 10.1002/cbin.70062

Shilin Li, Kebo Liu, Xiaoyang Li, Hao Zi, Kaiyuan Jiang

{"title":"TFAP2C Affects PI3K/AKT/mTOR Pathway-Mediated EMT for Glioblastoma Development Through Transcriptional Regulation.","authors":"Shilin Li, Kebo Liu, Xiaoyang Li, Hao Zi, Kaiyuan Jiang","doi":"10.1002/cbin.70062","DOIUrl":"https://doi.org/10.1002/cbin.70062","url":null,"abstract":"Transcription factor AP-2 gamma (TFAP2C) plays a pro-cancer role in various malignancies. Yet, the action of TFAP2C in glioblastoma (GBM) is unknown. This study aimed to investigate the effects of TFAP2C in GBM and the potential mechanism. TFAP2C knockdown in GBM cell lines was employed to examine its impact on cell proliferation, migration, and invasion (PMI), as well as epithelial-mesenchymal transition (EMT) development, and its association with the PI3K/AKT/mTOR (PAM) pathway by co-overexpressing PI3K or SC79 treatment (AKT agonist). The binding of TFAP2C and the PI3K promoter was predicted and validated. Finally, the above effects and mechanisms were verified in in vivo animal experiments. TFAP2C expression was strikingly heightened in human GBM cell lines and showed a negative correlation with patient survival. TFAP2C silencing inhibited GBM cell PMI, N-cadherin and Vimentin expression, and the PAM pathway, and activated E-cadherin and ZO-1 expression. Overexpression of PI3K or SC79 treatment reversed the above changes, suggesting that TFAP2C promotes GBM cell PMI and EMT via the PAM pathway. Mechanistically, TFAP2C binds to the promoter of PI3K and regulates PI3K transcription. Finally, the in vitro results were further validated in animal experiments. In conclusion, TFAP2C promotes PI3K transcription through direct binding to the promoter of PI3K and activates the PAM pathway to promote GBM proliferation and EMT, providing a potential therapeutic target for GBM.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144641950","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

Exploring Hippo YAP/TAZ Signaling: A Novel Avenue for Cardiovascular Disorders. 探索河马YAP/TAZ信号：心血管疾病的新途径

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-07-14 DOI: 10.1002/cbin.70052

Arwa Mithaiwala, Angel Godad

{"title":"Exploring Hippo YAP/TAZ Signaling: A Novel Avenue for Cardiovascular Disorders.","authors":"Arwa Mithaiwala, Angel Godad","doi":"10.1002/cbin.70052","DOIUrl":"https://doi.org/10.1002/cbin.70052","url":null,"abstract":"Significant attention has been paid to the Hippo signaling pathway and its effectors Yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) in cellular proliferation, survival, tissue homeostasis during development as well as cancer. While initially investigated in the context of oncogenesis, recent studies have just indicated its importance to cardiovascular diseases (CVD) like cardiac myocardial infarction (MI), cardiac hypertrophy, and heart failure (HF). This review focuses on therapeutic targets, regulatory mechanisms and signaling crosstalk between Hippo YAP/TAZ pathway with other traditional pathways like PI3K/AKT, TGF-β, WNT/β-catenin in CVD. Thus, although targeted YAP/TAZ activation in the myocardium may enhance regeneration/differentiation, its dysregulation promotes maladaptive cardiac remodeling characterized by hypertrophy and fibrosis. A better appreciation of the nuanced control on YAP/TAZ in different cardiovascular indications may point to an opportunity for precision therapeutics. In this review, we have discussed strategies to target specific components of the Hippo pathway as potential therapeutic approaches with implications for fibrosis reduction by LATS1/2 inhibition or cardiomyocyte survival promotion via MST1/2 suppression. The role of noncoding RNAs in YAP/TAZ activity modulation is further illustrated and provides us with possible therapeutic avenues that can be explored for noninvasive treatments.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144625472","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

UPF3B Accelerates the Growth of Liver Cancer Cells by Enhancing Autophagy via CDK12. UPF3B通过CDK12促进肝癌细胞自噬从而加速肝癌细胞生长。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-07-10 DOI: 10.1002/cbin.70060

Sijie Xie, Shuting Song, Xinlei Liu, Dongdong Lu

{"title":"UPF3B Accelerates the Growth of Liver Cancer Cells by Enhancing Autophagy via CDK12.","authors":"Sijie Xie, Shuting Song, Xinlei Liu, Dongdong Lu","doi":"10.1002/cbin.70060","DOIUrl":"https://doi.org/10.1002/cbin.70060","url":null,"abstract":"UPF3B encodes a protein that is part of a postsplicing multi-protein complex involved in both mRNA nuclear export and mRNA surveillance. Herein, we demonstrate that UPF3B accelerates the proliferation ability of liver cancer cells in vitro and in vivo. Moreover, UPF3B affects epigenetic regulation in human liver cancer cells. Moreover, ATAC-seq results show that chromatin accessibility is changed between rLV group and rLV-UPF3B group. Therefore, UPF3B alters transcriptome and proteome in liver cancer. In particular, UPF3B affects the heterogeneity of liver cancer and its microenvironment network. Furthermore, UPF3B promotes the modification ability of H3K4me3, H4K16Ac, and RNAPolII on promoter region of CDK12 and then increased the expression of CDK12. Strikingly, UPF3B enhances the interaction between LC3 and DOR, ATG4 and LC3, ATG3 and LC3, ATG3 and ATG12, ATG3 and ATG16L1, ATG3 and ATG7, ATG3 and ATG9A, and the expression of activated LC3, beclin1 dependent on CDK12. Ultimately, UPF3B increases the autophagy via CDK12 and then enhances the expression of ARAF, RRAS, CyclinD1, C-myc, PCNA, PKM2, CDK4, YB-1, H-Ras via CDK12-autophagy pathway. Importantly, our results indicate that CDK12 determines the oncogenic function of UPF3B. In conclusions, these results provide basis for research on liver cancer prevention and treatment.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599517","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

Metformin Promotes Osteogenic Differentiation of Adipose-Derived Stem Cells in Diabetic Osteoporosis by Regulating Autophagy. 二甲双胍通过调节自噬促进糖尿病骨质疏松症中脂肪干细胞的成骨分化。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-07-09 DOI: 10.1002/cbin.70061

Huayue Cao, Qilin Li, Yujin Gao, Jingxiang Li, Peiyang Yu, Xiaorong Lan, Shuanglin Peng, Jingang Xiao

{"title":"Metformin Promotes Osteogenic Differentiation of Adipose-Derived Stem Cells in Diabetic Osteoporosis by Regulating Autophagy.","authors":"Huayue Cao, Qilin Li, Yujin Gao, Jingxiang Li, Peiyang Yu, Xiaorong Lan, Shuanglin Peng, Jingang Xiao","doi":"10.1002/cbin.70061","DOIUrl":"https://doi.org/10.1002/cbin.70061","url":null,"abstract":"Patients with diabetic osteoporosis (DOP) face significant challenges in bone defect repair and regeneration. Adipose-derived stem cells (ASCs) have been widely used in bone tissue engineering due to their accessibility and multi-potency. However, DOP-ASCs exhibit lower capacity for osteogenic differentiation compared to control ASCs (CON-ASCs). In this study, we explored the effects of metformin (Met) on the autophagy and osteogenic capacity of DOP-ASCs. DOP mouse model was established with a high-fat and high-glucose diet combined with streptozotocin injection. After treating DOP-ASCs with Met and 3-methyladenine (3-MA), changes in autophagy levels and osteogenic differentiation capacity were observed by western blot analysis, real-time quantitative PCR (qPCR), immunofluorescence, alkaline phosphatase staining, alizarin red staining, and GFP-LC3 fluorescence labeling analysis. DOP-ASCs were cocultured with the Biphasic Calcium Phosphate (BCP), and implanted into the cranial defect area of DOP mice. The mice then received oral Met and intraperitoneal 3-MA injections for 3 months. The implanted BCP was assessed by micro-CT, HE and Masson staining. We observed a significantly reduced autophagic levels and capacity for osteogenic differentiation in DOP-ASCs, as compared to CON-ASCs. Met activated autophagy in DOP-ASCs and improved their osteogenic differentiation capacity. However, in the DOP + Met + 3MA group, both the autophagic level and the osteogenic differentiation capacity were suppressed. The results from the in vitro research and the in vivo outcomes agreed. Moreover, Met dramatically reduced p-PI3K and p-AKT expression. Met improves the osteogenic differentiation capacity by activating autophagy, an effect mediated through the PI3K/AKT signaling pathway.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144590562","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

RAD54L Is a Prognostic Biomarker and Demonstrate Correlation With Drug Sensitivity in Hepatocellular Carcinoma. RAD54L是肝细胞癌的预后生物标志物并与药物敏感性相关

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-07-05 DOI: 10.1002/cbin.70054

Tingting You, Hui Tang, Hui Ge, Chunmei Bai, Jianfeng Zhou

{"title":"RAD54L Is a Prognostic Biomarker and Demonstrate Correlation With Drug Sensitivity in Hepatocellular Carcinoma.","authors":"Tingting You, Hui Tang, Hui Ge, Chunmei Bai, Jianfeng Zhou","doi":"10.1002/cbin.70054","DOIUrl":"https://doi.org/10.1002/cbin.70054","url":null,"abstract":"Hepatocellular carcinoma (HCC), a leading cause of cancer-related mortality, is characterized by its aggressive nature and poor prognosis. This study investigates the role of RAD54L, a protein implicated in homologous recombination repair of DNA double-strand breaks, in the progression of HCC and its potential as a prognostic marker. Expression levels of RAD54L were assessed using transcriptomic data from The Cancer Genome Atlas and Gene Expression Omnibus databases. Kaplan-Meier survival curves and multivariate Cox regression analyses were conducted to evaluate the prognostic significance of RAD54L expression. Furthermore, the study explored immune infiltration, protein-protein interaction (PPI) networks, and functional enrichment analyses to elucidate the underlying mechanisms of RAD54L in HCC pathogenesis. Drug sensitivity was measured in the HepG2 cell line and GDSC database. Results showed that RAD54L was significantly upregulated at the mRNA level in HCC tissues (n = 369) compared to adjacent normal liver samples (n = 50), with high expression correlating with a poorer overall survival and disease-free interval. Functional enrichment analysis demonstrated that ATPase activity, helicase activity, and coenzyme binding pathways might be involved in RAD54L's effects on HCC pathogenesis. Additionally, knockdown of RAD54L in HepG2 cells resulted in reduced proliferation and increased sensitivity to gemcitabine treatment. In conclusion, higher expression of RAD54L is associated with poor prognosis in HCC and may enhance gemcitabine efficacy, suggesting its potential as both a prognostic biomarker and a therapeutic target in HCC management.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567222","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

Identification of a Pyruvate Ferredoxin Oxidoreductase in Acanthamoeba castellanii Cysts: A Key Enzyme in Cyst Energy Homeostasis. 棘阿米巴包囊中丙酮酸铁氧化还蛋白氧化还原酶的鉴定：包囊能量稳态的关键酶。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-07-05 DOI: 10.1002/cbin.70057

Luiz Fernando Carvalho-Kelly, Rafaella Oliveira da Costa, José Roberto Meyer-Fernandes

{"title":"Identification of a Pyruvate Ferredoxin Oxidoreductase in Acanthamoeba castellanii Cysts: A Key Enzyme in Cyst Energy Homeostasis.","authors":"Luiz Fernando Carvalho-Kelly, Rafaella Oliveira da Costa, José Roberto Meyer-Fernandes","doi":"10.1002/cbin.70057","DOIUrl":"https://doi.org/10.1002/cbin.70057","url":null,"abstract":"Pyruvate ferredoxin oxidoreductase (PFOR) is the main enzyme responsible for pyruvate decarboxylation under anaerobic conditions. This enzyme is very well characterized in a wide range of microorganisms, such as anaerobic bacteria and microaerophilic parasites; however, the presence of this enzyme in free-living amoebas (FLAs) has not been demonstrated. Acanthamoeba castellanii (A. castellanii) is an FLA that exhibits trophozoite and cyst forms during its life cycle. The trophozoite form possesses functional mitochondria that are responsible for ATP synthesis. The cyst form possesses a rudimental mitochondrial structure that seems to be not functional and anaerobically synthesizes ATP. In this study, we described the presence of a PFOR in A. castellanii (known as AcPFOR). The structure of this enzyme is very similar to that of PFOR, which has been characterized in other microorganisms, and the main domains responsible for the enzymatic activity of PFOR are present in AcPFOR. The cyst forms exhibited increased expression and enzymatic activity of PFOR. This enzyme is inhibited by nitazoxanide (a PFOR inhibitor), and drug administration was able to inhibit the encystment process by overstimulating autophagy. The inhibition of the enzyme also affects cyst viability, thus resulting in the inhibition of the excystation process. In conclusion, we demonstrated the importance of PFOR in A. castellanii cysts energy homeostasis, thereby indicating that this enzyme may be an interesting therapeutic target.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567221","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

COMMD1 Inhibits Epithelial Mesenchymal Transition (EMT) and Liver Metastasis in Cervical Cancer Through Modulation of the Twist1/E-Cadherin Pathway. COMMD1通过调控Twist1/E-Cadherin通路抑制宫颈癌上皮间充质转化（EMT）和肝转移。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-07-05 DOI: 10.1002/cbin.70049

Yue Zhang, Xiuli Wang, Ke Wang, Lei Sun, Shiying Yang, Xiaoguang Wang

{"title":"COMMD1 Inhibits Epithelial Mesenchymal Transition (EMT) and Liver Metastasis in Cervical Cancer Through Modulation of the Twist1/E-Cadherin Pathway.","authors":"Yue Zhang, Xiuli Wang, Ke Wang, Lei Sun, Shiying Yang, Xiaoguang Wang","doi":"10.1002/cbin.70049","DOIUrl":"https://doi.org/10.1002/cbin.70049","url":null,"abstract":"Our investigation was aimed at deciphering the potential role of copper metabolism MURR1 domain containing 1 (COMMD1) in cervical cancer tumorigenesis and metastasis, along with its underlying molecular mechanism, both in vitro and in vivo. To validate the research objectives, cervical cancer cell lines with stably overexpressed and knockdown COMMD1 were generated. In addition, an orthotopic murine model of cervical cancer with liver metastasis was constructed to elucidate the metastatic impact of COMMD1. Functional assays including CCK-8 assay, colony formation assay, scratch assay, and transwell invasion assay were conducted to evaluate the proliferation, migration, and invasion capabilities of cervical cancer cells. Western blot analysis and immunofluorescence double staining were performed to detect protein expression profiles and visualize actin cytoskeleton remodeling. Hematoxylin-eosin (H&E) staining and immunohistochemistry were utilized to characterize tumor histopathology and protein expression. Key findings revealed that COMMD1 was markedly downregulated in cervical cancer cell lines. Ectopic expression of COMMD1 potently impeded cell proliferation, colony formation, migration, and invasion of cervical cancer cells. Mechanistically, COMMD1, suppressed epithelial-mesenchymal transformation (EMT) by antagonizing the twist family bHLH transcription factor 1 (Twist1)/epithelial (E)-cadherin pathway, as evidenced by reduced expression of EMT-associated markers and restored E-cadherin membrane localization. In the orthotopic mouse model, COMMD1 overexpression significantly attenuated liver metastatic foci formation and blunted EMT progression. In conclusion, COMMD1 acts as a tumor suppressor in cervical cancer, with its antitumor effects primarily mediated by inhibiting Twist1-driven EMT and metastatic cascade.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567217","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

ZnTs: Key Regulators of Zn²⁺ Homeostasis in Diseases. znt：疾病中Zn2+动态平衡的关键调节因子。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-07-05 DOI: 10.1002/cbin.70056

Huimei Liu, Meilin Chen, Jingtong Duan, Ruirui Lu, Lanfang Li

{"title":"ZnTs: Key Regulators of Zn2+ Homeostasis in Diseases.","authors":"Huimei Liu, Meilin Chen, Jingtong Duan, Ruirui Lu, Lanfang Li","doi":"10.1002/cbin.70056","DOIUrl":"https://doi.org/10.1002/cbin.70056","url":null,"abstract":"Zinc (Zn2+) is an essential trace element that plays a crucial role in various biological functions. Aberrant Zn2+ homeostasis may lead to the occurrence and development of diseases. Zinc transporters, primarily classified into two families in humans: the ZnT (SLC30A) family and the ZIP (SLC39A) family, are critical regulators of Zn2+ homeostasis. The roles of ZnT-mediated Zn2+ homeostasis in diseases are an active area of research. The ZnT family comprises ten members, belonging to four subfamilies, which are widely distributed in various tissues and subcellular organelles. ZnTs mediate directional Zn2+ efflux, transporting cytoplasmic Zn2+ into extracellular compartments or sequestering it within intracellular vesicles. Accumulating evidence has shown that ZnT dysregulation or ZnT mutations can disrupt Zn2+ homeostasis, leading to the occurrence and development of diseases, such as cancer, cardiovascular disease, and neurodegenerative diseases. In this review, we focus on the distribution and structure of ZnTs. Furthermore, we synthesize recent advances in ZnT-mediated regulation of Zn2+ homeostasis in disease pathogenesis to guide the development of novel diagnostic and therapeutic strategies.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567223","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

Beyond Histones: Unveiling the Functional Roles of Protein Acetylation in Prokaryotes and Eukaryotes. 超越组蛋白：揭示蛋白乙酰化在原核生物和真核生物中的功能作用。

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-07-05 DOI: 10.1002/cbin.70055

Bruno Sousa Bonifácio, Ariely Barbosa Leite, Ana Caroline de Castro Nascimento Sousa, Suellen Rodrigues Maran, Antoniel Augusto Severo Gomes, Elton J R Vasconcelos, Nilmar Silvio Moretti

{"title":"Beyond Histones: Unveiling the Functional Roles of Protein Acetylation in Prokaryotes and Eukaryotes.","authors":"Bruno Sousa Bonifácio, Ariely Barbosa Leite, Ana Caroline de Castro Nascimento Sousa, Suellen Rodrigues Maran, Antoniel Augusto Severo Gomes, Elton J R Vasconcelos, Nilmar Silvio Moretti","doi":"10.1002/cbin.70055","DOIUrl":"https://doi.org/10.1002/cbin.70055","url":null,"abstract":"Lysine acetylation plays a crucial role in cellular processes and is found across various evolutionary organisms. Recent advancements in proteomic techniques revealed the presence of acetylation in thousands of non-histone proteins. Here, we conducted extensive meta-analysis of 48 acetylomes spanning diverse organisms, including archaea, bacteria, fungi, protozoa, worms, plants, insects, crustacea, fish, and mammals. Our analyzes revealed a predominance of a single acetylation site in a protein detected in all studied organisms, and proteins heavily acetylated, with > 5-10 acetylated-sites, were represented by Hsp70, histone, or transcription GTP-biding domain. Moreover, using gene enrichment approaches we found that ATP metabolic processes, glycolysis, aminoacyl-tRNA synthetase pathways and oxidative stress response are among the most acetylated cellular processes. Finally, to better explore the regulatory function of acetylation in glycolysis and oxidative stress we used aldolase and superoxide dismutase A (SODA) enzymes as model. For aldolase, we found that K147 acetylation, responsible to regulate human enzyme, conserved in all phylogenic clade, suggesting that this acetylation might play the same role in other species; while for SODA, we identified many lysine residues in different species present in the tunnel region, which was demonstrated for human and Trypanosoma cruzi, as negative regulator, also suggesting a conserved regulatory mechanism. In conclusion, this study provides insights into the conservation and functional significance of lysine acetylation in different organisms emphasizing its roles in cellular processes, metabolic pathways, and molecular regulation, shedding light in the extensive function of non-histone lysine acetylation.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567216","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

C/EBP-α Promotes Mitochondrial Fission and Inhibits the Activation of Hepatic Stellate Cells via YAP-Drp1 Pathway. C/EBP-α通过YAP-Drp1通路促进线粒体分裂并抑制肝星状细胞活化

IF 3.3 3区生物学

Cell Biology International Pub Date : 2025-07-03 DOI: 10.1002/cbin.70058

Chenjian Hou, Yajun Yan, Ying Su, Meili Wang, Ju Yang, Xiaoli Liu, Xuefeng Zhai, Yuxiang Wang, Xiuping Liu

{"title":"C/EBP-α Promotes Mitochondrial Fission and Inhibits the Activation of Hepatic Stellate Cells via YAP-Drp1 Pathway.","authors":"Chenjian Hou, Yajun Yan, Ying Su, Meili Wang, Ju Yang, Xiaoli Liu, Xuefeng Zhai, Yuxiang Wang, Xiuping Liu","doi":"10.1002/cbin.70058","DOIUrl":"https://doi.org/10.1002/cbin.70058","url":null,"abstract":"The activation of hepatic stellate cells (HSCs) plays a key role in the pathogenesis of liver fibrosis. However, the activation of HSCs requires energy from mitochondria-highly dynamic organelles. In our previous studies, we have confirmed that CCAAT/enhancer binding protein α (C/EBP-α) can inhibit the activation of HSCs, but whether it can affect the activation of HSCs by regulating mitochondrial dynamics is still unclear. In this study, we characterized the roles and mechanisms of C/EBP-α-mediated mitochondrial fission in regulating HSCs activation. We found that C/EBP-α upregulates Drp1 expression through inhibiting YAP expression, thus promoting mitochondrial fission and suppressing the activation of HSCs. In addition, in the HSCs with C/EBP-α overexpression, the epistatic roles of YAP and Drp1 in regulating mitochondrial biology and HSCs activation were interrogated with their respective inhibitors/agonists. Thus, we propose that mitochondrial fission plays an important role in the activation of HSCs and fibrosis that is regulated by a C/EBP-α-YAP-Drp1 axis.","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2025-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144552469","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