Cytojournal最新文献

{"title":"Vaspin inhibits ferroptosis: A new hope for treating myocardial ischemia-reperfusion injury.","authors":"Xuehong Lin, Laiyun Xin, Xianqing Meng, Duo Chen","doi":"10.25259/Cytojournal_141_2024","DOIUrl":"10.25259/Cytojournal_141_2024","url":null,"abstract":"<p><strong>Objective: </strong>Myocardial ischemia-reperfusion injury (MIRI) is a critical pathological basis for cardiovascular diseases. In recent years, the effect of ferroptosis on MIRI has attracted extensive attention. Vaspin, an adipose tissue-derived serine protease inhibitor, has multiple biological functions, including anti-inflammatory and antioxidant effects. This study aims to investigate the molecular mechanism by which vaspin alleviates MIRI by regulating hypoxia-inducible factor-1α (HIF-1α) and ferroptosis signaling pathways.</p><p><strong>Material and methods: </strong>A mouse model of myocardial ischemia/reperfusion (I/R) and a hypoxia/reoxygenation (H/R) model was used to evaluate the protective effects of vaspin on MIRI. The mechanism by which ferroptosis is modulated by the vaspin/HIF-1α signaling pathway was investigated by constructing a vaspin overexpression adenoviral vector. Myocardial infarct size and histological changes were assessed using triphenyltetrazolium chloride and hematoxylin-eosin staining. Ferroptosis-related proteins were detected by Western blot assay, and apoptosis and reactive oxygen species levels were analyzed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling. Iron content in myocardial tissue and cells was measured by enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>Myocardial I/R increased myocardial infarct size and serum lactate dehydrogenase (LDH) levels compared with the control group, indicating severe myocardial injury. Western blot results showed that MIRI reduced endogenous vaspin and HIF-1α levels and inhibited glutathione peroxidase 4. <i>In vivo</i> and <i>in vitro</i> vaspin overexpression treatment reduced infarct size, decreased LDH levels, inhibited ferroptosis pathway activity, and alleviated oxidative stress levels in myocardial tissues. In the H/R model, vaspin overexpression upregulated HIF-1α, inhibited ferroptosis markers, and reduced apoptosis and iron deposition. However, inhibiting HIF-1α reversed the cardioprotective and anti-ferroptotic effects of vaspin.</p><p><strong>Conclusion: </strong>Vaspin inhibits ferroptosis and upregulates the HIF-1α signaling pathway to mitigate myocardial I/R injury. The vaspin/HIF-1α pathway could be a potential target for MIRI prevention and treatment and offers fresh perspectives on ischemic heart disease management. Vaspin could be a novel cardioprotective agent that plays a significant role in the prevention and treatment of cardiovascular diseases.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"64"},"PeriodicalIF":2.5,"publicationDate":"2024-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11801648/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143366716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A case of lung adenocarcinoma expressing carbonic anhydrase IX and cluster of differentiation 10 antigen combined with renal clear cell carcinoma.","authors":"Yunjun Wang, Ting Wang, Hengming Zhang, Guohua Yu","doi":"10.25259/Cytojournal_106_2024","DOIUrl":"10.25259/Cytojournal_106_2024","url":null,"abstract":"<p><p>Few reports exist on dual primary lung and kidney tumors. Lung adenocarcinoma and renal clear-cell carcinoma are usually distinguished based on histological morphology and characteristic immunohistochemistry. This study describes a patient with concurrent lung adenocarcinoma and clear cell renal cell carcinoma, notable for their shared expression of both carbonic anhydrase IX (CA9) and cluster of differentiation 10 (CD10) markers, a phenomenon that has remained unreported in existing literature. We made a correct diagnosis based on histological morphology and immunohistochemical results, discussed the significance of CA9 and CD10 expression in lung adenocarcinoma, and provided insights for differential diagnosis, intending to offer pathologists relevant insights for diagnosing multiple primary malignant neoplasms.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"62"},"PeriodicalIF":2.5,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11801657/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143366370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preliminary study on the cellular and molecular mechanisms of Cms1 ribosomal small subunit homolog promoting hepatocellular carcinoma progression via activation of the homolog family member A/yes-associated protein 1 signaling pathway.","authors":"Yao Zheng, Aiyun Wang, Shuaijun Yu, Benzun Wei, Xiao Lyu","doi":"10.25259/Cytojournal_69_2024","DOIUrl":"10.25259/Cytojournal_69_2024","url":null,"abstract":"<p><strong>Objective: </strong>The precise mechanism of action of cms1 ribosomal small subunit homolog (CMSS1) in hepatocellular carcinoma (HCC) is yet unknown, although it may be essential to the malignant evolution of disease. The aim of this study was to reveal the role of CMSS1 in HCC and its possible mechanism.</p><p><strong>Material and methods: </strong>The expression of CMSS1 in different HCC cell lines was detected by quantitative real-time polymerase chain reaction and Western blot. The expression of CMSS1 in HCC cells was subsequently silenced, and the proliferation capacity of HCC cells was measured by colony formation assay, 5-ethynyl-2'-deoxyuridine (EdU) assay, and flow cytometry, and the migration and metastasis capacity of the HCC cells was measured by Transwell assay and Western blot. Finally, ras homolog family member A (RhoA) and yes-associated protein 1 (YAP1) were silenced, and the relationship between CMSS1, RhoA, and YAP1 was further discussed by immunofluorescence, colony formation assay, and EdU assay.</p><p><strong>Results: </strong>The experimental results showed that CMSS1 is highly expressed in HCC tissues and cell lines (<i>P</i> < 0.001). Further experiments demonstrated that CMSS1 promotes the malignant progression of HCC by activating the RhoA GTPase/YAP1 signaling pathway (<i>P</i> < 0.001). Inhibition of YAP1 could reverse the enhanced proliferation and colony formation ability induced by CMSS1 (<i>P</i> < 0.001). Silencing CMSS1 expression can inhibit epithelial- mesenchymal transition (<i>P</i> < 0.01). Moreover, silencing RhoA reduces the YAP1 nuclear translocation (<i>P</i> < 0.001).</p><p><strong>Conclusion: </strong>CMSS1 promotes the malignant progression of HCC by activating the RhoA GTPase/YAP1 signaling pathway.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"61"},"PeriodicalIF":2.5,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11801666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143366612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Surfeit 4 regulates aerobic glycolysis to enhanced proliferation, tumor stemness, invasion, and metastasis in oral squamous cell carcinoma.","authors":"Wei Yuan, Tao Tan, Linlin Lu, Chaofei Lu, Yan Zhang, Baojuan Liu","doi":"10.25259/Cytojournal_137_2024","DOIUrl":"10.25259/Cytojournal_137_2024","url":null,"abstract":"<p><strong>Objective: </strong>Oral squamous cell carcinoma (OSCC) is a common malignant tumor worldwide. Surfeit 4 (SURF4) is a member of the surfeit gene family and plays a regulatory role in various cellular processes, such as protein transport and lipid metabolism. Therefore, this study aims to investigate the regulatory role and mechanisms of SURF4 in OSCC.</p><p><strong>Material and methods: </strong>Serum samples were collected from the normal control and OSCC groups. The function of OSCCs was analyzed through Transwell, 5-ethynyl-2'-deoxyuridine incorporation, and Cell Counting Kit-8 assays. Selected proteins were measured by Western blot analysis. Additional vectors for the overexpression (OE) and knockdown of SURF4 were established. Aerobic glycolysis (AG) was detected through cellular glucose consumption and lactate production assays.</p><p><strong>Results: </strong>A significant increase was observed in protein and messenger RNA (mRNA) levels of serum SURF4 in OSCC patients compared with the control group (<i>P</i> < 0.001). The knockdown of SURF4 alleviated proliferation, invasion, and metastasis in OSCC (<i>P</i> < 0.001). Overexpressing SURF4 aggravated proliferation and invasion in OSCC and increased the levels of stem cell genes Octamer-binding Transcription Factor 4 and Sex-determining Region Y-box 2 (<i>P</i> < 0.001). Furthermore, adenosine triphosphate levels, lactate levels, and extracellular acidification rate were found to be elevated in the OE SURF4 group, along with higher levels of AG-related regulatory proteins (<i>P</i> < 0.001). Inhibiting AG with glycolysis inhibitor 2-deoxyglucose effectively impeded proliferation and invasion in OSCC.</p><p><strong>Conclusion: </strong>SURF4 plays a role in OSCC by regulating AG to enhance proliferation, tumor stemness, invasion, and metastasis.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"60"},"PeriodicalIF":2.5,"publicationDate":"2024-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683412/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Overlap syndrome of Erdheim-Chester disease and Langerhans cell histiocytosis: A case report.","authors":"Yingying Ding, Shanshan Chen, Guinian Huang, Xiaojuan Guo","doi":"10.25259/Cytojournal_174_2024","DOIUrl":"10.25259/Cytojournal_174_2024","url":null,"abstract":"<p><p>Langerhans cell histiocytosis (LCH) and Erdheim-Chester disease (ECD) are exceptionally rare disorders characterized by varied clinical presentations, posing several challenges for clinicians. The concomitant occurrence of LCH and ECD is exceedingly rare and has no known etiology. In this report, we present a rare case of mixed histiocytosis (both ECD and LCH) with multisystem involvement. The patient, a 49-year-old female, initially presented with a rash 2 years ago and progressively developed exophthalmos, fatigue, and shortness of breath. She lacked the mutation in codon 600 of exon 15 of B-Raf proto-oncogene (BRAF-V600E) and subsequently underwent treatment with corticosteroids, interferon-alpha, and chemotherapy, all of which proved ineffective. This work highlights the urgent need to improve treatment outcomes for such patients. Therefore, we discuss the latest advancements in understanding treatment strategies for mixed histiocytic syndromes.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"59"},"PeriodicalIF":2.5,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683406/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transglutaminase 2 inhibition ameliorates cardiac fibrosis in myocardial infarction by inducing M2 macrophage polarization <i>in vitro</i> and <i>in vivo</i>.","authors":"Alimujiang Maimaitijiang, Qingyu Huang, Yurong Wu, Shengjia Sun, Qiying Chen","doi":"10.25259/Cytojournal_32_2024","DOIUrl":"10.25259/Cytojournal_32_2024","url":null,"abstract":"<p><strong>Objective: </strong>Macrophages perform vital functions in cardiac remodeling after myocardial infarction (MI). Transglutaminase 2 (TG2) participates in fibrosis. Nevertheless, the role of TG2 in MI and mechanisms underlying macrophage polarization are unclear. This study aimed to discover the functions and possible mechanisms of TG2 in MI.</p><p><strong>Material and methods: </strong>C57BL/6 mice were classified into three groups (six mice per group): Sham, MI, and MI+GK921 groups. GK921 acts as a TG2 inhibitor. Cardiac function, myocardial cell apoptosis, fibrosis, and macrophage phenotype in mouse experiments were detected through echocardiography, terminal deoxynucleotidyl transferase dUTP nick end labeling, Masson staining, immunofluorescence, and flow cytometry, respectively. The <i>in vitro</i> study involved the treatment of mouse cardiac fibroblasts isolated from mice with transforming growth factor β1 (TGF-β1) and evaluation of fibrosis through the detection of the expressions of fibrosis-associated proteins using Western blot. Bone marrow-derived macrophages (BMDMs) obtained from mice were triggered by interleukin (IL)-4, and the type of macrophages was determined through flow cytometry.</p><p><strong>Results: </strong>In <i>in vivo</i> experiments, GK921 substantially improved cardiac injury and fibrosis, induced M2 macrophage polarization, and suppressed the TGF-β1/small mother against decapentaplegic 3 (Smad3) pathway in MI mice. Moreover, TG2 knockdown considerably decreased the expressions of fibrosis-associated proteins in TGF-β1-triggered mouse cardiac fibroblasts, which indicates the repressive effect of TG2 knockdown on fibrosis. In addition, the inhibition effect of TG2 downregulation on the TGF-β1/Smad3 pathway was proven in TGF-β1-treated mouse cardiac fibroblasts <i>in vitro</i>. Moreover, TG2 inhibition remarkably increased M2 macrophage polarization in IL-4-induced BMDMs.</p><p><strong>Conclusion: </strong>TG2 inhibition facilitated M2 macrophage polarization to provide protection against MI-caused cardiac fibrosis in mice, and these effects may be attained through modulation of the TGF-β1/Smad3 pathway.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"58"},"PeriodicalIF":2.5,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683372/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adenosine deaminase acting on RNA 2 provides neuroprotection by activating Kv1.1 channels in a rat epilepsy model.","authors":"Pingping Zhu, Wei Yuan, Wenquan Liu, Jian Wu, Pengzhen Wang, Bo Ning","doi":"10.25259/Cytojournal_53_2024","DOIUrl":"10.25259/Cytojournal_53_2024","url":null,"abstract":"<p><strong>Objective: </strong>Potassium voltage-gated channel sub-family A member 1 (Kv1.1), as a shaker homolog potassium channel, displays a special mechanism for posttranscriptional regulation called RNA editing. Adenosine deaminase acting on RNA 2 (ADAR2) can cause abnormal editing or loss of normal editing, which results in cell damage and related diseases. The relationship between Kv1.1 and editing enzyme ADAR2 in epileptic rats remains incompletely understood. We aimed to investigate the neuroprotective role of ADAR2 and its relationship with Kv1.1 in epileptic rats and the SH-SY5Y neuroblastoma cell line.</p><p><strong>Material and methods: </strong>A rat epilepsy model was induced <i>in vivo</i> using lithium chloride-pilocarpine. We investigated the effect of ADAR2 on epileptic rats through Western blotting, quantitative reverse transcription polymerase chain reaction (qRT-PCR), and histological analysis. Western blotting was aimed at investigating the effect of overexpression of ADAR2 and Kv1.1-interfering RNA (si-Kv1.1) for neuronal apoptosis.</p><p><strong>Results: </strong>The overexpression of ADAR2 in epileptic rats led to the increased mRNA and protein expression of Kv1.1 (<i>P</i> < 0.001) and B-cell leukemia/lymphoma 2 protein (Bcl-2) (<i>P</i> < 0.001), whereas the decreased expressions of Bcl-2-associated X protein and cleaved caspases-3/7 at protein levels (<i>P</i> < 0.0001; <i>P</i> < 0.0001; <i>P</i> < 0.01) detected by Western blotting and qRT-PCR experiments. Hematoxylin and eosin staining and Nissl staining revealed the neuroprotection provided by ADAR2 overexpression. The experiments demonstrated that Kv1.1 was regulated by ADAR2. ADAR2 overexpression increased neuronal survival in <i>in vivo</i> experiments through the elevation of Bcl-2 levels (<i>P</i> < 0.05) and reduction of cleaved caspase-3/7 activity (<i>P</i> < 0.0001; <i>P</i> < 0.01). In the recovery experimental group that involved silencing Kv1.1, the beneficial effects of overexpressing ADAR2 were no longer observed (<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>Our findings confirm that the upregulation of ADAR2 promotes Kv1.1 protein expression, which ultimately reduces neuronal damage in the hippocampus of animals with epilepsy.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"57"},"PeriodicalIF":2.5,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683407/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907816","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Receptor interacting serine/threonine kinase 2 promotes rheumatoid arthritis progression and partially regulates nuclear factor kappa B pathway.","authors":"Yanzheng Wang, Meiyu Xu, Xinxin Liu, Deheng Liu","doi":"10.25259/Cytojournal_63_2024","DOIUrl":"10.25259/Cytojournal_63_2024","url":null,"abstract":"<p><strong>Objective: </strong>Rheumatoid arthritis (RA) is a disabling systemic autoimmune disease worldwide; however, its molecular pathway remains largely unknown. Thus, this study aimed to explore the effects of receptor-interacting serine/threonine kinase 2 (RIPK2) on RA progression and its underlying mechanism.</p><p><strong>Material and methods: </strong>RIPK2 expression was analyzed using real-time quantitative polymerase chain reaction, immunohistochemical staining, and Western blot (WB) analysis in RA synovial tissues or cells. Cell viability or proliferation was determined using the cell counting kit-8 and 5-ethynyl-2'-deoxyuridine. Cell metastasis was analyzed using the transwell assay and wound healing assay. Flow cytometry was adopted to measure cell apoptosis. The level of inflammation-related factors was measured using the enzyme-linked immunosorbent assay. WB analysis was used to determine the expression level of nuclear factor kappa B (NF-κB) pathway-related genes.</p><p><strong>Results: </strong>RIPK2 was highly expressed in RA synovial tissues and cells. Transfection with RIPK2 short hairpin RNA plasmids reduced the gene expression level of RIPK2 in RA fibroblast-like synoviocytes (FLS) cells. Notably, RIPK2 silencing hindered the proliferation, invasion, and migration of tumor cells as well as accelerated the apoptosis of RA-FLS cells. Furthermore, RIPK2 silencing suppressed the RA-FLS cell inflammatory response and NF-κB pathway.</p><p><strong>Conclusion: </strong>RIPK2 silencing could retrain the malignant behavior and inflammatory response of RA-FLSs and partially modulate the NF-κB pathway.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"56"},"PeriodicalIF":2.5,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683368/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Methyltransferase-like 14 promotes the tumorigenesis and proliferation of pancreatic cancer cells through myc proto-oncogene signaling pathway.","authors":"Junru Li, Peng Wang, Fei Liu, Yuanyuan Li, Youyou Wu, Fengbo Wang, Jundong Du","doi":"10.25259/Cytojournal_105_2024","DOIUrl":"10.25259/Cytojournal_105_2024","url":null,"abstract":"<p><strong>Objective: </strong>Pancreatic cancer is characterized by low survival rate and rapid deterioration. Methyltransferase-like 14 (METTL14), as N6-methyladenosine (m6A) methyltransferase, is closely related to tumor progression. The purpose of this study is to look into how METTL14 affects pancreatic cancer tumorigenesis, cell division, and apoptosis.</p><p><strong>Material and methods: </strong>We examined and contrasted the levels of METTL14 protein and messenger RNA expression in human pancreatic ductal cells and human pancreatic cancer cells. After silencing or upregulating METTL14, the proliferative ability, migration ability, and cell apoptosis of pancreatic tumor cells was detected by colony-forming assay, wound scratch healing assay, cell counting kit 8 assay, and terminal deoxynucleotidyl transferasemediated 2'-deoxyuridine 5'-triphosphate-biotin nick end labeling assay. Following the use of c-Myc inhibitor (10058-F4), western blot analysis was carried out to investigate the key factor expression and c-Myc signaling pathway activation status.</p><p><strong>Results: </strong>METTL14 was preferentially expressed in human pancreatic cancer cells PANC-1 and SW1990 than in human normal pancreatic duct cells human pancreatic nestin-expressing cells (HPNE) (<i>P</i> < 0.001). Overexpression of METTL14 increased the tumorigenic and proliferative ability of pancreatic cancer cells. Overexpression of METTL14 decreased apoptosis rate. Western blot assay showed that nucleus b-catenin increased when METTL14 was overexpressed, and nucleus b-catenin decreased when METTL14 was silenced in PANC-1 cell (<i>P</i> < 0.01). The protein expression of other key factors, such as c-Myc, matrix metalloproteinase (MMP)-9, and MMP-2, were also affected. The use of c-Myc inhibitor (10058-F4) on the basis of OE-METTL14 reversed the effect of the overexpression of METTL14 on promoting the tumorigenesis and cell proliferation of pancreatic cancer cell lines PANC-1 and SW1990.</p><p><strong>Conclusion: </strong>METTL14 promoted the tumorigenesis and proliferation of pancreatic cancer cells by the c-Myc signaling pathway.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"55"},"PeriodicalIF":2.5,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683408/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907834","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fibronectin type III domain containing protein 5/irisin alleviated sepsis-induced acute kidney injury by abating ferroptosis through the adenosine 5'-monophosphate-activated protein kinase/nuclear factor erythroid-2-related factor 2 signaling pathway.","authors":"Shenghao Gui, Chaochao Zhu, Yunfeng Lu","doi":"10.25259/Cytojournal_62_2024","DOIUrl":"10.25259/Cytojournal_62_2024","url":null,"abstract":"<p><strong>Objective: </strong>Ferroptosis has been described in association with acute kidney injury (AKI)-induced sepsis. Fibronectin type III domain containing protein 5 (FNDC5)/irisin plays a crucial role in renal protection. The objective of this study was to investigate whether FNDC5/irisin is involved in AKI-induced sepsis by modulating ferroptosis, and the molecular mechanisms that may be involved.</p><p><strong>Material and methods: </strong>A sepsis-induced AKI model was built <i>in vivo</i> and <i>in vitro</i> through lipopolysaccharide (LPS) intervention. FNDC5, adenosine 5'-monophosphate-activated protein kinase (AMPK), phospho-AMPK (p-AMPK), nuclear factor erythroid-2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), glutathione peroxidase 4 (GPX4), and acyl-CoA synthetase long-chain family member 4 (ACSL4) concentrations in cells and mouse kidney tissues were appraised by Western blot. Pro-inflammatory cytokines concentrations in cell supernatants and mouse kidney tissues were appraised by enzyme-linked immunosorbent assay. Fe²⁺ concentration in cells and mouse kidney tissue was appraised by kit. The apoptosis rate of cells and mouse kidney tissue was measured by flow cytometry. Automatic biochemical analyzer was to test serum creatinine (SCr) and blood urea nitrogen (BUN). The kidney tissue sections from each groups were observed by hematoxylin and eosin staining.</p><p><strong>Results: </strong>LPS abated FNDC5 concentration in human kidney-2 cells and mouse kidney tissue (<i>P</i> < 0.001). Overexpression of FNDC5 can abated proinflammatory cytokines concentrations in cells and mouse kidney tissue (<i>P</i> < 0.01). Meanwhile, overexpression of FNDC5 can boost GPX4 protein concentration, abate ACSL4 protein, and abate Fe²⁺ concentration in cells and mouse kidney tissues (<i>P</i> < 0.05). In addition, the overexpression of FNDC5 can reduce the rate of apoptosis (<i>P</i> < 0.01). <i>In vivo</i> experiments showed that FNDC5 overexpression reduced serum BUN and SCr concentrations and alleviated pathological damage in the mouse renal tissues (<i>P</i> < 0.05) and exhibited a certain renal protective effect. FNDC5 overexpression can boost p-AMPK/AMPK, Nrf2, and HO-1 protein concentrations (<i>P</i> < 0.01).</p><p><strong>Conclusion: </strong>FNDC5/irisin improves sepsis-induced acute renal injury by abating ferroptosis through the AMPK/Nrf2 signaling pathway.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"54"},"PeriodicalIF":2.5,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683371/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907818","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}