Cytojournal最新文献

{"title":"The mechanism of prostaglandin E2 upregulation of programmed death ligand 1 expression promoting immune escape in non-small cell lung cancer.","authors":"Tian Wang, Lei Liu, Sen Liu","doi":"10.25259/Cytojournal_129_2025","DOIUrl":"10.25259/Cytojournal_129_2025","url":null,"abstract":"<p><strong>Objective: </strong>Non-small cell lung cancer (NSCLC) represents a major contributor to cancer-related mortality. This study aims to investigate the prostaglandin E synthase (PTGES) role in NSCLC, especially how prostaglandin E2 (PGE2), which is synthesized by PTGES prompts programmed death ligand 1 (PD-L1) expression, resulting in immune escape.</p><p><strong>Material and methods: </strong>The PTGES and PGE2 expression levels were tested in normal and NSCLC samples, respectively. An A549 cell line that overexpressed and knocked down PTGES was established, and cell multiplication, colony formation, and aggression were evaluated. The PD-L1 levels and cytotoxicity effect of CD8⁺ T cells were analyzed by co-culture with A549 cells. The expression levels of proteins involved in phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway and the effect of activation and inhibition on PD-L1 expression were investigated. The effect of PGE2 was further verified by establishing an <i>in vivo</i> xenograft mouse model.</p><p><strong>Results: </strong>The expression of PTGES in NSCLC cells notably increased compared with that in control cells (<i>P</i> < 0.001). Correspondingly, a significant upregulation of PGE2 levels was observed (<i>P</i> < 0.001). Overexpression of PTGES enhanced cell proliferation and aggression ability (<i>P</i> < 0.001), whereas knockdown of PTGES weakened these capabilities (<i>P</i> < 0.01). In the experiment of co-culture with CD8⁺ T cells, PD-L1 was upregulated (<i>P</i> < 0.01) and cytotoxicity was considerably reduced (<i>P</i> < 0.01) in the PTGES overexpression group. Meanwhile, PD-L1 was downregulated (<i>P</i> < 0.01) and cytotoxicity was enhanced (<i>P</i> < 0.01) in the PTGES knockdown group. Overexpression of PTGES was able to activate the PI3K/AKT/mTOR pathway (<i>P</i> < 0.01). Activation and inhibition of this pathway showed that PGE2 upregulated PD-L1 expression through this signaling pathway (<i>P</i> < 0.01). The mouse transplanted tumor model further verified the effect of PTGES expression on tumor growth and immune escape.</p><p><strong>Conclusion: </strong>This study confirmed that PGE2 promotes immune evasion of NSCLC by upregulating PD-L1, and the mechanism involves the activation of the PI3K/AKT/mTOR pathway. This research provides a novel theoretical basis for immunotherapy of NSCLC and emphasizes the clinical value of PTGES/PGE2 as a potential target.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"105"},"PeriodicalIF":3.1,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883099/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151119","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 promoting role of protein arginine methyltransferase 1 in cervical cancer: Mechanisms of angiogenesis and immune evasion.","authors":"Xiaoping Wang, Xiaoxia Zheng, Yingji Fang, Tingting Zheng, Jing Zhang, Zhongliang Li, Yanmei Hou","doi":"10.25259/Cytojournal_106_2025","DOIUrl":"10.25259/Cytojournal_106_2025","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;Cervical cancer (CC) is a leading factor in cancer-associated mortality among women worldwide. Protein arginine methyltransferase 1 (PRMT1) is involved in tumor growth, metastasis, and immune regulation in various types of cancer. However, the specific role of PRMT1 in CC remains unclear. This study aims to assess the expression pattern of PRMT1 in CC and its effects on tumor growth, angiogenesis, immune response, and metastasis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Material and methods: &lt;/strong&gt;We used quantitative reverse-transcription polymerase chain reaction and Western blot to detect the expression of PRMT1 in mouse tumor tissues and normal cervical tissues and the differential expression of PRMT1 in human cervical epithelial cells (HCerEpiC) and CC cell lines (HeLa). An ectopic CC mouse model was established and treated with anti-PRMT1 antibody or PRMT1 recombinant protein to evaluate PRMT1 expression in tumor tissues, tumor volume, weight, and histological changes. Transwell and tube formation assays were performed to assess the effects of PRMT1 on CC cell migration, invasion, and endothelial cell tube formation. The regulation of the cGAS-STING (cyclic GMP-AMP synthase-stimulator of interferon genes) signaling pathway in HeLa cells by PRMT1 was also investigated using PicoGreen staining and Western blot analysis.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;The expression of PRMT1 was noticeably higher in tumor tissues than in normal tissues (&lt;i&gt;P &lt;&lt;/i&gt; 0.001) as well as in HeLa than in HCerEpiC (&lt;i&gt;P &lt;&lt;/i&gt; 0.001). In the mouse model, anti-PRMT1 treatment significantly inhibited tumor growth and reduced PRMT1 expression (&lt;i&gt;P &lt;&lt;/i&gt; 0.001). Treatment with PRMT1 recombinant protein promoted tumor growth and increased PRMT1 expression (&lt;i&gt;P &lt;&lt;/i&gt; 0.001). Histological analysis revealed that anti-PRMT1 treatment led to tumor cell shrinkage, nuclear condensation, and tissue necrosis, whereas PRMT1 recombinant protein treatment promoted cell proliferation and nuclear enlargement. Moreover, anti-PRMT1 treatment suppressed the expression of angiogenesis-related markers (a-smooth muscle actin, Cluster of differentiation 31, and glucose transporter 1) and significantly increased CD8+ immune cell infiltration, while PRMT1 recombinant protein enhanced angiogenesis and inhibited CD8 expression (&lt;i&gt;P &lt;&lt;/i&gt; 0.001). Knockdown of PRMT1 (Sh-PRMT1) significantly inhibited HeLa cell migration and invasion, while overexpression of PRMT1 (Ov-PRMT1) significantly promoted these processes (&lt;i&gt;P &lt;&lt;/i&gt; 0.001). Tube formation assays showed that Sh-PRMT1 treatment suppressed tube formation in human umbilical vein endothelial cells, whereas Ov-PRMT1 increased the number of formed tubes (&lt;i&gt;P &lt;&lt;/i&gt; 0.001). Finally, Sh-PRMT1 treatment significantly increased the activation of the cGAS-STING signaling pathway, while Ov-PRMT1 suppressed its activity (&lt;i&gt;P &lt;&lt;/i&gt; 0.001).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;PRMT1 promotes CC progression by enhancing tumor growth, angiogenesis, a","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"104"},"PeriodicalIF":3.1,"publicationDate":"2025-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151151","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 \"A brief overview of imprint cytology in thoracic cytopathology\".","authors":"Nikola Gardić","doi":"10.25259/Cytojournal_214_2025","DOIUrl":"10.25259/Cytojournal_214_2025","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.25259/Cytojournal_124_2025.].</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"103"},"PeriodicalIF":3.1,"publicationDate":"2025-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883100/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151155","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":"Novel mechanism of tumor metastasis: DDX11-ATAD5 interaction mediates epithelial-mesenchymal transition to promote gallbladder cancer progression.","authors":"Lei Kong, Wei Li, Weishu Kong, Huali Yang","doi":"10.25259/Cytojournal_42_2025","DOIUrl":"10.25259/Cytojournal_42_2025","url":null,"abstract":"<p><strong>Objective: </strong>Molecular mechanisms underlying gallbladder cancer (GBC) progression remain incompletely understood. This study aims to investigate the role and molecular mechanism of DEAD/H-box helicase 11 (DDX11)-ATPase family AAA domain containing 5 (ATAD5) protein interaction in GBC pathogenesis.</p><p><strong>Material and methods: </strong>Cell proliferation, colony formation, and Transwell assays were performed to evaluate the effects of DDX11-ATAD5 interaction in GBC cells. Sequencing data were analyzed to assess DDX11 and ATAD5 expression in GBC tissues, and immunofluorescence co-localization and co-immunoprecipitation assays were conducted to verify the interaction between DDX11 and ATAD5. Subcutaneous xenograft and metastasis models were established to validate their functions <i>in vivo</i>, and E-cadherin and vimentin were detected by quantitative real-time polymerase chain reaction.</p><p><strong>Results: </strong>Both DDX11 and ATAD5 were upregulated in GBC tissues and exhibited direct protein-protein interaction (<i>P</i> < 0.05). Functional studies revealed that DDX11 promoted GBC cell proliferation, migration, and invasion while inhibiting apoptosis (<i>P</i> < 0.01). ATAD5 silencing markedly attenuated the oncogenic effects mediated by DDX11. <i>In vivo</i> experiments further confirmed that DDX11 overexpression enhanced subcutaneous tumor growth and metastasis in nude mice (<i>P</i> < 0.001). Mechanistically, the DDX11-ATAD5 complex promoted GBC cell invasion and metastasis by facilitating the epithelial-mesenchymal transition (EMT; <i>P</i> < 0.01).</p><p><strong>Conclusion: </strong>This study reveals a novel molecular mechanism whereby DDX11-ATAD5 interaction promotes GBC progression through EMT activation, providing potential therapeutic targets for GBC diagnosis and treatment.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"102"},"PeriodicalIF":3.1,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883107/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151130","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 novel candidate tumor biomarker progestin and adipoQ receptor 3 regulates cell metastasis through transforming growth factor-β pathway in hepatocellular carcinoma.","authors":"Xiaohui Liang, Yan Ding, Wenna Liu","doi":"10.25259/Cytojournal_138_2025","DOIUrl":"10.25259/Cytojournal_138_2025","url":null,"abstract":"<p><strong>Objective: </strong>Progestin and adipoQ receptor 3 (PAQR3) have been identified as a potential tumor suppressor in hepatocellular carcinoma (HCC), yet its role in metastasis remains unclear. This study examined PAQR3 expression in primary HCC and its regulation of cell metastasis and ferroptosis through the transforming growth factor-b (TGF-b) pathway.</p><p><strong>Material and methods: </strong>PAQR3 expression in HCC tissues was evaluated by immunohistochemistry, while western blotting (WB) and quantitative real-time polymerase chain reaction were used to assess its levels in HCC cells. Cell migration and invasion were analyzed using Transwell and wound-healing assays. WB was employed to measure epithelial-mesenchymal transition-related proteins. Ferroptosis was evaluated by measuring lipid peroxidation, iron accumulation, reactive oxygen species (ROS) levels, and the expression of ferroptosis-related proteins.</p><p><strong>Results: </strong>PAQR3 expression was significantly downregulated in HCC tissues and may serve as a prognostic marker (<i>P</i> < 0.001). PAQR3 overexpression suppressed HCC cell migration and invasion, elevated ROS, Fe²⁺, and lipid peroxidation, downregulated GPX4 and SLC7A11, and upregulated ACSL4, thereby promoting ferroptosis (<i>P</i> < 0.001). In addition, PAQR3 overexpression reduced TGF-b1, p-Smad3, and p-Smad2 (<i>P</i> < 0.001), while increasing Smad3 and Smad2, indicating suppression of the TGF-b pathway.</p><p><strong>Conclusion: </strong>These findings suggest that PAQR3 inhibits metastasis and induces ferroptosis in HCC through TGF-b pathway regulation.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"101"},"PeriodicalIF":3.1,"publicationDate":"2025-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883101/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151107","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":"Various genetic alterations observed in both benign and malignant oncocytic (Hürthle cell) neoplasms of the thyroid.","authors":"Chiara Jean Cocelli, Lisa Reid, Shuyue Ren","doi":"10.25259/Cytojournal_84_2025","DOIUrl":"10.25259/Cytojournal_84_2025","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;Oncocytic thyroid follicular neoplasms (ONs), including oncocytic adenoma (OA) and oncocytic carcinoma (OC), are distinct follicular cell-derived tumors with unique molecular profiles. Oncocytic changes can also occur in other situations, such as papillary thyroid carcinoma (PTC) and thyroiditis. Due to overlapping cytological features, distinguishing benign from malignant ONs preoperatively remains challenging. This study examines cytological patterns and genetic alterations in ONs and aims to enhance diagnostic accuracy.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Material and methods: &lt;/strong&gt;We retrospectively analyzed ON and oncocytic PTC (OPTC) cases from January 2018 to March 2025 at Cooper University Hospital, identifying 119 surgical resections (55 malignant, 62 benign, and two oncocytic non-invasive follicular thyroid neoplasms with papillary-like nuclear features. Sixty-five cases had fine-needle aspiration biopsy results categorized using The Bethesda System for Reporting Thyroid Cytopathology. Molecular examinations were performed in Afirma, ThyroSeq, or ThyGeNEXT/ThyraMIR. Statistical analyses included Wilcoxon Rank Sum tests, logistic regression, and Fisher's exact tests.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;No significant differences were observed between benign and malignant groups in terms of patient sex or tumor size; however, younger patient age was associated with malignant neoplasm within the cytology tested samples (&lt;i&gt;P&lt;/i&gt; = 0.0300). Molecular analysis showed that 3.6% (1/28) of malignant cases were negative for tested alterations, while 33.3% (12/36) of benign cases were negative (&lt;i&gt;P&lt;/i&gt; = 0.0035). Common mutations included eukaryotic translation initiation factor 1A X-linked (EIF1AX) (27.3%) in OCs and Harvey rat sarcoma viral oncogene homolog (HRAS) Q61R (41.2%) in OPTCs. In contrast, OA exhibited a higher frequency of chromosomal copy number alterations (33.3%) and variable other genetic changes.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;ONs pose diagnostic challenges due to significant cytological and molecular overlap between benign and malignant cases. Current thyroid molecular testing reveals a broad range of genetic alterations in ONs but lack sufficient specificity to reliably distinguish benign from malignancy in most instances. In this study, genetic alterations were detected in 66.6% (24/36) of OAs, and telomerase reverse transcriptase (TERT) mutations - typically associated with malignancy - were identified in two OAs. However, notably, certain mutations were exclusive to specific groups, such as B-Raf proto-oncogene, serine/threonine kinase (BRAF), anaplastic lymphoma kinase/echinoderm microtubule-associated protein-like 4 (ALK/EML4), and paired box 8 - peroxisome proliferator activator receptor gamma (PAX8-PPARG) in OPTCs or EIF1AX in OCs. Importantly, only 3.6% (1/28) of malignant OPTC/ONs were tested negative on molecular analysis, suggesting that ONs with negative molecular test results are more likely to be be","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"100"},"PeriodicalIF":3.1,"publicationDate":"2025-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151109","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":"Ubiquitin C-terminal hydrolase L5 promotes the development of renal cell carcinoma through the glycolysis mediated by the phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin pathway.","authors":"Lin Ruan, Shun Li, Liuyu Xu","doi":"10.25259/Cytojournal_100_2025","DOIUrl":"10.25259/Cytojournal_100_2025","url":null,"abstract":"<p><strong>Objective: </strong>Renal cell carcinoma (RCC) is a prevalent malignant tumor of the kidney that has considerable heterogeneity and intricate molecular pathways. Incidence and death rates associated with kidney cancer have been increasing steadily. Consequently, investigating its molecular basis and identifying new biomarkers for targeted therapies have become important. Ubiquitin C-terminal hydrolase L5 (UCHL5) has an effect on tumor initiation and progression. This study aims to explore the role of UCHL5 in promoting RCC development and identify related molecular mechanisms.</p><p><strong>Material and methods: </strong>Quantitative real-time polymerase chain reaction and Western blot (WB) analyses were employed to measure UCHL5 expression. Stable UCHL5 overexpression and knockdown cell lines were generated using lentiviral transfection in 786-O cells. Colony formation and 5-ethynyl-2'-deoxyuridine assays were used to assess cell proliferation. Cell migration was evaluated using scratch assays, while invasion capacity was determined by Transwell assays. Commercial kits were utilized to quantify glucose consumption and lactate production. WB was applied to detect proteins related to glycolysis and components of the Phosphoinositol 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway. The function of UCHL5 in RCC cells was validated <i>in vivo</i> through an animal tumor model.</p><p><strong>Results: </strong>The expression of UCHL5 increased in RCC cell lines (<i>P</i> < 0.01). Silencing UCHL5 significantly impaired the malignant behavior of RCC cells (<i>P</i> < 0.01), whereas its overexpression promoted this cellular behavior (<i>P</i> < 0.05). Reducing UCHL5 levels decreased glucose uptake, lactate secretion, and protein expression involved in glycolysis, while overexpression enhanced glycolytic activity in RCC cells (<i>P</i> < 0.01). Knockdown of UCHL5 diminished the phosphorylation of PI3K/AKT/mTOR pathway proteins (<i>P</i> < 0.05), whereas the opposite effect was observed upon overexpression (<i>P</i> < 0.01). Treatment with 740Y-P effectively reversed the suppression of glycolysis, proliferation, and metastasis caused by UCHL5 knockdown (<i>P</i> < 0.01). Conversely, LY294002 inhibited the glycolytic enhancement and aggressive phenotypes induced by UCHL5 overexpression (<i>P</i> < 0.01). Animal experiments further confirmed that UCHL5 downregulation suppressed RCC growth through the PI3K/AKT/ mTOR pathway (<i>P</i> < 0.01).</p><p><strong>Conclusion: </strong>UCHL5 activates the PI3K/AKT/mTOR cascade, which enhances the glycolysis of RCC cells and promotes the development of renal cancer. This study provides insights into the molecular mechanisms underlying the oncogenic role of UCHL5 in RCC.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"99"},"PeriodicalIF":3.1,"publicationDate":"2025-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151177","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":"Precision in practice: The diagnostic yield of endoscopic ultrasound guided fine needle aspiration/fine needle biopsy cytology in pancreatic mass lesions.","authors":"Ali Koyuncuer, Hüseyin Aykut, Emine Kanatsız, Kamil Özdil","doi":"10.25259/Cytojournal_161_2025","DOIUrl":"10.25259/Cytojournal_161_2025","url":null,"abstract":"","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"98"},"PeriodicalIF":3.1,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151140","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":"Oxoglutarate dehydrogenase-like may alleviate the inflammatory response process of epilepsy by inhibiting JAK/STAT signaling pathway through upregulating collagen type IV alpha 2.","authors":"Wenzeng Wang, Qiannan Song, Daqing Feng, Qun Chen, Tingting Guo, Hong Chen","doi":"10.25259/Cytojournal_251_2024","DOIUrl":"10.25259/Cytojournal_251_2024","url":null,"abstract":"<p><strong>Objective: </strong>Despite the availability of many epilepsy drugs, certain epilepsy patients still cannot be treated with medication. The dysfunction of oxoglutarate dehydrogenase-like (OGDHL) is related to neurodegeneration. This article aimed to explore the role of OGDHL on interleukin (IL)-1β-induced epileptic cell model and its molecular mechanism.</p><p><strong>Material and methods: </strong>An epileptic cell model was established using IL-1β. Quantitative real-time polymerase chain reaction was used to detect the expression levels of tumor necrosis factor-α, IL-1β, and IL-6 after different treatments. Western blot was used to detect the recovery effect of OGDHL overexpression on the IL-1-induced epilepsy model of CTX-TNA cells through the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway and collagen type IV alpha 2 (COL4A2) expression level. Meanwhile, the hypertrophy, viability, and apoptosis of CTX-TNA cells were = evaluated through terminal deoxynucleotidyl transferase dUTP nick end labeling staining, cell counting kit-8 assay, and glial fibrillary acidic protein expression. In addition, we evaluated the effect of the JAK/STAT signaling pathway agonist α7nAchR on the effects of OGDHL overexpression. The influence and possible mechanisms of OGDHL overexpression were comprehensively assessed through the above experimental methods.</p><p><strong>Results: </strong>Our results suggest that OGDHL overexpression can alleviate IL-1β-induced inflammatory response to epilepsy through the JAK/STAT signaling pathway and significant upregulation of COL4A2 expression level (<i>P</i> < 0.001). In addition, ODGHL overexpression can regulate the hypertrophy and apoptosis of CTX-TNA cells (<i>P</i> < 0.001). The effect of OGDHL overexpression on reducing epileptic inflammatory response was further demonstrated through the intervention of α7nAchR, which serves as an agonist in the JAK/STAT signaling pathway.</p><p><strong>Conclusion: </strong>ODGHL overexpression may inhibit the JAK/STAT signaling pathway by upregulating COL4A2 expression, and it inhibited the IL-1β-induced inflammation of CTX-TNA cells in an epileptic model.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"97"},"PeriodicalIF":3.1,"publicationDate":"2025-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12883102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146151192","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":"Prominent repair-like changes that mimic atypical squamous cells after radiation treatment in the lung: A report of two cases.","authors":"Benjamin L Petrykowski, Raul Virginio Rodriguez, Reginald Munden, Andrea Abbott, Mariam Alexander, Mary Richardson, Jessica A Forcucci, Maria Cecilia D Reyes","doi":"10.25259/Cytojournal_54_2025","DOIUrl":"10.25259/Cytojournal_54_2025","url":null,"abstract":"<p><p>Radiation changes in lung cytology specimens can lead to diagnostic challenges, especially during on-site evaluation. We present a case of two patients, both with a prior history of lung malignancy and subsequent radiation treatment, one with a metastatic high-grade undifferentiated pleomorphic sarcoma and the other with a small cell carcinoma. One was thought to be malignant, and one was thought to be atypical on-site. Common to both cases was a hypocellularity and a prominent repair-like/reactive change with polygonal cells or elongated fiber-like cells and dense cytoplasm mimicking atypical squamous cells in shape and cytoplasm. Knowledge of these prominent findings may help cytopathologists quickly recognize radiation changes at on-site evaluation and avoid overcalls.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"96"},"PeriodicalIF":3.1,"publicationDate":"2025-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12743453/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145851252","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}