Cytojournal最新文献

{"title":"Computer-assisted scatter plot analysis of cell and nuclear areas distinguishes urothelial carcinoma in urine cytology specimens.","authors":"Chinami Hoshino, Sayaka Kobayashi, Yoshimi Nishijima, Seiji Arai, Kazuhiro Suzuki, Masanao Saio","doi":"10.25259/Cytojournal_213_2024","DOIUrl":"10.25259/Cytojournal_213_2024","url":null,"abstract":"<p><strong>Objective: </strong>Image analysis in urine cytology typically focuses on individual cells, particularly nuclear features. This study aimed to analyze non-tumor and urothelial carcinoma cases by examining scatter plots of cell or cell cluster areas and the maximum nuclear area within them.</p><p><strong>Material and methods: </strong>The study included 192 cases: 52 negative and 140 positive. Whole slide images were generated using a virtual slide scanner, and image analysis was conducted with cytological analysis software. Scatter plots were created for cells/cell cluster areas and the largest connected nuclear areas (scatter plot for cells/cell cluster), as well as for nuclear area and perimeter (scatter plot for nucleus).</p><p><strong>Results: </strong>In the scatter plot for the nucleus, significant differences were noted between cytology-negative and cytology-positive groups (<i>P</i> = 0.0134). However, when divided into cytology-negative, non-invasive, and invasive groups, a significant difference was only found between negative and non-invasive groups (<i>P</i> = 0.0281), not between negative and invasive groups (<i>P</i> = 0.1266). In the scatter plot for cell/cell cluster, plotting cell cluster area (X-axis) and maximum nuclear area (Y-axis) revealed three distribution patterns: horizontal (X-axis), vertical (Y-axis), and diagonal. Cytology-negative cases mainly showed horizontal patterns, while cytology-positive cases exhibited vertical patterns. In the non-tumor group, horizontal patterns were dominant, while vertical patterns were common in non-invasive and invasive tumor groups. The pTa low-grade group mainly showed diagonal patterns, whereas the pTa high-grade, pTis, and pTis + pTa groups predominantly showed vertical patterns. The percentage of cell/cell clusters in tumor-rich areas (along with Y-axis) was significantly higher in non-invasive and invasive tumors compared to non-tumor cases (<i>P</i> < 0.0001), although lower in invasive tumors compared to non-invasive ones (<i>P</i> = 0.0299). In addition, neutrophil-rich images were significantly more common in stromal and muscle invasion groups than in non-invasion groups.</p><p><strong>Conclusion: </strong>In urine cytology, cellular overlap and cluster density were key factors for distinguishing malignant from benign cells. This image analysis algorithm was useful in identifying malignant clusters with large, connected nuclear regions. The algorithm could potentially detect both invasive and early-stage tumors, highlighting the need for further development of such tools for routine diagnosis.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"12"},"PeriodicalIF":2.5,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711845","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 peptidase 14 promotes neuron injury by stabilizing acyl-CoA synthetase long-chain family member 4 through deubiquitination.","authors":"Xiaoting Hao, Ying Liu","doi":"10.25259/Cytojournal_52_2024","DOIUrl":"10.25259/Cytojournal_52_2024","url":null,"abstract":"<p><strong>Objective: </strong>Ubiquitin-specific peptidase 14 (USP14) may be a target for stroke treatment. Our study aims to explore the molecular mechanism of USP14 in the stroke process.</p><p><strong>Material and methods: </strong>A stroke cell model was constructed using oxygen-glucose deprivation/reoxygenation (OGD/R)-induced SK-N-SH cells, and cell growth was assessed using cell counting kit 8 assay, EdU assay, and flow cytometry. Proinflammatory cytokine levels were tested through an enzyme-linked immunosorbent assay. The levels of USP14 and acyl-CoA synthetase long-chain family member 4 (ACSL4) were determined through Western blot and quantitative real-time polymerase chain reaction, whereas the interaction of USP14 and ACS14 was evaluated by co-immunoprecipitation assay.</p><p><strong>Results: </strong>OGD/R-induced SK-N-SH cell injury by enhancing ferroptosis and the knockdown of USP14 inhibited OGD/R-induced cell inflammation, apoptosis, and ferroptosis. Moreover, USP14 enhanced ACSL4 protein expression through deubiquitination. ACSL4 silencing mitigated neuron injury, and ACSL4 upregulation abolished USP14 knockdown-mediated inhibition of neuron injury.</p><p><strong>Conclusion: </strong>USP14 can enhance neuron injury through stabilizing ACSL4 protein expression.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"11"},"PeriodicalIF":2.5,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932950/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710989","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 phosphatase and tensin homolog deleted on chromosome ten inhibits lung cancer cell proliferation by suppressing the oncogene polo-like kinase 1 and inducing autophagy.","authors":"Weizhou Jiang, Pei Wang, Limin Huang","doi":"10.25259/Cytojournal_146_2024","DOIUrl":"10.25259/Cytojournal_146_2024","url":null,"abstract":"<p><strong>Objective: </strong>Lung cancer is one of the main causes of cancer-related mortality globally, and it poses considerable therapeutic challenges. Polo-like kinase 1 (PLK1) exhibits upregulation in lung cancer, and PLK1 silencing promotes autophagy in lung cancer cells, which inhibits tumor progression. The phosphatase and tensin homolog deleted on chromosome ten (PTEN) acts as a tumor suppressor gene. This study aimed to investigate whether PTEN regulates autophagy and inhibits lung cancer-cell proliferation by suppressing PLK1.</p><p><strong>Material and methods: </strong>In this study, we evaluated cell proliferation by silencing or overexpressing PLK1 and PTEN in A549 cells through 5-ethynyl-2'-deoxyuridine labeling and cloning experiments. The autophagy levels were detected through transmission electron microscopy, real-time quantitative polymerase chain reaction, and Western blot. Finally, the results of <i>in vitro</i> experiment were further verified using an <i>in vivo</i> xenograft tumor animal model.</p><p><strong>Results: </strong>The upregulation of PTEN suppressed PLK1 expression in lung cancer cells and reduced their proliferation rate. In addition, the overexpression of PTEN has been associated with the growth of lung cancer tumors. In parallel, the levels of autophagy of lung cancer cells rose in response to PTEN upregulation <i>in vivo</i> and <i>in vitro</i>.</p><p><strong>Conclusion: </strong>This study revealed that PTEN promotes the autophagy of lung cancer cells and inhibits cell proliferation and tumor growth by suppressing PLK1 expression. This finding provides a new strategy for lung cancer treatment by utilizing the autophagy-regulating effect of PTEN to inhibit lung cancer growth by targeting PLK1.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"10"},"PeriodicalIF":2.5,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434129","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 fatty acid-binding protein 4 improved sepsis-induced myocardial dysfunction through anti-apoptotic and antioxidant effects by mammalian target of rapamycin signaling pathway.","authors":"Zhilei Qiu, Kexing Zhou, Qinyao Qi, Wei Chen","doi":"10.25259/Cytojournal_157_2024","DOIUrl":"10.25259/Cytojournal_157_2024","url":null,"abstract":"<p><strong>Objective: </strong>One of the main complications of sepsis that is linked to poor clinical outcomes and high mortality is sepsis-induced myocardial dysfunction (SIMD). Fatty acid-binding protein 4 (FABP4) is a protein that is expressed in macrophages and adipose tissue and is involved in inflammation and apoptosis in various pathological processes. The purpose of this study was to investigate the role of FABP4 in SIMD.</p><p><strong>Material and methods: </strong>The H9c2 cell model of myocardial dysfunction induced by septicemia was established by lipopolysaccharide (LPS). Measurements of cell viability, apoptosis, reactive oxygen species levels, mitochondrial activity, and proinflammatory factor expression were used to assess FABP4's involvement in SIMD. In addition, the expression level of key proteins in the mammalian target of rapamycin (mTOR) signaling pathway was analyzed using Western blot. Finally, the combination of AZD-8055 further demonstrated the possibility of mTOR as a therapeutic target for SIMD.</p><p><strong>Results: </strong>Silencing FABP4 expression drastically increased H9c2 cell viability and mitochondrial function. In addition, by upregulating B-cell lymphoma-2 (Bcl-2) and downregulating Bcl-2 associated X protein, FABP4 silencing improved LPS-induced anti-apoptosis of H9c2 cells. Finally, silencing FABP4 alleviated SIMD through the mTOR signaling pathway. However, the therapeutic effect was inhibited when FABP4 silencing was combined with the mTOR inhibitor AZD-8055.</p><p><strong>Conclusion: </strong>Silencing FABP4 alleviates LPS-induced inflammatory response and apoptosis in H9c2 cells and enhances mitochondrial function through the mTOR signaling pathway.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"8"},"PeriodicalIF":2.5,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434110","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":"Jumonji domain-containing protein 6 promotes gastric cancer progression: Modulating immune evasion through autophagy and oxidative stress pathways.","authors":"Xinyue Zhang, Di Na","doi":"10.25259/Cytojournal_230_2024","DOIUrl":"10.25259/Cytojournal_230_2024","url":null,"abstract":"<p><strong>Objective: </strong>Immune response is crucial in the development of gastric cancer (GC), and Jumonji domain-containing protein 6 (JMJD6) plays an important role in mediating GC cell behavior. This study aims to elucidate the mechanisms through which JMJD6 affects autophagy and immune evasion in GC cells.</p><p><strong>Material and methods: </strong>Immunocytochemistry was employed to assess JMJD6 and programmed death-ligand 1 (PD-L1) levels in gastric cancer cell line (MKN-45) and gastric epithelial cell line cells. MKN-45 cells with JMJD6 knockdown and overexpression were generated. The effect of JMJD6 on MKN-45 cells was evaluated using cell counting kit-8 assay, cellular fluorescence staining, and Transwell assays. Western blot analysis and immunofluorescence techniques were employed to investigate the regulation of autophagy by JMJD6. Reactive oxygen species (ROS) levels were evaluated by applying ROS fluorescence staining. Meanwhile, the protein and gene expression levels of molecules related to antioxidant stress responses were assessed through immunofluorescence assays and quantitative real-time polymerase chain reactions, respectively.</p><p><strong>Results: </strong>The expression levels of JMJD6 and PD-L1 were elevated in GC cells (<i>P</i> < 0.001). JMJD6 overexpression enhanced MKN-45 cell migration, invasion, and colony formation <i>in vitro</i> (<i>P</i> < 0.001). In MKN-45 cells, the epithelial-mesenchymal transition was promoted by JMJD6 upregulation but was notably inhibited by JMJD6 knockdown (<i>P</i> < 0.001). JMJD6 overexpression increased the expression levels of Sequestosome 1, Microtubule-associated protein 1A/1B-light chain 3 (LC3)II/LC3I, and PD-L1 in MKN-45 cells, and autophagy activation further elevated PD-L1 levels (<i>P</i> < 0.001). In addition, JMJD6 overexpression reduced ROS production and increased the expression of molecules related to antioxidant stress response, with the reverse effects observed on JMJD6 knockdown (<i>P</i> < 0.001).</p><p><strong>Conclusion: </strong>JMJD6 notably facilitates GC progression and immune evasion by modulating autophagy and oxidative stress pathways.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"6"},"PeriodicalIF":2.5,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434078","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":"Hypoxia-induced S-phase kinase-interacting protein 2 knockdown repressed the progression of melanoma through extracellular signal-regulated kinase 1/2 pathway.","authors":"Yong Hu","doi":"10.25259/Cytojournal_117_2024","DOIUrl":"10.25259/Cytojournal_117_2024","url":null,"abstract":"<p><strong>Objective: </strong>Hypoxia intensely drives the development of malignant tumors, including skin cutaneous melanoma (SKCM). S-phase kinase-interacting protein 2 (SKP2) is known to participate in the progression of human tumors. The purpose of this study is to explore whether SKP2 acts as a hypoxic response gene during SKCM progression.</p><p><strong>Material and methods: </strong>SKP2 expression in SKCM tissues was analyzed using The Cancer Genome Atlas database. Anoxic experiments were conducted to simulate an anoxic environment. 5-Ethynyl-2'-deoxyuridine and colony formation assays were used to evaluate SKCM cell growth. Scratch healing and Transwell assays were applied to measure the migration and invasion abilities of SKCM cells. An immunoblotting assay was used to detect the levels of extracellular signal-regulated kinase (ERK)1/2 pathway proteins. In addition, the ERK-specific agonist LM22B-10 was added to confirm whether the ERK1/2 signaling pathway is required for SKP2-mediated SKCM progression under hypoxic conditions.</p><p><strong>Results: </strong>SKP2 was significantly upregulated in SKCM tissues and closely related to adverse outcomes in patients. Moreover, SKP2 levels increased in SKCM cells under normoxic conditions and further elevated under hypoxic conditions. SKP2 deficiency led to the reduced proliferation, migration, and invasion potential of cells under hypoxic conditions. Mechanically, SKP2 silencing blocked the ERK1/2 pathway in hypoxic cells, and the activation of the ERK1/2 pathway rescued the suppression effect of SKP2 on the hypoxia-induced progression of SKCM.</p><p><strong>Conclusion: </strong>SKP2 deficiency repressed the hypoxic-induced progression of SKCM through the ERK1/2 pathway. This novel discovery regarding the SKP2/ERK1/2 axis might provide new insights into the pathogenesis of SKCM.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"9"},"PeriodicalIF":2.5,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829309/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434076","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":"NPC intracellular cholesterol transporter 2 regulates the anti-apoptotic protein baculoviral inhibitor of apoptosis repeat containing 3 and affects drug resistance in gastric cancer.","authors":"Yanan Xu, Yanbo Wang, Wenyue Zhao, Fengli Liu","doi":"10.25259/Cytojournal_116_2024","DOIUrl":"10.25259/Cytojournal_116_2024","url":null,"abstract":"<p><strong>Objective: </strong>Cisplatin (DDP)-based chemotherapy medications are frequently used as the initial line of treatment for cancer patients, including those with stomach cancer. At present, DDP resistance is a frequent problem in chemotherapy for advanced gastric cancer (GC). This study aimed to investigate the function of NPC intracellular cholesterol transporter 2 (NPC2) in GC cells.</p><p><strong>Material and methods: </strong>The expression of NPC2 and baculoviral inhibitor of apoptosis repeat containing 3 (BIRC3) in gastric epithelial cells-1, BGC823, and BGC823/DDP cells was determined by Western blotting and quantitative real-time polymerase chain reaction, respectively. Subsequently, the proliferative capacity and viability of BGC823 cells were assessed by 3-(4,5-dimethylthiazol2-yl)-2.5-diphenyl-2-tetrazolium bromide, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling assay, and colony-formation assay. Finally, the association of NPC2 and BIRC3 with the nuclear factor kappa-B (NF-κB) pathway was determined by Western Blot.</p><p><strong>Results: </strong>In GC cells, NPC2 transcription increased, and DDP-resistant cells showed higher NPC2 expression levels than their parental cells (<i>P</i> < 0.001). In terms of mechanism, compared with parental cells, overexpressing NPC2, DDP-resistant cells showed resistance to DDP. Knocking down NPC2 increased the apoptotic response of DDP-resistant cells to DDP and blocked the cancer cells resistant to DDP exhibiting BIRC3, thereby promoting GC cell apoptosis (<i>P</i> < 0.001). Importantly, involving NF-κB signaling overturned the NPC2-mediated DDP resistance.</p><p><strong>Conclusion: </strong>NPC2 regulated BIRC3 and affected drug resistance in GC. Therefore, NPC2 and BIRC3 may be new targets for cancer patient treatment following DDP therapy and act as roadblocks to overcome chemotherapy resistance in GC.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"7"},"PeriodicalIF":2.5,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829312/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434081","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":"Relationship between transmembrane emp24 domain containing 2 expression and tumor stem cell characteristics in oral cancer.","authors":"Yanhui Wu, Shunchu Zhang, Guimei Zou","doi":"10.25259/Cytojournal_132_2024","DOIUrl":"10.25259/Cytojournal_132_2024","url":null,"abstract":"<p><strong>Objective: </strong>Transmembrane Emp24 Domain Containing 2 <b>(</b>TMED2) is a mediator of membrane protein trafficking involved in intracellular protein transport. Recent research suggests that TMED2 plays an important role in the development and metastasis of tumors; however, its exact mechanisms in oral cancer (OC) remain unclear. This study aims to elucidate the role and possible mechanisms of TMED2 in OC.</p><p><strong>Material and methods: </strong>We investigated the impact of TMED2 knockdown on the invasion, migration, and proliferation capabilities of OC cells. Furthermore, we analyzed the <i>in vitro</i> and <i>in vivo</i> interactions between TMED2 and polypeptide-N-acetylgalactosaminyltransferase 7 (GALNT7) as well as explored the regulatory function of TMED2 on GALNT7. The alterations in stem cell markers were assessed using clone formation assays, western blot, and quantitative real-time polymerase chain reaction.</p><p><strong>Results: </strong>The upregulation of TMED2 promoted the proliferation and invasion abilities of OC cells. Further analysis revealed that TMED2 enhanced the stem-like properties and tumorigenicity of OC cells by directly regulating the expression of GALNT7. <i>In vivo</i> and <i>in vitro</i> results suggested that silencing TMED2 expression reduced the incidence of OC.</p><p><strong>Conclusion: </strong>Our data imply that TMED2 stimulates GALNT7 transcription, which in turn amplifies the stem-like characteristics and carcinogenic potential of OC cells. Moreover, the block of TMED2 prevents cancers from growing and spreading <i>in vivo</i>. This finding provides a new therapeutic target for the treatment of OC and highlights the critical role of TMED2 in the condition.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"5"},"PeriodicalIF":2.5,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434107","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":"Fourth Cytopathology Monograph and Atlas Series Book Titled \"Cytopathology of Urine (& The Paris System)\" as Extension of Open Access Charter of Cytopathology Foundation Inc.","authors":"Vinod B Shidham, Shikha Bose, Zubair Baloch, Lester J Layfield","doi":"10.25259/Cytojournal_256_2024","DOIUrl":"10.25259/Cytojournal_256_2024","url":null,"abstract":"","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"4"},"PeriodicalIF":2.5,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829314/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434121","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":"E2F1-mediated <i>ESPL1</i> transcriptional activation predicts poor prognosis and promotes the proliferation of leiomyosarcoma.","authors":"Xiaojuan Yang, Guihua Miao, Qin Wang, Qin Yu, Qinsheng Hu, Gang Tan","doi":"10.25259/Cytojournal_178_2024","DOIUrl":"10.25259/Cytojournal_178_2024","url":null,"abstract":"<p><strong>Objective: </strong>Soft tissue and bone cancers, collectively known as sarcomas, constitute a diverse array of uncommon tumors originating from connective tissues. Among sarcomas, leiomyosarcoma (LMS) is one of the most frequently encountered subtypes. This study aims to investigate the expression, clinical significance, biological regulation, and dysregulation mechanisms of extra spindle pole bodies like 1 (<i>ESPL1</i>), a gene critical for cell cycle regulation in LMS.</p><p><strong>Material and methods: </strong>Bioinformatics analysis was performed using the data from The Cancer Genome Atlas-Sarcoma and Genotype-Tissue Expression datasets. Functional experiments to assess cell proliferation and the cell cycle were performed in LMS cells (SK-LMS-1) after <i>ESPL1</i> knockdown. Bioinformatics analyses were conducted to identify the potential transcriptional regulators of ESPL1. The regulatory relationship between <i>ESPL1</i> and the E2F transcription factor 1 (E2F1) was validated through the various molecular assays.</p><p><strong>Results: </strong><i>ESPL1</i> is significantly overexpressed in LMS compared with normal muscle tissue. High <i>ESPL1</i> expression is associated with a shorter progression-free interval (PFI) in sarcoma patients, particularly in the LMS subset. <i>ESPL1</i> expression might be an independent prognostic factor for poor overall survival and PFI in LMS patients. Functional studies in the LMS cell line SK-LMS-1 demonstrated that <i>ESPL1</i> knockdown slowed cell proliferation and increased G2/M cell cycle arrest, suggesting its crucial role in maintaining LMS cell viability and genomic integrity. Further bioinformatics analysis identified the E2F1 transcription factor as a key regulator of ESPL1 expression in LMS. Mechanistic investigations demonstrated that E2F1 interacts with the <i>ESPL1</i> promoter, leading to transcriptional activation.</p><p><strong>Conclusion: </strong>These findings highlight the ESPL1-E2F1 axis as a potential prognostic biomarker and therapeutic target in LMS.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"3"},"PeriodicalIF":2.5,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829311/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434045","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}