Cytojournal最新文献

{"title":"Digital transformation and artificial intelligence integration in cytopathology: From standardization to emerging semi-quantitative paradigms.","authors":"Yasemin Akca","doi":"10.25259/Cytojournal_186_2025","DOIUrl":"10.25259/Cytojournal_186_2025","url":null,"abstract":"","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"29"},"PeriodicalIF":2.2,"publicationDate":"2026-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13255159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148254040","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":"SOX2 promotes the progression of hepatocellular carcinoma by targeting FOXJ3 and activating the PI3K/AKT pathway to regulate autophagy and mitophagy.","authors":"Zhigang Zhang, Wanhua Ren","doi":"10.25259/Cytojournal_164_2025","DOIUrl":"10.25259/Cytojournal_164_2025","url":null,"abstract":"<p><strong>Objectives: </strong>Sex-determining region Y-box transcription factor 2 ( SOX2) has been implicated in tumorigenesis across various cancers. This study sought to characterize the expression pattern of SOX2 in hepatocellular carcinoma (HCC) and elucidate its potential mechanism in promoting HCC progression by targeting Forkhead box J3 (FOXJ3) and regulating the phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway, autophagy, and mitophagy.</p><p><strong>Material and methods: </strong>SOX2 expression was examined in normal liver epithelial (THLE2) and HCC (Huh7) cells. It was modulated by shRNA-mediated knockdown and plasmid-based overexpression. 5-Ethynyl-2'-deoxyuridine (EdU) fluorescence staining assay, Transwell assays, and flow cytometry were performed to evaluate cell viability and motility. Autophagy and mitophagy were assessed by Western blotting and transmission electron microscopy, and mitochondria-lysosome co-localization was visualized by immunofluorescence staining. The roles of SOX2 and FOXJ3 in the PI3K/AKT signaling pathway were investigated.</p><p><strong>Results: </strong>SOX2 was markedly upregulated in HCC cells (<i>P</i> <0.001). SOX2 overexpression enhanced the viability and motility of Huh7 cells and inhibited apoptosis, whereas SOX2 knockdown elicited opposite effects (<i>P</i> <0.001). Mechanistically, SOX2 upregulated autophagy-related proteins Microtubule-Associated Protein 1 Light Chain 3 ( LC3)-II/LC3-I and p62, promoted autophagosome formation, increased PTEN-induced kinase 1 ( PINK1) and p-COX4 levels, and facilitated mitochondria-lysosome co-localization (<i>P</i> <0.05). Co-overexpression of FOXJ3 reversed the promotive effects of SOX2 on cell proliferation, migration, autophagy, and mitophagy and attenuated PI3K/AKT pathway activation (<i>P</i> <0.001).</p><p><strong>Conclusion: </strong>SOX2 promotes HCC progression by negatively regulating FOXJ3, thereby activating the PI3K/AKT signaling pathway and inducing autophagy and mitophagy. The potential SOX2-FOXJ3-PI3K/AKT axis may serve as a novel regulatory pathway underlying HCC development and represents a potential target for therapeutic intervention.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"28"},"PeriodicalIF":2.2,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13255168/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148254059","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 inappropriate thyroid-stimulating hormone secretion syndrome after thalidomide treatment.","authors":"Yanju Zhu, Juan Chen","doi":"10.25259/Cytojournal_173_2025","DOIUrl":"10.25259/Cytojournal_173_2025","url":null,"abstract":"<p><p>Thalidomide is used for the management of several diseases, including the treatment of certain dermatological conditions. We report a case of thyroid dysfunction, characterized by a high serum thyroid-stimulating hormone (TSH) level accompanied by high free triiodothyronine (FT3) and free thyroxine (FT4), in a patient with preexisting hypothyroidism and human immunodeficiency virus (HIV) infection during thalidomide treatment. The case provides a novel pattern of thyroid dysfunction induced by thalidomide, differing from classical thyroid disease. We recommended a measurement of baseline thyroid function and TRAb before thalidomide treatment, every 2 weeks during the initial 1-3 months, and then monthly.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"27"},"PeriodicalIF":2.2,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13255163/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148254074","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":"Tumor-associated macrophage-derived chemokine ligand 5 regulates the Hypoxia-inducible factor-1α/vascular endothelial growth factor signaling pathway to promote breast cancer invasion and migration.","authors":"Yongyun Zhu, Mingxiang Zhang, Zhengzhi Zhu","doi":"10.25259/Cytojournal_6_2025","DOIUrl":"10.25259/Cytojournal_6_2025","url":null,"abstract":"<p><strong>Objective: </strong>Tumor-associated macrophages (TAMs) are important components of the breast cancer (BC) microenvironment that contributes to tumor progression by secreting cytokines. Chemokine ligand 5 (CCL5) expression is upregulated in BC, but the specific mechanism of TAM-derived CCL5 in BC microenvironment remains elucidated. This article aims to explore the role of TAM-derived CCL5 in the progression of BC.</p><p><strong>Material and methods: </strong>M2-type TAMs were induced from Tohoku Hospital Pediatrics-1 (THP-1) monocytes. CCL5 expression in TAM cells was evaluated. The biological effects of recombinant or TAM-derived CCL5 on ZR-75-30 cells were examined using proliferation, migration, invasion assays, and epithelial-mesenchymal transition (EMT) markers. CCL5 was silenced in TAMs and hypoxia-inducible factor-1α (HIF-1α) was overexpressed to explore the downstream signaling pathway.</p><p><strong>Results: </strong>CCL5 expression was significantly increased in TAMs compared with that in BC cells (<i>P</i> < 0.001). Recombinant CCL5 and TAM-conditioned medium promoted ZR-75-30 cell proliferation, migration, and invasion and EMT (<i>P</i> < 0.01), whereas CCL5 knockdown in TAMs markedly reversed these effects (<i>P</i> < 0.001). EMT-related changes, including decreased E-cadherin expression and increased Vimentin, matrix metalloproteinase (MMP)2, and MMP9 expression levels, were reversed by CCL5 silencing (<i>P</i> < 0.01). Inhibition of CCL5 significantly reduced HIF-1α and vascular endothelial growth factor (VEGF) expression levels (<i>P</i> < 0.001), and these reductions were rescued by HIF-1α overexpression (<i>P</i> < 0.01). Functional rescue experiments confirmed that HIF-1α overexpression restored cell proliferation and invasion and EMT suppressed by CCL5 knockdown. Angiogenesis was suppressed by CCL5 silencing and subsequently restored by HIF-1α overexpression (<i>P</i> < 0.001).</p><p><strong>Conclusion: </strong>TAM-derived CCL5 plays an oncogenic role in BC by regulating HIF-1α/VEGF pathway-mediated malignancy and angiogenesis.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"26"},"PeriodicalIF":2.2,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13192363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148018445","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":"Fibrinogen-like protein 1 induces the formation of an immunosuppressive microenvironment by upregulating fibronectin 1 to promote immune evasion in bladder cancer.","authors":"Keyao Hu, Lei Luo, Peng Li, Xiaofei Wang, Lijiang Sun","doi":"10.25259/Cytojournal_80_2025","DOIUrl":"10.25259/Cytojournal_80_2025","url":null,"abstract":"<p><strong>Objectives: </strong>The role of fibrinogen-like protein 1 (FGL1) in the immune microenvironment in bladder cancer has been extensively studied, but the specific regulatory pathways require further investigation.</p><p><strong>Materials and methods: </strong>The overexpression vector of FGL1 or small interfering RNA was transfected into RT4 cells, and cell growth was observed. Tumor cells with altered FGL1 expression were co-incubated with peripheral blood mononuclear cells to simulate the immune microenvironment of bladder cancer <i>in vitro</i>, and the number and function of immune cells were monitored. The potential interacting proteins of FGL1 were predicted using an online bioinformatics database. Fibronectin 1 (FN1) was selected as the follow-up research object and was overexpressed or knocked down to explore its effect on tumor cell growth and immune microenvironment. A mouse model of transplanted tumor <i>in vitro</i> was established to explore FGL1 knockdown on tumor growth and immune microenvironment <i>in vivo</i>.</p><p><strong>Results: </strong>FGL1 was abnormally overexpressed in bladder cancer and enhanced RT4 cells' migration, invasion, and proliferation. Its knockdown inhibited tumor cell growth. FGL1 decreased CD4 and CD8+T cell proportion, increased the number of Treg cells, promoted CD8+T cell apoptosis, inhibited interferon-gamma, and upregulated the secretion level of interleukin-10. Its knockdown had the opposite effect. FN1 was identified as an interacting protein of FGL1 and was positively regulated by FGL1 to promote the growth of RT4 cells. In the FGL1-induced tumor immunosuppressive microenvironment, blocking FN1 reversed the situation. <i>In vivo</i> studies showed that FGL1 silencing inhibited the growth of subcutaneously transplanted tumors in mice, which was related to the inhibition of FGL1 and FN1 expression.</p><p><strong>Conclusion: </strong>FGL1 promotes bladder cancer immune evasion by upregulating FN1. Our results provide a new reference for the immunotherapy of bladder cancer.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"25"},"PeriodicalIF":2.2,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13192362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148018361","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 and validation of a multiparameter prognostic model for extranodal natural killer/T-cell lymphoma: Integration of clinical, pathological, and molecular biomarkers.","authors":"Shishou Wu, Yifei Liu, Lei Jiang, Licai An, Yuanfeng Zhang, Yu Pan, Liling Song, Yunjun Wang, Guohua Yu","doi":"10.25259/Cytojournal_34_2025","DOIUrl":"10.25259/Cytojournal_34_2025","url":null,"abstract":"<p><strong>Objectives: </strong>The objectives of the study are to develop and validate a novel prognostic model for extranodal natural killer/T-cell lymphoma (ENKTCL) by integrating clinical and pathological parameters.</p><p><strong>Material and methods: </strong>We retrospectively analyzed 106 patients with ENKTCL (2008-2020) from the Department of Pathology of Yantai Yuhuangding Hospital and the Affiliated Hospital of Nantong University, constructing the novel international prognostic index (NIPI) model through multivariable Cox regression of immunohistochemistry (IHC) markers (age, MTP53, Ki-67, lactate dehydrogenase, hemoglobin, platelet-tolymphocyte ratio) and quantitative dot blot (QDB) tumor microenvironment features.</p><p><strong>Results: </strong>The model demonstrated significant risk stratification (<i>P</i> < 0.001) with a 3-year area under the curve of 0.72 (IHC) and 0.80 (QDB), outperforming Ann Arbor staging (<i>P</i> > 0.05) and existing international prognostic index (<i>P</i> = 0.00036)/natural killer lymphoma prognostic index (<i>P</i> = 0.00017) models. The QDB-based implementation showed superior prognostic discrimination (<i>P</i> = 0.00014), highlighting its potential for precise individualized therapy.</p><p><strong>Conclusion: </strong>NIPI provides improved risk stratification for ENKTCL, and QDB-based analysis offers enhanced precision in individualized therapy. This model addresses the unmet needs for ENKTCL prognostication and warrants further multicenter validation.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"24"},"PeriodicalIF":2.2,"publicationDate":"2026-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098387/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786352","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":"Topoisomerase II binding protein 1-interacting checkpoint and replication regulator promotes lung adenocarcinoma proliferation by regulating myelocytomatosis oncogene signaling pathway.","authors":"Yi Zhao, Yuan Feng, Mantao Guo, Linrui Li","doi":"10.25259/Cytojournal_24_2025","DOIUrl":"10.25259/Cytojournal_24_2025","url":null,"abstract":"<p><strong>Objectives: </strong>This study aims to investigate the role of topoisomerase II binding protein 1-interacting checkpoint and replication regulator (TICRR) on the proliferation of lung adenocarcinoma (LUAD) and its potential molecular mechanism as well as to provide a new strategy to improve LUAD treatment.</p><p><strong>Material and methods: </strong>The expression level of TICRR in patients with LUAD was analyzed on the basis of the Cancer Genome Atlas program database, and loss- and gain-of-function experiments were conducted to validate whether TICRR promoted the proliferation of LUAD cells. Then, pathway enrichment analysis and luciferase reporter assays were performed to dissect the potential mechanism.</p><p><strong>Results: </strong>Overexpression of TICRR in patients with LUAD was associated with poor survival (<i>P</i> < 0.001). In addition, overexpression of TICRR aggravated LUAD cell proliferation, which was ameliorated by TICRR depletion. In addition, TICRR could activate the myelocytomatosis oncogene (MYC) signaling pathway by regulating Bcl-2-associated X protein and Cyclin B1, which are the pivotal effectors of the MYC signaling pathway.</p><p><strong>Conclusion: </strong>TICRR plays a critical role in fostering the progression of LUAD by regulating the MYC signaling pathway.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"23"},"PeriodicalIF":2.2,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786763","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":"Cytology at the crossroads: Safeguarding equity in the molecular era.","authors":"Cristina Díaz Del Arco","doi":"10.25259/Cytojournal_203_2025","DOIUrl":"10.25259/Cytojournal_203_2025","url":null,"abstract":"","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"22"},"PeriodicalIF":2.2,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786308","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":"Mapping the function of EF-hand domain-containing protein 2 and determining its clinical relevance in non-small-cell lung cancer through single-cell transcriptomics.","authors":"Xueping Luo, Feng Zhang, Zhiyu Li, Chucheng Zhong, Xiaozhen Shen","doi":"10.25259/Cytojournal_29_2025","DOIUrl":"10.25259/Cytojournal_29_2025","url":null,"abstract":"<p><strong>Objective: </strong>This study aims to explore the cellular composition and transcriptional variability within the tumor microenvironment (TME) of non-small-cell lung cancer (NSCLC) using single-cell RNA sequencing (scRNAseq) and to assess the role of EF-hand domain-containing protein 2 (EFHD2) in tumor progression and its involvement in relevant signaling pathways.</p><p><strong>Material and methods: </strong>We analyzed scRNA-seq datasets to map the cellular and transcriptional landscape of NSCLC tumors. Immunohistochemistry (IHC) was employed to validate the expression of EFHD2 and assess immune cell infiltration in clinical samples. To further investigate the functional effect of EFHD2, we performed Western blot and quantitative real-time polymerase chain reaction analyses as well as cell proliferation, migration, invasion, and apoptosis assays. We also explored the janus kinase (JAK)-signal transducers and activators of transcription (STAT) signaling pathway as a potential underlying mechanism.</p><p><strong>Results: </strong>The scRNA-seq analysis revealed that epithelial cells were the predominant population within the TME, alongside endothelial cells, fibroblasts, macrophages, and a small proportion of stem cells. EFHD2 expression exhibited considerable variability, with higher levels associated with clusters enriched in transcriptionally active and immunomodulatory pathways. The IHC results demonstrated elevated EFHD2 expression and immune cell infiltration in tumor tissues compared with adjacent non-tumor tissues.</p><p><strong>Conclusion: </strong>EFHD2 expression in the NSCLC TME correlates with immune cell infiltration and may play a significant role in tumor progression and immune modulation. The JAK-STAT signaling pathway may be a potential mechanism underlying the effect of EFHD2. This work provides a new avenue for targeted therapy in NSCLC.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"21"},"PeriodicalIF":2.2,"publicationDate":"2026-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786803","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-specific protease 5 promotes breast cancer progression by stabilizing Forkhead box M1 through deubiquitination.","authors":"Xiaoyan Wang, Tingting Chen, Songsong Wu, Youyi Wu","doi":"10.25259/Cytojournal_39_2025","DOIUrl":"10.25259/Cytojournal_39_2025","url":null,"abstract":"<p><strong>Objective: </strong>Breast cancer continues to be a leading and aggressive cancer in women. Despite improvements in early treatment, challenges such as rapid tumor proliferation, metastasis, and drug resistance persist. This research examines how the deubiquitinase ubiquitin-specific protease 5 (USP5) maintains Forkhead box M1 (FOXM1) protein stability and its impact on the advancement of breast cancer.</p><p><strong>Material and methods: </strong>Data from The Cancer Genome Atlas were utilized to investigate the expression patterns and interactions of USP5 and FOXM1 in breast cancer. The breast cancer cell lines were subjected to functional testing, including invasion, migration, and proliferation. The expression and interaction of USP5 and FOXM1 were examined using quantitative real-time polymerase chain reaction, Western blot, and co-immunoprecipitation analyses. Protein stability and ubiquitination assays were performed to evaluate the effect of USP5 on FOXM1 stability.</p><p><strong>Results: </strong>USP5 stabilized the FOXM1 protein by deubiquitination. Overexpression of USP5 increased FOXM1 levels, while USP5 knockdown accelerated FOXM1 degradation. The deubiquitinating enzyme USP5 inhibited the proteasomal degradation of FOXM1, enhancing its stability. Functional assays showed that USP5 overexpression promoted breast cancer cell progression, while USP5 knockdown inhibited these malignant phenotypes. <i>In vivo</i> analysis showed that FOXM1 knockdown reduced tumor volume, and USP5 overexpression with FOXM1 knockdown increased tumor size. The findings suggest that USP5 promotes breast cancer progression by regulating FOXM1 stability.</p><p><strong>Conclusion: </strong>USP5 enhances breast cancer progression by stabilizing FOXM1 through deubiquitination.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"18"},"PeriodicalIF":2.2,"publicationDate":"2026-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098382/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786825","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}