Analytical Cellular Pathology最新文献

{"title":"YTHDF3 Promoted Gastric Cancer Progression by Facilitating m⁶A-Dependent Degradation of APC mRNA.","authors":"Cao Zhang, Jun Wen, Zijian Liu, Ruyi Li, Yaqin He","doi":"10.1155/ancp/5045743","DOIUrl":"10.1155/ancp/5045743","url":null,"abstract":"<p><strong>Background: </strong>Stomach adenocarcinoma (STAD) is a highly prevalent malignancy. YTH domain family protein 3 (YTHDF3), an m⁶A reader, correlates with worse survival outcomes in STAD. The aim was to study the impact of YTHDF3 on STAD cells and its underlying regulatory mechanisms.</p><p><strong>Methods: </strong>Epidemiologically, the GEPIA and Kaplan-Meier Plotter databases were used to examine YTHDF3 expression in STAD and to assess its association with prognosis, with poor prognosis defined by overall survival (OS). Clinical parameters were also analyzed to validate the prognostic value of YTHDF3. Experimentally, STAD patients were selected as the study objects. Immunofluorescence was used to confirm YTHDF3 expression in STAD tissues. In vitro assays examined YTHDF3/Adenomatous polyposis coli (APC) regulation of Wnt signaling.</p><p><strong>Results: </strong>Epidemiologically, YTHDF3 elevation in STAD (p < 0.05) predicted poorer OS (hazard ratio [HR] = 1.46, 95% confidence interval [95% CI]: 1.17-1.81, p = 0.00066). High YTHDF3 expression was also significantly associated with advanced T stage (p = 0.0069), N stage (p = 0.0088), and positive distant metastasis (p = 0.0076). Experimentally, elevated YTHDF3 expression was observed in STAD tissues and cells (all p < 0.001). Silencing YTHDF3 suppresses AGS malignancy and promotes apoptosis. Conversely, YTHDF3 overexpression aggravated the malignant phenotype of STAD (all p < 0.001). Mechanistically, silencing YTHDF3 promoted APC expression (p < 0.001) in an m⁶A-dependent manner. Rescue experiments proved silencing APC reversed YTHDF3-knockdown-mediated repression of Wnt/β-catenin signaling and AGS cell malignancy (all p < 0.001).</p><p><strong>Conclusion: </strong>YTHDF3 promoted STAD progression by regulating APC mRNA degradation.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e5045743"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13576909/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148971925","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":"Xinlikang Capsule Alleviates Chemotherapy-Induced Fatigue by Inhibiting the PI3K/AKT-mTOR-FoxO Pathway.","authors":"Suzhou Huang, Yiheng Zhang, Tianle Ma, Lu Zhang, Xingxing Lu, Huihua Fang, Gaohong Lv, Zhipeng Chen, Xin Liu, Lina Zhang, Li Wu","doi":"10.1155/ancp/8879160","DOIUrl":"10.1155/ancp/8879160","url":null,"abstract":"<p><strong>Objective: </strong>Chemotherapy-induced fatigue (CIF) remains a clinically challenging condition with limited therapeutic options. This study aimed to elucidate the therapeutic potential and underlying mechanisms of the multiherbal Xinlikang (XLK) capsule against CIF using an integrated strategy that combined network pharmacology prediction with experimental validation.</p><p><strong>Methods: </strong>A murine CIF model was established using 5-fluorouracil (5-FU). XLK was administered at various doses to evaluate its efficacy through comprehensive assessments, including behavioral tests (weight-bearing swimming, tail suspension, and grip strength), histopathology (hematoxylin-eosin [H&E] and periodic acid-Schiff [PAS] staining), and metabolic indices (lactate and ATP levels). To investigate the mechanisms, an integrated network pharmacology approach was employed to identify bioactive components of XLK, predict their potential targets, and construct a \"component-target-pathway\" network. Core signaling pathways implicated in CIF were prioritized via protein-protein interaction (PPI) and KEGG enrichment analyses. Key predictions were subsequently verified by Western blot analysis.</p><p><strong>Results: </strong>XLK treatment significantly ameliorated fatigue-like behaviors, improved muscle glycogen storage, and restored lactate and ATP homeostasis in CIF mice (all p  < 0.05). Network pharmacology predicted that the anti-CIF effect of XLK was closely associated with the regulation of energy metabolism-related pathways, particularly the PI3K/AKT-mTOR-FoxO signaling axis. Experimental validation confirmed that XLK significantly modulated the expression and phosphorylation levels of key proteins (e.g., p-PI3K, p-AKT, and p-mTOR) within this pathway in the skeletal muscle or relevant tissues of CIF model mice (all p  < 0.05).</p><p><strong>Conclusion: </strong>XLK enhances cellular energy homeostasis by regulating the PI3K/AKT-mTOR-FoxO signaling axis, thereby alleviating CIF. These findings provide a mechanistic rationale for the clinical application of XLK against CIF.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e8879160"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147437207","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":"RETRACTION: Myosin 1b Participated in the Modulation of Hypoxia/Reoxygenation-Caused H9c2 Cell Apoptosis and Autophagy.","authors":"Analytical Cellular Pathology","doi":"10.1155/ancp/9869070","DOIUrl":"10.1155/ancp/9869070","url":null,"abstract":"","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e9869070"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13125337/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147787065","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":"Identification of the Antioxidant Enzyme B166 as a Novel Biomarker for Patients With Glioblastoma Multiforme.","authors":"Weiqiang Liu, Bingwu Wang, Fanhua Kong, Cindy Cheung","doi":"10.1155/ancp/6120748","DOIUrl":"10.1155/ancp/6120748","url":null,"abstract":"<p><p>This study aimed to explore the regulatory role of sterol regulatory element-binding protein 1 (SREBP1) in the antioxidant enzyme B166 and to examine the prognostic and therapeutic potential of B166 in glioblastoma multiforme (GBM). RNA-seq data from TCGA and GTEX databases were analyzed to explore the relationship between B166 and GBM, as well as between B166 and SREBP1. Functional experiments were performed to determine whether SREBPs could regulate B166 expression level and to identify the major regulator of B166. Immunofluorescence staining was performed to investigate the cellular distribution of B166 in GBM. Quantitative reverse transcription polymerase chain reaction was employed to determine the regulatory effects of SREBP1-a. CellROX Deep Red dye was applied to detect mitochondrial reactive oxygen species (ROS) levels. The results revealed that B166 protein was significantly upregulated in GBM tissues compared with lower-grade gliomas and normal brain tissues (p<0.0001). The B166 expression level was elevated through SREBP1-a-mediated regulation in GBM, simultaneously decreasing endogenous ROS levels to maintain cellular redox homeostasis and preserve normal mitochondrial function. Reducing SREBP1 level decreased both RNA and protein expression levels of B166. Overexpression of the active form of SREBP1-a elevated the protein levels of B166 in both the mitochondria and nucleus. Pharmacological suppression of SREBP1 or genetic inhibition of B166 disrupted redox homeostasis, resulting in elevated oxidative stress and rapid cell death. In conclusion, B166 may serve as a promising therapeutic target for GBM. Its overexpression could enhance ROS elimination, highlighting its potential therapeutic benefits for GBM patients.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e6120748"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147437196","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":"Gliosarcoma: A Reappraisal of Neuroradiological, Surgical, Morphological, and Radiotherapeutic Characteristics of a Cohort From South Italy Single-Center.","authors":"Ida Rizzuto, Antonio Ieni, Sarah Caroline Scarcella, Valentina Sciacca, Vincenzo Fiorentino, Claudio Napoli, Maurizio Martini, Antonino Germanò, Francesca Granata, Stefano Pergolizzi, Giovanni Tuccari","doi":"10.1155/ancp/4966984","DOIUrl":"10.1155/ancp/4966984","url":null,"abstract":"<p><p>Gliosarcoma (GS) is a rare and aggressive variant of glioblastoma multiforme (GBM), characterized by a biphasic histopathological pattern featuring both glial and mesenchymal components. Accounting for 2% of all GBM cases, this brain tumor is known for its poor prognosis, rapid progression, and resistance to conventional treatments. Despite advances in molecular profiling and multimodal treatment strategies, GS remains a therapeutic challenge due to their highly invasive nature and limited response to standard regimens. The purpose of this study was to characterize the neuroradiological, surgical, clinicopathological, and radiotherapeutic profiles of a cohort of patients affected by GS, including two recurrences of disease.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e4966984"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580779/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147437162","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":"Regulation of Cell Function and Myeloid-Derived Suppressor Cell Chemotaxis by hsa_circ_0006466-miR-1286-PDGFRA/B Axis in Triple Negative Breast Cancer.","authors":"Fengqin Gao, Mingkai Gong, Yufeng Cao, Xiaoyi Liu, Jian Cui, Bing Du, Rongrong Dou, Chuankui Wei, Hongming Song","doi":"10.1155/ancp/2285318","DOIUrl":"10.1155/ancp/2285318","url":null,"abstract":"<p><strong>Background: </strong>Circular RNAs (circRNAs) play critical regulatory roles in diverse biological processes of breast cancer. This study aimed to investigate the circRNAs potentially related to immunity in triple-negative breast cancer (TNBC).</p><p><strong>Methods: </strong>We identified the dysregulated circRNAs in breast cancer using Gene Expression Omnibus (GEO) datasets. Then, their targeting microRNAs (miRNAs) were searched and overlapped with the miRNAs upstream of immune-associated genes. An immune-related circRNA-miRNA-mRNA network was constructed. Hsa_circ_0006466-miR-1286-PDGFRA/B axis was verified from perspectives of expression levels, binding relationships, cell functions, and regulation on myeloid-derived suppressor cells (MDSCs).</p><p><strong>Results: </strong>A total of 28 circRNAs were identified to be dysregulated and related to the immune system in TNBC. The immune-related circRNA-miRNA-mRNA network consisted of 28 circRNAs, 106 miRNAs, and 205 mRNAs. Hsa_circ_0006466 and PDGFRA/B mRNA were upregulated in TNBC patients and positively correlated with MDSC levels. miR-1286 was downregulated in TNBC patients and negatively correlated with MDSC levels. Cotransfection experiments, luciferase reporter assay, and RNA pull-down analyses confirmed hsa_circ_0006466-miR-1286-PDGFRA/B axis. Hsa_circ_0006466 inhibited TNBC cell migration/invasion and proliferation via miR-1286-PDGFRA/B. MDSC differentiation from THP-1 and chemotaxis in TNBC cell medium were moderated by hsa_circ_0006466-miR-1286-PDGFRA/B axis.</p><p><strong>Conclusions: </strong>Our study identifies hsa_circ_0006466 as an immune-related circRNA in TNBC, functioning as a ceRNA to sponge miR-1286 and upregulate PDGFRA/B expression, thereby promoting MDSC-mediated immunosuppression and TNBC progression. Targeting this axis may offer a dual therapeutic strategy to suppress TNBC aggressiveness and reverse immune evasion.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e2285318"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13580802/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147437192","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":"RETRACTION: Depletion of lncRNA MEG3 Ameliorates Imatinib-Induced Injury of Cardiomyocytes via Regulating miR-129-5p/HMGB1 Axis.","authors":"Analytical Cellular Pathology","doi":"10.1155/ancp/9761979","DOIUrl":"10.1155/ancp/9761979","url":null,"abstract":"","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e9761979"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13263405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148240302","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":"Momordica charantia Attenuates Hepatic Steatosis in High-Fat, High-Sucrose Diet-Induced Obese Mice.","authors":"Hyun-Min Woo, Se-Yeong Park, Young-Hee Jo, Sung-Jin Lee, Soo Ho Yeon, Hee-Soo Han, Tae Hoo Yi, Yeon Ju Kim, Yong-Mu Kim, Hyocheol Bae","doi":"10.1155/ancp/2235628","DOIUrl":"10.1155/ancp/2235628","url":null,"abstract":"<p><p>High-fat, high-sucrose (HFHS) diet consumption is a major contributor to obesity and liver-related metabolic disorders. Momordica charantia ethanolic extract powder (MC), derived from a traditional climbing plant, has been shown to exert multiple biological activities, including exhibiting antidiabetic, antioxidant, and antiinflammatory activities. Building on these properties, the present study investigated the potential effects of MC on hepatic lipid metabolism and obesity-related parameters in mice fed a HFHS diet. Male C57BL/6J mice (6 weeks old) were fed an HFHS diet for 4 weeks and subsequently divided into four dietary groups, receiving either continued HFHS, Cissus quadrangularis (CQ; positive control), MC 125 (125 mg/kg), or MC 250 (250 mg/kg) for an additional 12 weeks. Compared with the HFHS group, MC supplementation was associated with lower body weight gain, hepatic lipid accumulation, and epididymal adipocyte size. Histological findings were consistent with these changes in adipose tissue. At the molecular level, MC supplementation was associated with altered hepatic expression of genes involved in lipid metabolism, including decreased expression of the lipogenesis-related genes SREBP-1c, ACC, FAS, and SCD1, as well as alterations in C/EBPα and PPARγ expression. In addition, the expression of fibrosis-related genes Col1α1 and αSMA was decreased in the MC-supplemented groups. These findings suggest that MC supplementation may modulate hepatic lipid metabolism- and fibrosis-related gene expression in HFHS diet-fed mice. Collectively, the present findings suggest that MC may influence metabolic responses associated with chronic consumption of a HFHS diet.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13700938/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149276263","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":"Deployment of Artificial Intelligence in Clinical Oral Pathology: Evidence Summary and Implementation Gaps.","authors":"J H Shazia Fathima, Mugundan Raghavelu Narendran, Mohammed Sharique Ahmed Quadri, Thilla Sekar Vinothkumar, K A Kamala, Mohmed Isaqali Karobari","doi":"10.1155/ancp/9281281","DOIUrl":"10.1155/ancp/9281281","url":null,"abstract":"<p><strong>Background: </strong>Whole-slide imaging (WSI) has shifted pathology toward digital workflows, creating the foundation for applying artificial intelligence (AI) to diagnostic tasks. This review summarises validated AI applications in diagnostic pathology, with an emphasis on clinical performance, regulatory developments and the practical barriers that affect implementation.</p><p><strong>Methods: </strong>A structured search of PubMed, Scopus and Google Scholar identified English-language, peer-reviewed studies from January 2020 to May 2025. Eligible studies applied AI to diagnostic, grading or prognostic tasks in human tissue, used a pathologist-confirmed reference standard and included external or multi-centre validation.</p><p><strong>Results: </strong>More than 150,000 digital slides were represented across the included studies. Reported performance metrics demonstrated strong diagnostic accuracy across several validated applications. Large meta-analyses and externally validated studies reported sensitivity values exceeding 96% and specificity above 93% for selected cancer-detection tasks, while other studies demonstrated high agreement for Gleason grading (QWK up to 0.862) and biomarker quantification (Ki-67 ICC 0.98).</p><p><strong>Conclusion: </strong>AI has the capacity to strengthen diagnostic pathology by improving consistency, measurement and efficiency. Moving from experimental use to routine reporting will require broad validation across centres, enhanced model transparency, strong quality-assurance systems and close cooperation between developers and pathologists.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":"e9281281"},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13519655/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148834146","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":"Correction to \"GTSE1 Facilitates the Malignant Phenotype of Lung Cancer Cells via Activating AKT/mTOR Signaling\".","authors":"","doi":"10.1155/ancp/9862178","DOIUrl":"10.1155/ancp/9862178","url":null,"abstract":"","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2026 1","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13686285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149240194","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}