Cytojournal最新文献

{"title":"Diagnostic accuracy of the Yokohama system for reporting breast fine-needle aspiration cytology and breast imaging-reporting and data system in breast lesions.","authors":"Shakthivel V, Sana Ahuja, Sufian Zaheer, Swarna Swarna, Mukul Singh, Chintamani Chintamani","doi":"10.25259/Cytojournal_167_2025","DOIUrl":"10.25259/Cytojournal_167_2025","url":null,"abstract":"<p><strong>Objectives: </strong>The Yokohama system standardizes fine-needle aspiration cytology (FNAC) reporting for breast lesions, while the breast imaging-reporting and data system (BI-RADS) categorizes lesions based on imaging risk assessment. This study aimed to evaluate the diagnostic accuracy of FNAC using the Yokohama System in correlation with BI-RADS classifications.</p><p><strong>Material and methods: </strong>A retrospective analysis was conducted on 188 breast lesion cases that underwent FNAC and were categorized using the BI-RADS system. The breast FNAs were classified according to the Yokohama System and compared with histopathological diagnoses to calculate the risk of malignancy (ROM). The ROM for the BI-RADS categories was also determined. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were calculated for both.</p><p><strong>Results: </strong>According to the Yokohama classification, 5.9%, 52.1%, 4.8%, 8.5%, and 28.7% were classified as non-diagnostic, benign, atypical, suspicious, and malignant, respectively. The majority of cases were classified as BIRADS 3 (23.9%) and 5 (23.9%), followed by 4a (22.3%). Higher Yokohama and BI-RADS categories were more prevalent among malignant cases, with 64.9% in Yokohama category 5 and 51.9% in BI-RADS 5. Sensitivity was highest in Yokohama Scenario C (81.8%), while specificity (96.4%) and PPV (92.6%) were highest in Scenario A. When BI-RADS 4b, 4c, 5, and 6 were considered malignant, Scenario C had the highest sensitivity (87.0%) and NPV (90.4%), while Scenario B demonstrated the highest diagnostic accuracy (87.7%).</p><p><strong>Conclusion: </strong>FNAC using the Yokohama System and imaging-based BI-RADS classification both show high diagnostic accuracy for breast lesions. While their individual performance is comparable, further studies are needed to explore whether combining these modalities improves diagnostic outcomes in clinically indeterminate cases.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"20"},"PeriodicalIF":2.2,"publicationDate":"2026-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098381/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786832","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":"BDNF facilitates ectopic endometrial stromal cell growth, invasion, migration and glycolysis in endometriosis via upregulating GLUT1.","authors":"Yapeng Han, Yang Yu, Yaguang Han, Wei Guan, Jieming Li, Boyi Feng, Chang Sun, Hong Ying Kuang","doi":"10.25259/Cytojournal_169_2024","DOIUrl":"10.25259/Cytojournal_169_2024","url":null,"abstract":"<p><strong>Objective: </strong>Brain-derived neurotrophic factor (BDNF) is considered to participate in regulating the endometriosis (EM) process. However, other functions and mechanisms of BDNF in EM progression still need to be further studied.</p><p><strong>Material and methods: </strong>Ectopic/normal endometrial stromal cells (ESCs) were isolated from EM tissues/normal control endometrial tissues. BDNF mRNA expression in EM tissues and normal control endometrial tissues was analyzed through quantitative real-time polymerase chain reaction. The protein levels of BDNF and glucose transporter 1 (GLUT1) were detected by Western blot. The function of ESCs was determined through cell counting kit 8 assay, 5-ethynyl-2'-deoxyuridine assay, flow cytometry, Transwell assay, and wound healing assay. The interaction between BDNF and GLUT1 was assessed through a co-immunoprecipitation assay and immunofluorescence staining.</p><p><strong>Results: </strong>BDNF expression was elevated in EM tissues and ectopic ESCs. Functional experiments revealed that BDNF knockdown repressed ectopic ESC proliferation, invasion, migration, and glycolysis and promoted apoptosis. In terms of mechanism, BDNF interacted with GLUT1 to enhance its protein expression. In addition, the repressing effect of BDNF knockdown on ectopic ESCs' growth, invasion, migration, and glycolysis was abolished by GLUT1 overexpression.</p><p><strong>Conclusion: </strong>Our study showed that BDNF could facilitate ectopic ESC function by interacting with GLUT1, thereby providing basic information for finding an effective therapeutic target of EM.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"19"},"PeriodicalIF":2.2,"publicationDate":"2026-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098390/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786996","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":"Destaining hematoxylin and eosin stains and restaining for immunohistochemistry has diagnostic value for cytology samples.","authors":"Mohammad M Al-Attar, Tianle Zou, Salwa Khedr, Min Zhang, Karen Dresser, Andrew H Fischer","doi":"10.25259/Cytojournal_171_2025","DOIUrl":"10.25259/Cytojournal_171_2025","url":null,"abstract":"<p><strong>Objectives: </strong>The use of one antibody per slide for immunohistochemical (IHC) studies is difficult to interpret when neoplastic cells are sparse, mixed with complex mixtures of other cells, or are obscured by the IHC stain itself. To accurately assign IHC results to particular neoplastic cells, we developed and validated a technique of destaining hematoxylin and eosin (H&E) stains and restaining (DSRS) by IHC on cytology cell block sections and studied its utility.</p><p><strong>Materials and methods: </strong>We identified 9 patients with fine needle aspiration (FNA) samples performed for a variety of tumors. Specimens were collected and made into ThinPreps and cell blocks. Cell block serial H&E stains revealed a rich background of benign cells, with rare scattered atypical cells arranged singly or in small clusters. Select H&E slides were scanned, destained, and then restained with one IHC biomarker per H&E. Slide scanning and image synchronization were used in tracking neoplastic cells. IHC results were validated for the DSRS process for all antibodies without the need for modification of the IHC protocol. Diagnoses rendered on the limited FNA samples were compared with those made on core biopsies, resections, or cytologic samples with ample cell quantity.</p><p><strong>Results: </strong>DSRS of the limited FNA samples did not compromise the quality of tissues or IHC, and comparison of the limited FNA diagnosis and final diagnosis rendered on more adequate specimens revealed concordant and accurate diagnosis in 89% (8/9) of cases, in contrast to a concordance rate of 22% (2/9) before the use of DSRS while the immunostain interpretation accuracy rate is 100% (9/9).</p><p><strong>Conclusion: </strong>DSRS of cytology cell block sections allows IHC stains to be ascribed to particular cells, enabling diagnosis when material is sparse, when diagnostic cells are admixed with other cell types, and when the IHC stain itself would otherwise obscure the identity of cells. DSRS provides an inexpensive alternative to other, more advanced techniques such as multiplex IHC or immunofluorescence.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"17"},"PeriodicalIF":2.2,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786315","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":"Koilocytes in the era of molecular viral detection: Still a useful cytopathic effect of human papillomavirus?","authors":"Haissa O Brito, Leonardo Maciel, Rui Miguel Gil da Costa","doi":"10.25259/Cytojournal_168_2025","DOIUrl":"10.25259/Cytojournal_168_2025","url":null,"abstract":"","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"14"},"PeriodicalIF":2.2,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786791","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":"SA4503 plays a protective role in post-resuscitation injury by reducing apoptosis caused by mitochondrial dysfunction and endoplasmic reticulum stress through the activation of sigma-1 receptor.","authors":"Yijie Wang, Yi Li, Haiyan Zhao, Rong Liu, Jilin Yang, Ting Li, Chen He, Jiahong Qin","doi":"10.25259/Cytojournal_55_2025","DOIUrl":"10.25259/Cytojournal_55_2025","url":null,"abstract":"<p><strong>Objective: </strong>Cardiac arrest followed by resuscitation can induce brain injury, and currently, there are no effective treatments for brain damage after cardiopulmonary resuscitation (CPR), necessitating the exploration of additional therapeutic strategies and prevention approaches. This study aimed to investigate the mechanism of action by which SA4503 activates the Sigma-1 receptor (Sig-1R) to protect against ischemic brain injury in both <i>in vitro</i> and <i>in vivo</i> models. The goal of this study was to provide theoretical support for SA4503 as a potential therapeutic agent and promote clinical intervention research for post-resuscitation brain injury following CPR.</p><p><strong>Material and methods: </strong>This study explored the mechanism underlying the ability of Sig-1R activation to mitigate brain injury following cardiac arrest and resuscitation in rats through both <i>in vivo</i> and <i>in vitro</i> models. The methods used include enzyme-linked immunosorbent assay, magnetic resonance imaging, Western blot analysis, and flow cytometry.</p><p><strong>Results: </strong>The <i>in vivo</i> results demonstrated that the Sig-1R agonist SA4503 significantly attenuated neurological deficits in rats subjected to CPR. <i>In vitro</i> mechanistic investigations revealed that SA4503 potently reversed Sig-1R protein downregulation, reduced apoptosis, ameliorated mitochondrial dysfunction, and reduced endoplasmic reticulum (ER) stress in the oxygen-glucose deprivation/reperfusion (OGD/R) group.</p><p><strong>Conclusion: </strong>This study further confirms that Sig-1R activation confers protective effects against brain injury following cardiac arrest and resuscitation, as well as against OGD/R-induced injury in HT22 cells. The underlying mechanism involves the mitigation of apoptosis driven by mitochondrial dysfunction and ER stress.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"16"},"PeriodicalIF":2.2,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098388/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786837","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":"Upregulation of itchy E3 ubiquitin protein ligase contributes to endometrial cancer through promoting forkhead box P1 degradation.","authors":"Yong-Hong Zhang, Hai-Yang Yu, Chun-Fang Li, Jian-Chao Li","doi":"10.25259/Cytojournal_51_2024","DOIUrl":"10.25259/Cytojournal_51_2024","url":null,"abstract":"<p><strong>Objective: </strong>Endometrial cancer (EC) is one of the most prevalent cancers affecting the female reproductive system and originates from the uterine epithelium, posing a significant health burden to postmenopausal women. As an E3 ubiquitin ligase, itchy E3 ubiquitin protein ligase (ITCH) plays a key role in the progression of multiple kinds of solid cancers, but its function in EC remains unclear. This work aims to explore the roles of ITCH during the carcinogenesis of EC.</p><p><strong>Material and methods: </strong>The messenger RNA (mRNA) level of ITCH in 47 paired EC tissue and adjacent non-tumor controls was examined by quantitative polymerase chain reaction. The protein level of ITCH in formalin-fixed paraffin-embedded EC tissue and adjacent non-tumor controls from 47 patients with EC was detected by immunohistochemistry. Data on the RNA levels of ITCH and forkhead box P1 (FOXP1), along with prognostic information for 541 patients with EC, were obtained from the Human Protein Atlas database. A chromatin immunoprecipitation assay was employed to investigate the interaction between FOXP1 and the promoter of the KRAS proto-oncogene GTPase (KRAS).</p><p><strong>Results: </strong>Both ITCH mRNA and protein levels are upregulated in EC tissues. Patients with lower ITCH expression exhibit prolonged overall survival. In EC tissue samples, ITCH protein level negatively correlates with the FOXP1 protein level. ITCH interacts with FOXP1 in EC cells and promotes its ubiquitination and subsequent degradation. FOXP1 inhibits KRAS expression in EC cells by binding to its promoter region. ITCH overexpression suppresses the FOXP1-KRAS axis, leading to increased proliferation and reduced apoptosis of EC cells.</p><p><strong>Conclusion: </strong>ITCH functions as an oncogene in EC, promoting carcinogenesis by inducing FOXP1 degradation and upregulating KRAS expression.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"15"},"PeriodicalIF":2.2,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098380/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147786811","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":"Silencing C-X-C motif chemokine receptor inhibited autophagy of hippocampal neurons in epileptic mice by upregulating TWIK-related K⁺ Channel 1.","authors":"Hong Chen, Wenzeng Wang, Daqing Feng, Qun Chen, Tingting Guo, Qiannan Song","doi":"10.25259/Cytojournal_252_2024","DOIUrl":"10.25259/Cytojournal_252_2024","url":null,"abstract":"<p><strong>Objective: </strong>Epilepsy is a neurological disease whose onset causes a variety of sequelae, reducing the standard of living. TWIK-related K⁺ channel 1 (TREK-1) has been linked to epilepsy. C-X-C motif chemokine receptor (CXCR2) is a potential target for the treatment of epilepsy inflammation. This work aims to observe the effect of CXCR2 expression on neuron autophagy and TREK-1 expression in the hippocampus of epileptic mice.</p><p><strong>Material and methods: </strong>An animal model of epilepsy was established, and the <i>CXCR2</i> gene was silenced. The expression of TREK-1, interleukin (IL)-1b, tumor necrosis factor-a, and IL-6 in the hippocampus of mice was detected by quantitative real-time polymerase chain reaction. Autophagy-related proteins beclin-1 and microtubule-associated protein light chain 3 (LC3) were examined by Western blot. Cell proliferation and activity were analyzed using cell counting kit-8 and 5-Bromodeoxyuridine assays.</p><p><strong>Results: </strong>Compared with that in the normal group, TREK-1 expression decreased and CXCR2 expression increased significantly in the hippocampus of epileptic model mice (<i>P</i> < 0.01). Two autophagy markers, beclin-1 and LC3 II/LC3 I, showed an increased expression in the hippocampal regions of the epileptic model group (<i>P</i> < 0.01). In addition, B-cell lymphoma 2 (Bcl-2)-associated X protein levels increased and Bcl-2 levels decreased in the epileptic mice (<i>P</i> < 0.01). After CXCR2 silencing, the expression of proinflammatory factor in the hippocampus of epileptic mice significantly decreased (<i>P</i> < 0.01). <i>In vitro</i>, cell viability and proliferation increased significantly after silencing CXCR2 (<i>P</i> < 0.05). Meanwhile, the expression levels of TREK-1 and Bcl-2 significantly increased (<i>P</i> < 0.001) and the levels of autophagy markers decreased <i>in vivo</i> and <i>in vitro</i> (<i>P</i> < 0.01). <i>In vivo</i>, CXCR2 expression did not change significantly after silencing TREK-1. After silencing TREK-1 and overexpressing CXCR2, the proliferation ability of HT22 cells decreased significantly (<i>P</i> < 0.001).</p><p><strong>Conclusion: </strong>Epileptic mice's hippocampal neuronal damage can be ameliorated by CXCR2 suppression. One possible explanation is that epileptic mice's hippocampus tissues express more TREK-1, which prevents excessive neuronal autophagy and lowers apoptosis.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"13"},"PeriodicalIF":2.2,"publicationDate":"2026-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12997642/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147487722","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":"Zinc finger TRAF-type containing 1 can promote the progression and metastasis of lung adenocarcinoma.","authors":"Yang Yu, Qian Zhao, Liang Song","doi":"10.25259/Cytojournal_49_2025","DOIUrl":"10.25259/Cytojournal_49_2025","url":null,"abstract":"<p><strong>Objective: </strong>Lung adenocarcinoma is a type of lung cancer that falls under the category of non-small cell carcinoma. Given its high incidence, it has attracted considerable attention. Zinc finger TRAF-type containing 1 (ZFTRAF1) was found in a two-hybrid yeast screening with muine galectin-3. However, the link between ZFTRAF1 and lung adenocarcinoma was unclear. This study aimed to explore the influencing mechanism of ZFTRAF1 on lung adenocarcinoma.</p><p><strong>Material and methods: </strong>In this study, by silencing or overexpressing ZFTRAF1, we investigated the migration and invasion ability of A549 and HCC827 cells. In addition, the polarization effect of ZFTRAF1 on macrophages was evaluated through flow cytometry and quantitative real-time polymerase chain reaction. Finally, tumor growth and development were evaluated through histological analysis <i>in vivo</i> and Western Blot analysis <i>in vitro</i>.</p><p><strong>Results: </strong>ZFTRAF1 was down-regulated in normal lung cells. Silencing of ZFTRAF1 inhibited migration, invasion of A549 and HCC827 cells, and the formation of tumors. Reduction of the expression of ZFTRAF1 inhibited the epithelial-mesenchymal transition, suppressed the phosphoinositide 3-kinase-protein kinase B pathway, and enhanced the polarization of M1 macrophages. In addition, the overexpression of ZFTRAF1 showed an opposite trend compared with its silencing in A549 and HCC827 cells.</p><p><strong>Conclusion: </strong>ZFTRAF1 promotes lung cancer development. Regulating the expression level of ZFTRAF1 to interfere with the growth and migration of lung adenocarcinoma may be a new strategy for the treatment of lung adenocarcinoma. In addition, the theoretical foundation for ZFTRAF1's therapeutic use is provided in this work.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"12"},"PeriodicalIF":2.2,"publicationDate":"2026-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12997640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147488099","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":"Integrin β1 in osteoblast differentiation and migration during acute bone loss after fracture: Regulation of extracellular signal-regulated kinase 1/2 signaling pathway.","authors":"Jingjie Luan, Jing Li, Jianhang Wang","doi":"10.25259/Cytojournal_36_2025","DOIUrl":"10.25259/Cytojournal_36_2025","url":null,"abstract":"<p><strong>Objective: </strong>Integrin β1 (ITGB1) reportedly participates in osteoblast differentiation, mineralization, and migration. Nevertheless, its role and underlying mechanism in osteoblast differentiation and migration during acute bone loss after fracture are not yet clear. This research was designed to measure the role of ITGB1 in osteoblast differentiation and migration and the underlying mechanism.</p><p><strong>Material and methods: </strong>ITGB1 expression was assessed in MC3T3-E1 cells at different incubation times (0, 4, 7, 14, 21, and 28 days) through quantitative real-time polymerase chain reaction. Alkaline phosphatase (ALP) activity determination, ALP staining, and Alizarin red staining were performed to evaluate the differentiation degree of osteoblasts. Western blot was performed to detect the expression of markers related to osteoblast differentiation. Osteoblast migration ability was determined by wound healing and transwell assays. The molecular mechanism by which ITGB1 modulated the differentiation and migration of osteoblasts was examined by Western blot.</p><p><strong>Results: </strong>ITGB1 expression increased significantly after 14, 21, and 28 days of osteoblast differentiation. ITGB1 increases enhanced osteoblast differentiation and migration; conversely, reduced ITGB1 inhibits osteoblast differentiation and migration. Mechanically, ITGB1 facilitated the activation of extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway, and the suppression of the ERK ERK1/2 pathway attenuated the effects of ITGB1 on osteoblast differentiation and migration.</p><p><strong>Conclusion: </strong>ITGB1 plays an important role in osteoblast differentiation and migration by activating the ERK1/2 signaling pathway, which may provide novel insights into bone injury treatment.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"11"},"PeriodicalIF":2.2,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12997641/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147487796","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 effect of Wilms tumor 1-associated protein on ferroptosis and immune escape in non-small-cell lung cancer by mediating N6-methyladenosine modification of Twist1.","authors":"Xianghui Yang, Jiazhi Li, Yueyong Li, Min Li, Luogen Peng, Li Zhao, Lijuan Zou","doi":"10.25259/Cytojournal_114_2025","DOIUrl":"10.25259/Cytojournal_114_2025","url":null,"abstract":"<p><strong>Objective: </strong>Non-small-cell lung cancer (NSCLC) is one of the most frequently occurring and aggressive cancers globally, but its complex molecular mechanisms remain only partially understood. This study investigated the effects of Wilms tumor 1-associated protein (WTAP) on NSCLC cell ferroptosis and immune escape through N6-methyladenosine (m6A) modification of twist family BHLH transcription factor 1 (Twist1).</p><p><strong>Material and methods: </strong>Western blot and reverse transcription-quantitative polymerase chain reaction were used to assess Twist1 expression in NSCLC cell lines and its circular structure. Small interfering RNAs targeting Twist1 and WTAP were transfected into H2170 cells, and their effects on cell viability, apoptosis, ferroptosis markers (reactive oxygen species [ROS], malondialdehyde [MDA], and Fe²⁺), and immune escape were evaluated using cell counting kit-8, flow cytometry, terminal deoxynucleotidyl transferase dUTP Nick-End labeling, ROS staining, and enzyme-linked immunosorbent assay. Co-culture with CD8⁺ T cells was employed to assess cytotoxicity and exhaustion marker expression (Lymphocyte activation gene-3, Programmed cell death protein 1, and T-cell immunoreceptor with Ig and ITIM domains). Magna methylated RNA immunoprecipitation, photo-activatable ribonucleoside-enhanced cross-linking and immunoprecipitation, and treatment with the methylation inhibitor 3-Deazaneplanocin A (3-DAA) confirmed the m6A modification of Twist1 and WTAP's regulatory role.</p><p><strong>Results: </strong>Twist1 was dramatically elevated in the NSCLC cell lines (<i>P</i> < 0.05). Knockdown of Twist1 inhibited NSCLC cell viability; promoted apoptosis; increased ROS, MDA, and Fe²⁺ levels; enhanced the cytotoxicity of CD8⁺ T cells; and reduced the expression of exhaustion markers (<i>P</i> < 0.05). These effects were partially reversed by the ferroptosis inhibitor Fer-1. WTAP expression increased in the NSCLC cells, and its knockdown markedly reduced the m6A modification and expression of Twist1 (<i>P</i> < 0.05). Furthermore, overexpression of Twist1 partially reversed the inhibitory effects of WTAP knockdown on NSCLC cell proliferation, ferroptosis, and immune escape (<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>Twist1 is highly expressed in NSCLC. It promotes NSCLC progression by enhancing ferroptosis and immune escape. WTAP-mediated m6A methylation plays a critical role in regulating Twist1 expression. The WTAP/Twist1 axis may serve as a potential therapeutic target for NSCLC.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"23 ","pages":"10"},"PeriodicalIF":2.2,"publicationDate":"2026-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12997639/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147487708","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}