Cytojournal最新文献

{"title":"Chloride intracellular channel 6 inhibits hepatocellular carcinoma progression by modulating immune cell balance and promoting tumor cell apoptosis.","authors":"He Zhou, Yue Xi, Xueyang Chen","doi":"10.25259/Cytojournal_183_2024","DOIUrl":"10.25259/Cytojournal_183_2024","url":null,"abstract":"<p><strong>Objective: </strong>Chloride intracellular channel 6 (CLIC6) is essential for the development of cancer, and it is widely studied for the treatment of various cancers. This study aimed to explore the potential mechanisms of CLIC6 in the treatment of hepatocellular carcinoma (HCC).</p><p><strong>Material and methods: </strong>Initially, a subcutaneous xenograft model of HCC was established. The model groups were treated with varying levels of CLIC6 recombinant protein. After 21 days, tumor and liver tissues were harvested. Tumor size and weight were measured, and hematoxylin-eosin staining was used to assess histopathological changes in the tumor tissues. Terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick-end labeling staining was employed to evaluate apoptosis in tumor tissue cells. Quantitative real-time polymerase chain reaction and Western blot were utilized to analyze cytokine messenger ribonucleic acid ( mRNA) levels in the liver or tumor tissues, and immunohistochemistry was conducted to assess cytokine expression.</p><p><strong>Results: </strong>CLIC6 significantly inhibits tumor proliferation and enhances apoptosis in tumor tissue cells. CLIC6 markedly reduces the mRNA levels of interleukin (IL)-6, IL-1β, interferon-γ, tumor necrosis factor-α, and IL-17A in liver tissue when increasing transforming growth factor-β and IL-4 mRNA levels. CLIC6 potentially modulates Th cell balance by regulating forkhead box protein P3, GATA-binding protein 3, T-box expressed in T cell, and retinoic acid receptor-related orphan receptor γt (ROR-γt) expression, thereby restraining HCC progression in mice. Moreover, CLIC6 mitigates hepatic oxidative damage via the Janus tyrosine kinase 1/signal transducer and activator of the transcription pathway, attenuates c-Jun N-terminal kinase (JNK) phosphorylation, and modulates apoptosis-related proteins, effectively hindering HCC development.</p><p><strong>Conclusion: </strong>CLIC6 demonstrates potent antitumor effects in HCC through inhibition of proliferation, promotion of apoptosis, modulation of cytokine levels, regulation of immune cell balance, and attenuation of oxidative stress pathways.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"20"},"PeriodicalIF":2.5,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711844","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":"Ankyrin repeat domain 1 is dysregulated in keloids and suppresses keloid fibroblast growth, migration, and extracellular matrix deposition.","authors":"Weiqi Wu, Yuan Si, Juan Yang, Liuyan Wen, Jingrong Li","doi":"10.25259/Cytojournal_111_2024","DOIUrl":"10.25259/Cytojournal_111_2024","url":null,"abstract":"<p><strong>Objective: </strong>The etiology and specific pathological mechanisms of keloids remain elusive. Array expression profiling has revealed dysregulation of the transcription cofactor ankyrin repeat domain 1 (ANKRD1) in keloid fibroblasts. The present study focused on examining the expression pattern of ANKRD1 in keloids and assessing its function in human keloid fibroblasts (HKFs).</p><p><strong>Material and methods: </strong>Differential mRNA expression profiles in keloid fibroblasts were investigated by analyzing data from gene expression omnibus (GEO) datasets. Immunohistochemistry assays were performed to verify the expression patterns of ANKRD1 and claudin 11 (CLDN11) in keloid tissue samples. Functional studies were conducted by transfecting HKFs with either a small interfering RNA (siRNA) targeting ANKRD1 (siANKRD1) or ANKRD1-overexpressing plasmids. The functional impact of ANKRD1 was assessed using cell proliferation, flow cytometry, and Transwell migration assays. mRNA expression was evaluated using reverse transcription polymerase chain reaction, and protein expression was determined using Western blotting.</p><p><strong>Results: </strong>Analysis of the GEO series (GSE) GSE44270 revealed eight differentially expressed mRNAs, with ANKRD1 and CLDN11 being the top two downregulated mRNAs. ANKRD1 expression was observed to be lower in keloid tissues than in normal skin tissues, whereas CLDN11 expression showed no significant difference between the two groups. ANKRD1 overexpression suppressed HKF proliferation, migration, and the expression levels of collagen I, fibronectin, matrix metallopeptidase 9, whereas the opposite effects were observed on ANKRD1 knockdown. ANKRD1 did not affect apoptotic cell levels.</p><p><strong>Conclusion: </strong>ANKRD1 is downregulated in keloids and inhibits the growth, migration, and extracellular matrix deposition of keloid fibroblasts. Thus, ANKRD1 may function as a suppressor in keloid formation.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"17"},"PeriodicalIF":2.5,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711842","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":"Ailanthone inhibits bladder cancer tumor and cell proliferation, epithelial-mesenchymal transition, and activation of the Janus kinase/signal transducer and activator of transcription 3 signaling pathway.","authors":"Jian Li, You Lv, Sheng Xue, Wenyong Li, Xiaole Zhang","doi":"10.25259/Cytojournal_166_2024","DOIUrl":"10.25259/Cytojournal_166_2024","url":null,"abstract":"<p><strong>Objective: </strong>Ailanthone (AIL), a medicinal component with antitumor properties, was distilled from <i>Ailanthus altissima</i>. The aim of this work was to probe the cancer-fighting effect of AIL on bladder cancer (BC) cells and the molecular basis of this effect.</p><p><strong>Material and methods: </strong>We developed a subcutaneous BC mouse model and then administered AIL treatment. The effects of AIL on tumor tissue integrity and apoptosis were analyzed using hematoxylin and eosin (H&E) staining and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining methods. Furthermore, we investigated the effect of AIL on the Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) pathway and associated proteins through quantitative reverse transcription polymerase chain reaction and Western blot analysis. Various concentrations of AIL were applied to BC cells, and its effects on cell survival, motility, and apoptosis were detected through cell counting kit-8 assay, Transwell assay, and flow cytometry. In addition, we examined the influence of AIL on apoptosis-related proteins and epithelialmesenchymal transition (EMT)-related proteins in BC cells through Western blot analysis.</p><p><strong>Results: </strong>AIL significantly suppressed the growth and migration of 5637 and T24 cells while promoting apoptosis (<i>P</i> < 0.05, <i>P</i> < 0.01, and <i>P</i> < 0.001). In addition, AIL increased the levels of cell death-associated proteins (<i>P</i> < 0.05, <i>P</i> < 0.01, and <i>P</i> < 0.001) and reversed EMT in BC cells. <i>In vivo</i>, AIL treatment reduced tumor growth and lowered the transcriptional levels of interleukin (IL)-6, IL-10, and IL-23, which are activation factors in the JAK/STAT3 signaling pathway. It also decreased the phosphorylation levels of JAK1, JAK2, and STAT3 in tumor tissues (<i>P</i> < 0.05 and <i>P</i> < 0.01).</p><p><strong>Conclusion: </strong>AIL exhibits multiple anticancer effects, such as BC cell growth suppression, apoptosis enhancement, reversion of EMT reversion, tumor growth, and JAK/STAT3 pathway activation suppression.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"16"},"PeriodicalIF":2.5,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711841","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":"Suppression of regulatory factor X 7 alleviates airway remodeling and inflammation in childhood asthma.","authors":"Yahui Wu, Tiansheng Dai, Jingwen Qin, Jian Guo, Jitao Fan, Jun Mei, Xiaoli Li, Fang Liu","doi":"10.25259/Cytojournal_138_2024","DOIUrl":"10.25259/Cytojournal_138_2024","url":null,"abstract":"<p><strong>Objective: </strong>Childhood asthma is a chronic heterogeneous syndrome composed of distinct disease entities or phenotypes. This study was conducted to characterize regulatory factor X 7 (RFX7) in childhood asthma.</p><p><strong>Material and methods: </strong>Two available transcriptome datasets (GSE65204 and GSE27011) were used to analyze regulatory factor X (RFX) family members in childhood asthma. Random forest, logistic regression, and linear support vector machine (SVM) analyses were performed to construct an RFX-based classification model. Airway smooth muscle cells (ASMCs) were induced through platelet-derived growth factor-BB (PDGF-BB) for an asthma <i>in vitro</i> model. RFX7 expression was measured through immunoblotting. RFX7 was knocked out by transfection of RFX7 small-interfering RNAs, and then airway remodeling and inflammation were assayed.</p><p><strong>Results: </strong>Among RFX family members, RFX3, RFX7, and RFX-associated protein displayed differential expression in childhood asthma versus healthy controls. Thus, SVM, logistic regression, and random forest-based machine learning models were built. The random forest model presented the best diagnostic efficacy (area under the curve [AUC] = 1 and 0.67 in discovery and verification sets). RFX7 was found to be effective in diagnosing childhood asthma (AUC = 0.724 and 0.775 in discovery and verification sets). In addition, RFX7 was overexpressed in PDGF-BB-stimulated ASMCs (^✶ ^✶ <i>P</i> < 0.01). Silencing RFX7 remarkably attenuated the proliferative and migrative capacities of ASMCs with PDGF-BB stimulation (^✶ ^✶ <i>P</i> < 0.01). In addition, RFX7 was positively related to neutrophil infiltration in childhood asthma, and its knockdown downregulated the levels of pro-inflammatory cytokines in PDGF-BB-stimulated ASMCs (^✶ ^✶ <i>P</i> < 0.01).</p><p><strong>Conclusion: </strong>The findings of this study indicate that RFX7 is a novel molecule that is correlated with airway remodeling and inflammation in childhood asthma, providing insights into the mechanism underlying this disease and its potential clinical importance.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"15"},"PeriodicalIF":2.5,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710694","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":"Pulmonary extranodal NK/T-cell lymphoma: A clinicopathological analysis of five patients.","authors":"Qing Li, Yunxiao Zhang, Hui Sun, Xue Wang, Di Wu","doi":"10.25259/Cytojournal_177_2024","DOIUrl":"10.25259/Cytojournal_177_2024","url":null,"abstract":"<p><strong>Objective: </strong>Our goal was to investigate the clinicopathological features of extranodal natural killer (NK)/T-cell lymphoma (ENKTL).</p><p><strong>Material and methods: </strong>A total of five newly identified (5 biopsy samples) untreated cases of pulmonary ENKTL were collected between January 2016 and January 2024. The clinical characteristic pathology features on hematoxylin-eosin-staining sections, immunohistochemistry stating, treatment responses, and prognoses were retrospectively analyzed.</p><p><strong>Results: </strong>Among the five patients, four were male and one was female, and their ages varied between 48 and 63 years. All five patients were initially diagnosed with stage IV disease. Histological examination revealed either scattered or localized clusters of highly pleomorphic tumor lymphocytes associated with necrosis and a significant presence of inflammatory cells. Most tumor cells expressed cluster of differentiation (CD)3, T-cell intracellular antigen-1, and granzyme B, whereas there was an absence of CD20, CD79a, or CD5 expression. The expression of CD56 was detected in four out of the five patients. Only two patients were tested for programmed cell death ligand 1, with one out of two patients exhibiting positivity (Tumor Proportion Score (TPS) 80%). The Ki-67 proliferation index varied from 40% to 90%. All patients tested positive for Epstein- Barr virus-encoded ribonucleic acid (RNA) (EBER) through fluorescence <i>in situ</i> hybridization (FISH). Five of the patients died during follow-up. Four of these patients underwent standard chemotherapy, with survival durations ranging from 3 to 24 months. One patient received only supportive treatment, resulting in a survival time of 1 month.</p><p><strong>Conclusion: </strong>Pulmonary ENKTL is an uncommon, aggressive cancer associated with a bleak prognosis. The likelihood of misdiagnosis is high because of the presence of necrotic lesions and various cell types. Accurate diagnosis relies heavily on immunohistochemistry and EBER FISH. The aim of our study was to facilitate improved diagnosis of pulmonary ENKTL and to identify treatment strategies for affected individuals.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"14"},"PeriodicalIF":2.5,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932977/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710462","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 physiological and pathogenic roles of yes-associated protein/transcriptional co-activator with PDZ-binding motif in bone or skeletal motor system-related cells.","authors":"Yao Huang, Xueqian Ouyang, Jinghua Tan, Zhenyu Meng, Xiuwen Ma, Yiguo Yan","doi":"10.25259/Cytojournal_237_2024","DOIUrl":"10.25259/Cytojournal_237_2024","url":null,"abstract":"<p><p>Yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) are the primary downstream effectors of the Hippo signaling pathway. This pathway plays a crucial role in regulating organ size, maintaining tissue homeostasis, and controlling cellular processes such as fate determination and tissue development. This review provides an overview of the current understanding of how the transcriptional regulators YAP and TAZ contribute to the physiological and pathological processes in tissues and cells associated with the skeletal motor system. The underlying molecular mechanisms and mechanical transduction were reviewed.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"13"},"PeriodicalIF":2.5,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143710640","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":"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":"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}