Cytojournal最新文献

{"title":"Lysine acetyltransferase 5 contributes to diabetic retinopathy by modulating autophagy through epigenetically regulating autophagy-related gene 7.","authors":"Qi Gao, Yanjun Lai, Shuai He, Yanhua Wang, Guochao Zhang, Xinyu Zhu, Shifang Zhuang","doi":"10.25259/Cytojournal_187_2024","DOIUrl":"10.25259/Cytojournal_187_2024","url":null,"abstract":"<p><strong>Objective: </strong>Diabetic retinopathy (DR) is a prevalent and serious complication among individuals with diabetes, significantly compromising their visual acuity and overall quality of life. Lysine acetyltransferase 5 (KAT5), an essential catalytic subunit of the nucleosome acetyltransferase of the H4 complex, is implicated in the development of various diseases, including neurological disorders, breast cancer, and lung cancer. However, the function of KAT5 in DR remains poorly understood. This study aims to investigate the influence of KAT5 on autophagy (Atg) during DR.</p><p><strong>Material and methods: </strong>Experiments were conducted using streptozotocin (STZ)-treated rats to induce diabetes and observe changes in KAT5 expression and its effect on Atg. Retinal tissues and RF/6A cells were utilized to analyze the expression levels of various proteins and their involvement in Atg and apoptosis. KAT5 depletion and Atg7 knockdown were performed to further understand their roles in the process.</p><p><strong>Results: </strong>The eyeballs of STZ-treated rats showed increased expression of KAT5. Depletion of KAT5 attenuated STZ-induced DR injury in rats. The retinal tissues of STZ-treated rats exhibited reduced expression of B-cell lymphoma-2 (Bcl-2) and increased levels of BCL-2-associated X protein and cleaved caspase 3, which could be reversed by KAT5 depletion. STZ treatment induced expression of Beclin-1 and microtubule-associated protein 1 light chain 3B in retinal tissues, and KAT5 knockdown blocked this effect. In monkey retinal choroidal endothelial ( RF/6A) cells, high glucose (HG) treatment decreased 5-ethynyl-2'-deoxyuridine-positivecells and increased terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive cells, which were reversed by KAT5 depletion. KAT5 depletion also attenuated HG-induced apoptosis and Atg in RF/6A cells. Mechanistically, KAT5 depletion reduced histone H3 lysine 27 acetylation and ribonucleic acid ( RNA) polymerase II enrichment on the Atg7 promoter, leading to a decrease in the messenger RNA ( mRNA) and protein expression of Atg7. Atg7 knockdown suppressed Atg in RF/6A cells under HG conditions and reversed the effect of KAT5 depletion on cell apoptosis and Atg.</p><p><strong>Conclusion: </strong>The findings suggest that KAT5 contributes to DR by modulating Atg through epigenetic regulation of Atg7. KAT5 emerges as a valuable target for DR treatment, providing a fresh perspective on the disease's pathogenesis and laying the foundation for the development of potential therapeutic strategies.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"22"},"PeriodicalIF":2.5,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711850","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":"Prominin 2 knockdown inhibits the growth, migration, and invasion of non-small cell lung cancer cells by repressing phosphatidylinositol 3 kinase/protein kinase B pathway.","authors":"Biao He, Ze Chen, Liang Zhong, Xiaoyong Pang","doi":"10.25259/Cytojournal_118_2024","DOIUrl":"10.25259/Cytojournal_118_2024","url":null,"abstract":"<p><strong>Objective: </strong>The prognosis of patients with non-small cell lung cancer (NSCLC) is poor, and this malignancy represents a grievous danger to human health due to its high rates of recurrence and metastasis. Previous studies have linked prominin 2 (PROM2) to certain cancers. However, the impact of PROM2 on the biological behavior of NSCLC cells and regulatory pathways has rarely been explored. Therefore, the study aims to elucidate the roles and regulatory mechanisms of PROM2 in the cell function of NSCLC by interfering with PROM2.</p><p><strong>Material and methods: </strong>PROM2 messenger ribonucleic acid (mRNA) and protein expression levels in NSCLC cells were analyzed by applying quantitative real-time polymerase chain reaction and Western blot analysis. Phosphatidylinositol 3 kinase (PI3K), protein kinase B (AKT), and phosphorylated-AKT (p-AKT) protein levels were evaluated through Western blot analysis. Cell counting kit-8 and Transwell assays were used to evaluate NSCLC cell proliferation, migration, and invasion.</p><p><strong>Results: </strong>PROM2 mRNA protein levels drastically increased in NSCLC tissues and cells. High PROM2 mRNA level was related to the poor prognosis of patients with NSCLC. PROM2 silencing remarkably repressed NCI-H520 and A549 cell proliferation, migration, and invasion. Furthermore, PI3K and p-AKT protein levels clearly decreased after PROM2 silencing. Importantly, rescue experiments elucidated that PI3K/AKT pathway activation could reverse the inhibitory effect of PROM2 silencing on the proliferation, migration, and invasion of NCI-H520 and A549 cells.</p><p><strong>Conclusion: </strong>This study verified that PROM2 knockdown inhibits the growth, migration, and invasion of NSCLC by repressing the PI3K/AKT pathway.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"21"},"PeriodicalIF":2.5,"publicationDate":"2025-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711851","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":"Exploration of immunocytochemical biomarkers related to central lymph node metastasis in papillary thyroid microcarcinoma.","authors":"Lulu Rong, Jie Wang, Qian Wang, Yanli Zhu, Wenhao Ren","doi":"10.25259/Cytojournal_162_2024","DOIUrl":"10.25259/Cytojournal_162_2024","url":null,"abstract":"<p><strong>Objective: </strong>The presence of central lymph node metastasis (CLNM) represents a critical determinant in ascertaining the necessity for surgical intervention in patients with papillary thyroid microcarcinoma (PTMC). However, the predominant current methodologies for confirming the central lymph node status in clinical practice are hampered by the low predictive accuracy of preoperative ultrasound examination and the high risk of preoperative fine needle aspiration (FNA). Consequently, the objective of this study is to investigate and identify specific immunocytochemical biomarkers for predicting CLNM in PTMC patients based on preoperative thyroid FNA samples.</p><p><strong>Material and methods: </strong>In this study, the messenger ribonucleic acid sequencing data of pathological tumor stage 1 (pT1) papillary thyroid carcinoma (PTC) accompanied by pathological node stage information were initially retrieved from The Cancer Genome Atlas database. The differential expression genes (DEGs) between the pT1N1-PTC group and the pT1N0-PTC group were ascertained through bioinformatics methodology. Subsequently, these DEGs were imported into Cytoscape software to identify hub genes. Ultimately, immunohistochemical and immunocytochemical staining were employed to validate whether the biomarkers corresponding to the main hub genes demonstrated statistical significance in predicting CLNM within propensity score-matched PTMC samples.</p><p><strong>Results: </strong>In this study, a total of 292 DEGs and 10 hub genes were successfully identified. Subsequently, immunohistochemical and immunocytochemical staining were conducted on 208 PTMC cases selected through propensity score matching. Among these 208 cases, the biomarkers (Cytokeratin 5/6 [CK5/6], Chromogranin A [CgA], and Pair box gene 2 [Pax-2]) corresponding to the main hub genes (Cytokeratin 5 [KRT5], Cytokeratin 6 [KRT6A], Chromogranin A [CHGA], and PAX2) were subjected to immunohistochemical staining in postoperative thyroidectomy specimens, the immunohistochemical staining results revealed a statistically significant difference in CK5/6 expression between PTMCs with and without CLNM (<i>P</i> = 0.002). Subsequently, CK5/6 immunocytochemical staining performed on preoperative thyroid FNA liquid-based samples further corroborated that CK5/6 expression was more prone to being positive in PTMCs with CLNM (<i>P</i> = 0.010).</p><p><strong>Conclusion: </strong>CK5/6 is a valuable immunocytochemical biomarker capable of predicting the occurrence of CLNM in PTMC patients prior to surgery.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"18"},"PeriodicalIF":2.5,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711847","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":"Exploring miR-3148's impact on Krüppel-like factor 6-driven mitophagy and apoptosis in myocardial ischemic injury.","authors":"Chusheng Huang, Lipeng Li, Hailong Deng, Jincheng Su, Qingjun Wei, Ying He, Lei Xian","doi":"10.25259/Cytojournal_209_2024","DOIUrl":"10.25259/Cytojournal_209_2024","url":null,"abstract":"<p><strong>Objective: </strong>Myocardial infarction (MI) is a leading cause of death worldwide, accounting for millions of fatalities annually. The injury and repair of cardiomyocytes are closely associated with the changes in gene expression. MicroRNAs could serve as a potential target for MI treatment. This work aims to investigate the role of miR-3148 in mitochondrial dynamics during acute MI (AMI) with a specific focus on its regulatory mechanisms in mitophagy and apoptosis, which could reveal potential therapeutic targets for AMI treatment.</p><p><strong>Material and methods: </strong>MiR-3148 levels in patients with AMI and experimental models were measured to assess the effects of miR-3148 on cardiomyocyte viability under oxygen and glucose deprivation (OGD). The present investigation involved monitoring mitophagy markers, including PTEN-induced kinase 1 (PINK1), parkin RBR E3 ubiquitin-protein ligase (Parkin), Beclin1, and microtubule-associated protein 1A/1B light chain 3 II/I (LC3 II/I) ratio, as well as apoptotic markers such as cysteine-aspartic acid protease (Caspase) 9, Caspase 3, and cytochrome C (Cyt C). In addition, Krüppel-like factor 6 (KLF6) was examined as a target of miR-3148.</p><p><strong>Results: </strong>MiR-3148 was significantly elevated in patients with AMI and models. MiR-3148 overexpression reduced cardiomyocyte viability, whereas miR-3148 knockdown protected against OGD injury. The inhibition of miR-3148 activated mitophagy, as shown by the increased PINK1, Parkin, Beclin1 levels, and LC3 II/I ratios, and reduced sequestosome 1 (p62), and apoptotic markers levels. MiR-3148 directly targeted KLF6, reducing its expression. The suppression of KLF6 aggravated OGD injury by disrupting PINK1/Parkin-mediated mitophagy and enhancing apoptosis. Attenuating KLF6 expression reversed the protective effects of miR-3148 inhibition, indicating reciprocal regulation.</p><p><strong>Conclusion: </strong>In myocardial ischemic injury, miR-3148 modulates PINK1/Parkin-mediated mitophagy and apoptosis through KLF6 regulation. This finding highlights miR-3148 as a key factor in the pathogenesis of AMI and as a potential therapeutic target.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"19"},"PeriodicalIF":2.5,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11932976/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143711848","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":"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}