Analytical Cellular Pathology最新文献

{"title":"Peroxiredoxin 1 Promotes Proinflammatory Cytokine Secretion in Human Dysplastic Oral Keratinocytes and Mouse Tongue Precancerous Tissues.","authors":"Min Zhang, Wenjing Li, Jing Li, Wenchao Wang, Lingyu Li, Yunping Lu, Min Wang, Xiaofei Tang","doi":"10.1155/ancp/6577043","DOIUrl":"10.1155/ancp/6577043","url":null,"abstract":"<p><p>Oxidative stress, a widespread phenomenon involved in many pathological conditions, may be closely related with the progression of oral leukoplakia (OLK). Under chronic inflammation, oxidative stress could stimulate the local formation of a tumor-specific microenvironment in some types of cancer, though not well defined in oral cancer even in OLK. Peroxiredoxin 1 (Prx1), a widely expressed sulfhydryl antioxidant protein, is overexpressed in various tumors and affects tumorigenesis, cell proliferation, apoptosis, invasion, and metastasis. Prx1 also acts as a potent proinflammatory factor. Nuclear factor (NF)-κB is a member of the core dimeric transcription factor family that coordinates the inflammatory response. To investigate the role of Prx1 in oxidative stress-related inflammation in OLK, a coculture model of human dysplastic oral keratinocyte (DOK) and human epidermal fibroblast (HFF) was established and stimulated with H₂O₂. Cellular reactive oxygen species (ROS) and Prx1 levels in DOK were determined via flow cytometry and western blotting, respectively. Additionally, the levels of the inflammatory factors, interleukin (IL)-6, IL-8, IL-10, and interferon (IFN)-γ, in the conditioned medium were determined via enzyme-linked immunosorbent assay (ELISA). DOK nuclear expression of NF-κB was detected via immunofluorescence assay and western blotting. Moreover, the expression levels of inflammatory factors and the nuclear expression of NF-κB were examined in 4-nitroquinoline-1-oxide (4NQO)-induced tongue precancerous tissues of mice. H₂O₂ increased Prx1 levels and nuclear expression levels of NF-κB in DOKs and mouse tongue precancerous tissues and elevated the levels of IL-6, IL-8, IL-10, and IFN-γ secreted in the culture supernatants and mouse tongue tissues. However, <i>Prx1</i> knockdown in DOK and mouse tongue tissues attenuated the upregulation of inflammatory factor and nuclear NF-κB expression levels. Overall, our results suggest that oxidative stress increases Prx1 expression, which promotes inflammatory factor expression by activating NF-κB in human DOK and mouse tongue precancerous tissues.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"6577043"},"PeriodicalIF":2.6,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11972860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804579","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":"Recombinant Human Endostatin Suppressed the Biological Behavior of Human Umbilical Vein Endothelial Cells Under Hypoxic and Hypoxic/Starvation Conditions In Vitro.","authors":"Yongsheng Jia, Cuicui Zhang, Jimin Zhao, Chuanxiang Hu, Xiaoyong Yang, Yan Zhang","doi":"10.1155/ancp/3475731","DOIUrl":"10.1155/ancp/3475731","url":null,"abstract":"<p><p>Recombinant human endostatin (rh-endostatin) has been shown to act as an inhibitor of angiogenesis. Previous studies have indicated that rh-endostatin combined with chemotherapy can improve the objective response rate (ORR), time to progression (TTP), and clinical benefit rate (CBR) without increasing toxicity. However, this function has seldom been reported in normal cells. The aim of our study was to explore the effect of rh-endostatin on the biological behavior of human umbilical vein endothelial cells (HUVECs) under different conditions in vitro. Confluent HUVECs were cultured under normoxic, hypoxic, or hypoxic/starvation (H/S) conditions and then treated with rh-endostatin. An MTT assay was used to assess cell proliferation, and HUVEC tube formation and migration were assessed via a cell tubule formation assay and a migration assay. The expression of endoglin (CD105) was assessed by flow cytometry (FCM). Rh-endostatin inhibited the proliferation, migration, and tube formation of HUVECs under normoxic, hypoxic, and H/S conditions. Compared with that in the normoxia group, the expression of CD105 was not different in the hypoxia 24 h group, but in the starvation and hypoxia/starvation groups, the expression of CD105 was upregulated. Rh-endostatin downregulated the expression of CD105 under all the study conditions. Here we found rh-endostatin suppressed the biological behavior of HUVECs under hypoxic and H/S conditions. As the concentration increased, the effect of rh-endostatin on the biological behavior of HUVECs was not greatly enhanced. Rh-endostatin did not promote malignant biological behavior or CD105 expression. Since CD105 may induce endothelial-to-mesenchymal transition in HUVECs, we hypothesized that rh-endostatin may inhibit the malignant biological behavior of HUVECs under hypoxic conditions in vitro.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"3475731"},"PeriodicalIF":2.6,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11972857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143804561","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":"Chemopreventive Potential of Paddy Waste: A Promising Approach Against Benign Prostate Hyperplasia in Spontaneously Hypertensive Rats.","authors":"Azman Seeni, Atif Amin Baig, Mogana Das Murtey","doi":"10.1155/ancp/4029625","DOIUrl":"10.1155/ancp/4029625","url":null,"abstract":"<p><p><b>Background:</b> Benign prostate hyperplasia (BPH) is common in elderly men. Previously, paddy waste (both husk and straw) reportedly had chemopreventive potential. The main aim of this study was to explore the chemopreventive properties of paddy waste against prostate disease. This study determines the antiproliferative activity of the paddy waste product in spontaneously hypertensive rats (SHRs). <b>Methods:</b> Aqueous methanol extracts of paddy husk and straw were administered to SHRs for 17 weeks via drinking water, with no observed toxicity on dietary intake, body weight, liver, or kidney. The study used 18 male SHRs to model primary hypertension and 6 male Wistar Kyoto (WKY) rats as normotensive controls. The SHRs were divided into three groups: control (<i>n</i> = 6), paddy husk treated (<i>n</i> = 6, 15 mg/kg), and paddy straw treated (<i>n</i> = 6, 15 mg/kg), with treatment delivered in drinking water. <b>Results:</b> It managed to reduce blood pressure (72.0 mmHg; <i>p</i>  < 0.01) and the size of the ventral prostate to around 0.05% (<i>p</i>  < 0.01). Histological analysis revealed antiproliferative signs such as a reduction in the number of acini (7.50; <i>p</i>  < 0.01), epithelial height (10.55 µm; <i>p</i>  < 0.01), and epithelial acinar area (18.17%; <i>p</i>  < 0.01). Aqueous methanol extracts have arrested the cell cycle by downregulating (<i>p</i>  < 0.01) proliferative marker, Ki-67, and proliferating cell nuclear antigen (PCNA). Prostate cell growth is arrested by downregulation of androgen receptor (AR) which inhibited AR mRNA transcription (RTPCR analysis) and induced cell cycle arrest at the S phase through p27 and cyclin E2 (western blot analysis). <b>Conclusion:</b> In conclusion, paddy waste product especially husk is a better chemopreventive agent against prostate disease.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"4029625"},"PeriodicalIF":2.6,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11925631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143671417","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":"Decoding Osteosarcoma's Lactylation Gene Expression: Insights Into Prognosis, Immune Dynamics, and Treatment.","authors":"Cheng Peng, Chaoqun You, Shuang Cao, Linfei Cheng, Jiaji Ren, Jiashi Cao, Jing Wang, Tielong Liu","doi":"10.1155/ancp/6517238","DOIUrl":"https://doi.org/10.1155/ancp/6517238","url":null,"abstract":"<p><p>Osteosarcoma (OS), characterized by a complex tumor microenvironment, poses challenges in treatment, metastasis, and therapy resistance. This study examined the impact of lactylation, a posttranslational modification, on gene expression and tumor behavior in OS, particularly its influence on prognosis, immune cell infiltration, and chemotherapy response. Utilizing data from the Gene Expression Omnibus series accession number 21257 (GSE21257) and the Therapeutically Applicable Research to Generate Effective Treatments on Osteosarcoma (TARGET-OS) datasets, the investigation focused on analyzing the expression profiles of 267 lactylation modifier genes, which were selected from a total of 336 lactylation-related genes compiled from various studies in the literature. The methods included unsupervised clustering using \"ConsensusClusterPlus\" heatmap generation with \"pheatmap\" pathway analysis from several databases, and immune cell infiltration assessment using the \"single-sample Gene Set Enrichment Analysis (ssGSEA)\" function. The research revealed 36 significant lactylation-related genes in OS, categorizing them into two clusters with distinct survival and biological characteristics. One cluster demonstrated poor prognosis due to increased tumor cell proliferation and specific immune cell variations, also showcasing genes that enhance tumor growth and metastasis, thus indicating its aggressive nature and adverse outcomes for patients. These insights are crucial for understanding the molecular mechanisms of OS and identifying therapeutic targets. Therefore, the study elucidates the role of lactylation-related genes in the prognosis, pathogenesis, and treatment response of OS, laying the groundwork for further exploration into potential therapeutic targets and the underlying mechanisms within OS.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"6517238"},"PeriodicalIF":2.6,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11870760/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143544059","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":"The Association of <i>VDR/FokI</i> Gene Polymorphism and Protein Expression With Histopathological Alterations in Patients With Thyroid Colloid Nodule.","authors":"Mariwan F Abdalfatah, Abdullah A Shareef, Lana S Saleh, Mustafa F Rajab, Shukur W Smail, Saman S Abdulla, Harem Khdir Awla, Rivan H Ishaac, Kazhal S Ibrahim, Mazyar J Ahmed, Fairuz A Kakasur, Khder Hussein Rasul","doi":"10.1155/ancp/6796922","DOIUrl":"10.1155/ancp/6796922","url":null,"abstract":"<p><p><b>Objective:</b> Colloid nodules are common and benign thyroid lesions that usually progress slowly and are asymptomatic. It requires follow-up because untreated colloid nodules may develop into malignant tumor. The study aimed to examine the contributions of vitamin D receptor (VDR) expression, VDR/FokI (rs2228570) genotypes, and serum vitamin D level to the susceptibility to colloid nodules. <b>Methods:</b> One hundred forty subjects (80 patients and 60 controls) were enrolled and VDR FokI was determined by PCR in formalin fixed paraffin embedded (FFPE) blocks of the patients and blood of controls. Moreover, VDR protein expression was evaluated by immunohistochemistry using specific VDR monoclonal antibody in the tissue sections of patients and serum vitamin D were measured simultaneously using enzyme-linked immunosorbent assay (ELISA). <b>Results:</b> Sixty-two (77.5%) cases showed strong immunoreactivity score (IRS) of cytoplasmic staining. Strong IRS were significantly observed in samples with larger nodule size (<i>p</i> value: 0.0094), multinodules (<i>p</i> value: 0.0054), and carriers of CC genotypes (<i>p</i> value: 0.0034). TT homozygous genotype revealed significantly (<i>p</i> value: 0.029 and odds ratio (OR): 0.11) protective factor for colloid nodules. In addition, nodule size was significantly (<i>p</i> value: 0.016) larger among CC carriers. Moreover, vitamin D level and category were nonsignificantly difference between patients and controls. <b>Conclusion:</b> Our results reveal prominent cytoplasmic VDR expression, suggesting a distinct distribution pattern and offering valuable insights into its potential role in colloid nodules. VDR expression increases with increasing size and number of nodules. Regarding FokI genotypes, TT genotype was less likely to develop colloid nodule. These findings contribute to our understanding of cellular characteristics of this condition and may have implications for future research and clinical management.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"6796922"},"PeriodicalIF":2.6,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11858711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143505324","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":"Circular RNA Circ_0079226 Plays an Oncogenic Role in Gastric Cancer via the miR-155-5p/FOXK1/AKT Pathway.","authors":"Hui Zhang, Zhisheng Huang, Yingyun Zhong","doi":"10.1155/ancp/6619550","DOIUrl":"10.1155/ancp/6619550","url":null,"abstract":"<p><p><b>Background:</b> Circular RNA (circRNA) is implicated in various biological processes, including the progression of gastric cancer (GC). The specific functions and underlying mechanisms of circ_0079226 in GC are unknown. <b>Methods:</b> We examined cancerous and adjacent noncancerous tissues from 25 patients with GC to evaluate circ_0079226, miR-155-5p, and forkhead transcription factor K1 (FOXK1) expression. Pearson's correlation analysis was used to assess the relationships among these RNAs. We examined their functional roles utilizing in vitro (cell cytotoxicity kit-8, wound healing, and Transwell invasion assays) and in vivo (xenograft mouse models) approaches. Molecular mechanisms were investigated using bioinformatics, dual-luciferase reporter assays, and rescue experiments, while quantitative real-time PCR, western blot, immunohistochemistry (IHC), fluorescence in situ hybridization (FISH), and protein immunofluorescence (IF) were used to detect gene expression. <b>Results:</b> We found that circ_0079226 and FOXK1 levels were elevated, while miR-155-5p was reduced in GC tissues and cells. An inverse correlation existed between FOXK1 and miR-155-5p, while a direct correlation was observed between FOXK1 and circ_0079226. Circ_0079226 facilitated GC cell proliferation, migration, invasion, and in vivo tumor growth. It functions by sequestering miR-155-5p, which directly targets FOXK1. High miR-155-5p expression mitigated the effects of circ_0079226 on GC cells, and the reintroduction of FOXK1 reversed the inhibitory effects of miR-155-5p. Circ_0079226 boosts FOXK1 and its associated downstream signaling pathways, including FAK, AKT, and p-AKT, through competitive binding with miR-155-5p. <b>Conclusions:</b> In conclusion, circ_0079226 is implicated in GC cell proliferation and metastasis by modulating the miR-155-5p/FOXK1/AKT pathway, presenting it as a potential therapeutic target.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"6619550"},"PeriodicalIF":2.6,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11842135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143469723","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":"SLC1A4 Promotes Malignant Transformation of Hepatocellular Carcinoma by Activating the AKT Signaling.","authors":"Jiaoyun Zheng, Jian Gong","doi":"10.1155/ancp/1115184","DOIUrl":"10.1155/ancp/1115184","url":null,"abstract":"<p><p>Due to the difficulty in early diagnosis and the lack of treatment for advanced disease, the mortality rate of hepatocellular carcinoma (HCC) is high, and the 5-year overall survival rate is low at present. SLC1A4 is a neutral amino acid transporter, but its regulatory role and mechanism in HCC are still unclear. Through analyzing the TCGA database and clinical tissue specimens, this study uncovered the high expression of SLC1A4 in tumor tissues of HCC. Worse more, a high level of SLC1A4 may lead to a poor prognosis of HCC. Mechanically, silencing SLC1A4 inhibited the phosphorylation activation of AKT by suppressing the ubiquitin modification of AKT at lysine 63 and amino acid influx represented by D-serine, decreasing the protein level of <i>β</i>-catenin in the cell nucleus and suppressing the transcriptional activity of c-Myc and EpCAM promoters. As a result, silencing SLC1A4 inhibited the proliferation, migration, and stemness of hepatic cancer cells, which was successfully reversed by the introduction of exogenous AKT. Moreover, epithelial-mesenchymal transition (EMT) in vitro and metastasis potential in vivo of hepatic cancer cells was suppressed by the downregulated SLC1A4 level. In conclusion, SLC1A4 promotes the malignant transformation of HCC through activating signal transduction mediated by AKT. The findings in this study suggested that SLC1A4 may be a diagnostic indicator for the early HCC and a therapeutic target for the advanced HCC.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"1115184"},"PeriodicalIF":2.6,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11824774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143415930","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":"DDX21 Is a Potential Biomarker for Predicting Recurrence and Prognosis in Hepatocellular Carcinoma.","authors":"Chengjie Ji, Qing Zhong, Huilan Su, Xiaoli Xue, Renxiang Yang, Na Li","doi":"10.1155/ancp/1018820","DOIUrl":"10.1155/ancp/1018820","url":null,"abstract":"<p><p>DEAD-box helicase 21 (DDX21) is a conserved Asp-Glu-Ala-Asp (DEAD) box RNA helicase with multiple functions that is involved in various cellular processes and diseases. However, the role of DDX21 in the recurrence and prognosis of hepatocellular carcinoma (HCC) patients remains unknown. In the current study, we examined the protein expression of DDX21 in HCC tissues through immunohistochemical staining and analyzed the correlation between DDX21 protein expression and clinical outcome via Kaplan-Meier survival analysis. The Cox proportional hazards regression model was used to assess the interrelationships between the outcome and variable over time. Our results showed that increased expression of DDX21 protein was observed in HCC tissues compared with paracancerous tissues and was associated with advanced BCLC stage. Recurrent HCC patients had higher levels of DDX21 protein than nonrecurrent cases. Notably, DDX21 was an independent risk factor for predicting worse overall survival and recurrence-free survival in HCC patients. Furthermore, lack of DDX21 abated the growth and mobility of Hep3B cells. Taken together, our data highlight the clinical significance of DDX21 in the recurrence and prognosis of HCC patients and indicate that targeting DDX21 may represent an effective therapeutic strategy for the treatment of HCC.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"1018820"},"PeriodicalIF":2.6,"publicationDate":"2025-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11760617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143047819","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":"Development of a Novel Prognostic Model for Lung Adenocarcinoma Utilizing Pyroptosis-Associated LncRNAs.","authors":"Hong-Yan Bai, Tian-Tian Li, Li-Na Sun, Jing-Hong Zhang, Xiu-He Kang, Yi-Qing Qu","doi":"10.1155/ancp/4488139","DOIUrl":"10.1155/ancp/4488139","url":null,"abstract":"<p><p>Lung cancer is a highly prevalent and fatal cancer that seriously threatens the safety of people in various regions around the world. Difficulty in early diagnosis and strong drug resistance have always been difficulties in the treatment of lung cancer, so the prognosis of lung cancer has always been the focus of scientific researchers. This study used genotype-tissue expression (GTEx) and the cancer genome atlas (TCGA) databases to obtain 477 lung adenocarcinoma (LUAD) and 347 healthy individuals' samples as research subjects and divided LUAD patients into low-risk and high-risk groups based on prognostic risk scores. Differentially expressed gene (DEG) analysis was performed on 25 pyroptosis-related genes obtained from GeneCards and MSigDB databases in cancer tissues of LUAD patients and noncancerous tissues of healthy individuals, and seven genes were significantly different in cancer tissues and noncancerous tissues among them. Coexpression analysis and differential expression analysis of these genes and long noncoding RNAs (lncRNAs) found that three lncRNAs (AC012615.1, AC099850.3, and AO0001453.2) had significant differences in expression between cancer tissues and noncancerous tissues. We used Cox regression and the least absolute shrinkage sum selection operator (LASSO) regression to construct a prognostic model for LUAD patients with these three pyroptosis-related lncRNAs (pRLs) and analyzed the prognostic value of the pRLs model by the Likaplan-Meier curve and Cox regression. The results show that the risk prediction model has good prediction ability. In addition, we also studied the differences in tumor mutation burden (TMB), tumor immune dysfunction and rejection (TIDE), and immune microenvironment with pRLs risk scores in low-risk and high-risk groups. This study successfully established a LUAD prognostic model based on pRLs, which provides new insights into lncRNA-based LUAD diagnosis and treatment strategies.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"4488139"},"PeriodicalIF":2.6,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11745560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143015017","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":"High Glucose-Induced Senescent Fibroblasts-Derived Exosomal miR-497 Inhibits Wound Healing by Regulating Endothelial Cellular Autophagy via ATG13.","authors":"Changjiang Liu, Yuting Liu, Yifeng Yu, Siyuan Huang, Chao Sun, Dong Zhang, Aixi Yu","doi":"10.1155/ancp/8890200","DOIUrl":"10.1155/ancp/8890200","url":null,"abstract":"<p><p><b>Background:</b> Fibroblasts play a crucial role in diabetic wound healing, and their senescence is the cause of delayed wound repair. It was reported that fibroblasts can secrete exosomes that can mediate a vital role in diabetic complications. Our purpose is to examine the biological function of high glucose (HG)-induced senescent fibroblasts from the perspective of exosomes and reveal the mechanism at cellular and animal levels. <b>Methods:</b> HG-induced senescent fibroblasts were measured by senescence-associated <i>β</i>-galactosidase staining and immunofluorescence. Flow cytometry, 5-ethynyl-2'-deoxyuridine (edu), and cell counting kit 8 (CCK-8) assay were applied to detect apoptosis and cell viability. Fibroblasts and endothelial cells were cocultured, and the migration and angiogenesis abilities were detected by scratch, transwell, and tube formation assays. Exosomes were isolated and identified from fibroblasts that were treated differently. Then, the function of exosomes was investigated in cells and mice, including examining the cellular phenotype changes, detecting the autophagy levels, and evaluating the wound healing rate. Furthermore, the potential mechanism by which senescent fibroblast-derived exosomes inhibit wound healing was examined via bioinformatics, real-time quantitive polymerase chain reaction (qPCR), transfection, and dual-luciferase assays. <b>Results:</b> It illustrated that HG-induced senescent fibroblasts exhibited adverse impacts on cellular proliferation, migration, and angiogenesis of endothelial cells via secreting exosomes, and senescent fibroblast-derived exosomes (S-Exos) can delay skin wound defects in mice. Subsequent differential analysis of the GSE153214 and GSE48417 datasets elucidated that miR-497 was the biomarker in the senescent fibroblasts. Interestingly, the miR-497 levels were also elevated in S-Exos. Its overexpression can regulate human umbilical vein endothelial cell function by regulating autophagy via targeting ATG13. Furthermore, <i>in vivo</i> experiments also illustrated that miR-497 can delay wound healing and reduce autophagy. <b>Conclusions:</b> Our study demonstrated that exosomes from senescent fibroblasts can impair endothelial cell function and impede diabetic wound healing. The underlying mechanism was that fibroblast-derived exosomal miR-497 can target ATG13 to reduce autophagy, offering insight into new therapy for diabetic complications and other diseases.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2025 ","pages":"8890200"},"PeriodicalIF":2.6,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11742073/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143015079","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}