Cytojournal最新文献

{"title":"Phosphatase and tensin homolog accelerate the inflammatory injury and glycolysis of chondrocytes through TP53 protein-mediated p38MAPK pathway activation in a high-glucose environment.","authors":"Jian Ding, Chenghua Yang, Xiaofeng Li","doi":"10.25259/Cytojournal_199_2024","DOIUrl":"10.25259/Cytojournal_199_2024","url":null,"abstract":"<p><strong>Objective: </strong>Chronic metabolic diseases represent a high-risk factor for osteoarthritis. In particular, diabetes has been proven to be closely related to the occurrence of osteoarthritis in cases called diabetic osteoarthritis (DAO). A large number of studies have shown that phosphatase and tensin homolog (PTEN) are involved in the progression of osteoarthritis; however, the mechanism of PTEN in DAO remains unclear. Accordingly, this study aimed to explore the regulatory role of PTEN in inflammatory injury and glycolysis during the progression of DAO.</p><p><strong>Material and methods: </strong>Primary chondrocytes treated with high glucose (HG) were transfected with the small interfering (si) RNA of PTEN or tumor suppressor protein p53 (TP53). Then, cell viability and apoptosis, inflammatory factor secretion, and the protein expression of matrix metalloproteinase 13 and collagen II were detected. Subsequently, we examined glucose uptake, lactate production, reactive oxygen species (ROS) content, and the protein expression of glycolysis-related molecules, namely hexokinase2 and lactate dehydrogenase A, in PTEN knockdown primary chondrocytes. Then, primary chondrocytes were transfected with siRNA against PTEN (siPTEN) alone or together with plasmid DNA (pcDNA)-TP53 to detect changes in cellular inflammatory damage and glycolysis, and thus, determine whether the p38 mitogen-activated protein kinase (p38MAPK) pathway affects the inflammatory damage and glycolysis of chondrocytes by introducing SB203580, which is a p38 pathway inhibitor.</p><p><strong>Results: </strong>PTEN protein expression was up-regulated (<i>P</i> < 0.05) in rat primary chondrocytes in an HG environment, accompanied by decreased cell viability (<i>P</i> < 0.05), increased apoptosis (<i>P</i> < 0.05), increased secretion of inflammatory factors (<i>P</i> < 0.05), and aggravated degradation of the cell matrix (<i>P</i> < 0.05). In addition, HG-treated chondrocytes exhibited abnormal metabolism, which was manifested by increased glucose uptake (<i>P</i> < 0.05), lactate content (<i>P</i> < 0.05), ROS generation (<i>P</i> < 0.05), and expression of glycolysis-related molecules (<i>P</i> < 0.05). Meanwhile, the transfection of si-PTEN inhibited PTEN protein expression and reversed the inflammatory injury and glycolysis of chondrocytes caused by an HG environment. TP53 is a PTEN-binding protein, and its expression is positively regulated by PTEN. Similar to the role of PTEN, TP53 silencing reversed the inflammatory injury (<i>P</i> < 0.05) and glycolysis (<i>P</i> < 0.05) of chondrocytes caused by an HG environment. Further mechanistic studies have shown that PTEN promotes the inflammatory injury (<i>P</i> < 0.05) and glycolysis (<i>P</i> < 0.05) of chondrocytes by up-regulating the expression of TP53. Moreover, by introducing SB203580, a p38 pathway inhibitor, we confirmed that this process was mediated by activating the p38MAPK pathway.</p><p><strong>Conclusion: <","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"75"},"PeriodicalIF":3.1,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12596799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145490591","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":"Transcriptional enhanced associate domain factor 1 regulates cortactin-binding protein 2 N-terminal-like to control cell apoptosis in thyroid cancer.","authors":"Qian Ma, Liyong Zhang, Shan Jiang, Wenxin Zhao","doi":"10.25259/Cytojournal_140_2024","DOIUrl":"10.25259/Cytojournal_140_2024","url":null,"abstract":"<p><strong>Objective: </strong>Understanding the molecular mechanisms underlying papillary thyroid carcinoma (PTC) is crucial for identifying drug targets. This research aims to elucidate molecular interactions between transcriptional enhanced associate domain factor 1 (TEAD1) and cortactin-binding protein 2 N-terminal-like (CTTNBP2NL) in PTC cells and assess their effect on cell proliferation, apoptosis, and clonogenicity.</p><p><strong>Material and methods: </strong>Transcriptome data were used to identify differences in TEAD1 and CTTNBP2NL in PTC tissues. The correlation of gene expression with overall patient survival was analyzed. Laboratory experiments were conducted using thyroid papillary carcinoma 1 (TPC1) cells, where the overexpression of TEAD1 and the downregulation of CTTNBP2NL were manipulated. The regulatory dynamics between the two genes were confirmed through molecular biochemistry experiments. The effects on cell proliferation were evaluated using cell proliferation assays, and the impact on clonogenicity was assessed through colony formation assays.</p><p><strong>Results: </strong>Significant differences in TEAD1 and CTTNBP2NL were observed in PTC, with both genes showing strong correlations with overall patient survival. In TPC1 cells, the overexpression of TEAD1 remarkably mitigated the negative effects caused by CTTNBP2NL downregulation, reduced cell proliferation, and increased apoptosis. Quantitative polymerase chain reaction and Western blot analyses confirmed the regulatory relationship between TEAD1 and CTTNBP2NL. The overexpression of TEAD1 markedly enhanced the proliferative capacity of cells, while silencing CTTNBP2NL resulted in diminished cell growth. Clonogenic assays revealed that TEAD1 promoted colony formation, indicating its role in boosting cell survival and proliferation.</p><p><strong>Conclusion: </strong>TEAD1 plays a critical compensatory role in PTC cells by alleviating the adverse effects of CTTNBP2NL deficiency, thereby promoting cell survival and growth. Hence, TEAD1 could serve as a potential therapeutic target.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"74"},"PeriodicalIF":3.1,"publicationDate":"2025-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12596791/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145490792","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":"Synchronous primary cancers involving the endometrium and fallopian tube: A case report.","authors":"Qin Cao, Xiaoting Zhou, Danju Luo, Shuang Guo, Bangxing Huang","doi":"10.25259/Cytojournal_17_2025","DOIUrl":"10.25259/Cytojournal_17_2025","url":null,"abstract":"<p><p>The co-occurrence of uterine and adnexal malignancies poses significant diagnostic challenges in distinguishing synchronous primary tumors from metastatic lesions. This study presents a rare case of concurrent dedifferentiated endometrial carcinoma (DEC) and high-grade serous tubal carcinoma and highlights the critical role of integrated pathological and molecular analyses. A 58-year-old woman presented with a 2-month history of irregular vaginal bleeding. Transvaginal ultrasound demonstrated endometrial thickening (1 cm) with intrauterine fluid accumulation. Hysteroscopic biopsy confirmed endometrioid adenocarcinoma. The patient underwent laparoscopic radical hysterectomy with bilateral adnexectomy and pelvic lymphadenectomy. Histopathological examination identified two distinct neoplasms: (1) DEC (microsatellite instability-high subtype) located at the left uterine fundus and (2) High-grade serous carcinoma (SET subtype: solid, endometrioid-like, transitional patterns) in the right fallopian tube. Following surgery, six cycles of adjuvant chemotherapy with TP regimen (liposomal paclitaxel plus carboplatin) were administered. The patient remains disease-free at a 46-month follow-up. This case underscores the diagnostic complexity of synchronous gynecological malignancies. Comprehensive immunohistochemistry combined with molecular characterization is essential for accurate tumor classification, which directly determines staging precision and therapeutic decision-making. The favorable long-term outcome in this case suggests potential clinical implications for dual primary management strategies.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"73"},"PeriodicalIF":3.1,"publicationDate":"2025-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12596763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145490627","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":"1α, 25-dihydroxyvitamin D3 attenuates tumor necrosis factor-α-induced endothelial cell injury by modulating the tumor necrosis factor-α/nuclear factor kappa-B pathway.","authors":"Yangyang Xia, Sixiu Liu, Qiuyuan Shao, Yuan Feng, Bo Jin, Qingyan Zhang","doi":"10.25259/Cytojournal_220_2024","DOIUrl":"10.25259/Cytojournal_220_2024","url":null,"abstract":"<p><strong>Objective: </strong>Cardiovascular (CV) diseases remain the leading cause of death in modern societies, with endothelial dysfunction being the common pathology of CV diseases with various etiologies. Therefore, effectively regulating the function of endothelial cells is considered the key to the future treatment of various CV diseases. Low levels of vitamin D and its analogs have been shown to be associated with endothelial dysfunction in various diseases. However, the underlying mechanism remains unknown. Here, we conducted an <i>in vitro</i> study to evaluate the effects of 1α,25-dihydroxyvitamin D3 (1α, 25(OH)2D3), the active form of vitamin D, on adhesion molecule expression in human endothelial cells. The possible mechanism involved in this process was also explored.</p><p><strong>Material and methods: </strong>Human umbilical vein endothelial cells were cultured and treated according to the experimental requirements. Western blotting and reverse transcription polymerase chain reaction were used to evaluate the expression of vascular cell adhesion molecule-1 (VCAM-1) and E-selectin. Chromatin immunoprecipitation (ChIP) assays, immunofluorescence, Western blotting, and coimmunoprecipitation were used to assess the effects of 1α, 25(OH)2D3 on nuclear factor kappa-B (NF-κB) signaling.</p><p><strong>Results: </strong>1α, 25(OH)2D3 inhibited VCAM-1 and E-selectin mRNA and protein expression after tumor necrosis factor-α (TNF-α) stimulation. Moreover, 1α, 25(OH)2D3 affected TNF-α-induced IκBα phosphorylation and p65 NF-κB activation, leading to the inhibition of p65 expression. A ChIP assay revealed that TNF-α increased p65 binding to the promoters of VCAM-1 and E-selectin, which was suppressed by 1α, 25(OH)2D3. These effects were abrogated by a specific vitamin D receptor siRNA (VDR-siRNA). Coimmunoprecipitation revealed that 1α, 25(OH)2D3 induced increased binding of the vitamin D receptor to p65, which inhibited the ability of p65 to bind to target gene promoters.</p><p><strong>Conclusion: </strong>1α, 25(OH)2D3 regulates adhesion molecule expression in endothelial cells through the TNF-α/NF-κB pathway, laying the foundation for the clinical application of 1α, 25(OH)2D3 in the treatment of CV diseases.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"70"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12596787/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145490416","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":"Regulator of chromosome condensation 1 and broad-complex, tramtrack and bric a brac domain-containing protein is involved in ovarian cancer growth and drug resistance.","authors":"Gaowa Zhao, Xiaochao Xiao, Limeng Song, Bangruo Qi","doi":"10.25259/Cytojournal_268_2024","DOIUrl":"10.25259/Cytojournal_268_2024","url":null,"abstract":"<p><strong>Objective: </strong>Ovarian cancer (OC) is the most common and deadliest cancer in women worldwide. The high incidence and mortality rates highlight the serious threat that OC poses to women's health. Regulator of chromosome condensation (RCC1) and broad-complex, tramtrack and bric a brac ( BTB) domain-containing protein 1 (RCBTB1), which includes the RCC1 and BTB domains, is a cell proliferation-related protein. This study aims to reveal the role of RCBTB1 in OC and its possible pathway.</p><p><strong>Material and methods: </strong>The expression of RCBTB1 in OC cells was measured by quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC). Transwell assay, wound-healing assay, clone formation assay, IHC, immunofluorescence, and methylthiazolyldiphenyl-tetrazolium bromide assay were used to evaluate the effect of silencing RCBTB1 <i>in vivo</i> and <i>in vitro</i>. The neurofibromin 1 (NF1)/rat sarcoma (Ras) signal axis was determined by Western Blot, qRT-PCR, and immunofluorescence.</p><p><strong>Results: </strong>The A2780 cells had increased RCBTB1 expression (<i>P</i> < 0.01). By suppressing Ras signaling, RCBTB1 silencing hindered the proliferation of OC cells with Kirsten rat sarcoma viral oncogene (KRAS) mutations. RCBTB1 activated protein kinase kinase Cε, which degrades NF1. RCBTB1 also plays a key role in the Ras/ extracellular regulated protein kinase (ERK) signal axis by inhibiting Ras GTPase. RCBTB1 knockdown may alleviate mitogen-activated protein kinase kinase ( MEK) inhibitor resistance in KRAS-mutated OC by inhibiting Ras/ERK signaling.</p><p><strong>Conclusion: </strong>RCBTB1 may regulate the NF1/Ras signaling axis, which is critical for OC and MEK inhibitor resistance. This research offers a unique therapeutic approach for ovaries with KRAS mutations and uncovers a previously unknown connection between RCBTB1 and NF1/Ras signaling.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"71"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12596774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145490623","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":"Alginate oligosaccharides alleviates gestational diabetes mellitus through reducing oxidative stress and improving gut microbiota.","authors":"Ping Zhang, Chun Qin Ding, Yun Wang, Ping Du, Mei-Ling Tian","doi":"10.25259/Cytojournal_182_2024","DOIUrl":"10.25259/Cytojournal_182_2024","url":null,"abstract":"<p><strong>Objective: </strong>Gestational diabetes mellitus (GDM) has significant implications for maternal and neonatal health and constitutes a considerable health challenge that requires intervention. The primary factors contributing to GDM are oxidative stress and dysbiosis of the gut microbiota. Alginate oligosaccharides (AOS), known for their antioxidant properties and ability to modulate the balance of gut microbiota, may offer a promising therapeutic option for managing GDM. In this investigation, we aim to clarify the specific therapeutic effects and underlying mechanisms of AOS in GDM.</p><p><strong>Material and methods: </strong>Mice with GDM were administered various agents, including AOS and deltamethrin, to investigate the impact of AOS on gut microbiota composition, insulin resistance (IR), pancreatic cell apoptosis, and hepatic gluconeogenesis. Biochemical markers associated with GDM, IR, and hepatic gluconeogenesis were analyzed. Cell experiments were introduced to confirm the effects of AOS on high-glucose-induced liver cell damage.</p><p><strong>Results: </strong>Mice with GDM exhibited an imbalance in the gut microbiota, increased IR, enhanced liver gluconeogenesis, and activated the nuclear factor-erythroid 2 related factor 2/heme oxygenase-1 pathway in the liver. The administration of AOS restored gut microbiota equilibrium and reduced cell apoptosis in pancreatic cells, oxidative stress, IR, and hepatic gluconeogenesis, leading to improvements in parameters associated with islet β-cell functionality and insulin sensitivity. AOS also increased cell viability and decreased the inflammatory cytokine release induced by high glucose in QSG 7701 liver cells.</p><p><strong>Conclusion: </strong>Treatment with AOS offers protection against IR, and hepatic gluconeogenesis by diminishing oxidative stress and modulating the gut microbiota in mice with GDM. Hence, AOS is a promising intervention for GDM.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"72"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12596804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145490431","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":"Fine needle aspiration diagnosis of Kikuchi's lymphadenitis in axillary lymphadenopathy: A rare condition with an unusual presentation site.","authors":"Azaa Salim Al-Zakwani, Bushra Said Al-Hatrooshi","doi":"10.25259/Cytojournal_108_2024","DOIUrl":"10.25259/Cytojournal_108_2024","url":null,"abstract":"<p><p>Kikuchi's lymphadenitis (KL) is a benign, self-limited, reactive condition with unknown etiology, usually seen in young women of Asian descent. It is most commonly seen in the cervical lymph nodes; however, in rare cases, axillary lymph nodes are involved. Cytological diagnosis is possible with adequate lymph node sampling by fine needle aspiration in the proper clinical setting. Pathologists face some difficulties in making the diagnosis of KL due to overlapping findings among other conditions, such as tuberculosis, lupus lymphadenitis, non-specific reactive conditions, and even malignant lymphoma. Diagnosis by cytopathology has the advantage of using minimally invasive interventions, which avoid the unnecessary excision of the lymph node for this benign condition. Herein, we report a case of KL in a patient who presented with right axillary lymphadenopathy.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"69"},"PeriodicalIF":3.1,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12514765/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145281614","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":"Liquid-based cytology in the era of multi-omics and artificial intelligence integration.","authors":"Sana Ahuja, Sufian Zaheer","doi":"10.25259/Cytojournal_89_2025","DOIUrl":"10.25259/Cytojournal_89_2025","url":null,"abstract":"","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"68"},"PeriodicalIF":3.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12514761/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145281577","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":"Membrane-spanning 4 domains subfamily A member 4A inhibition promotes M1 macrophage polarization and enhances anti-gastric cancer immune response.","authors":"Xinyue Zhang, Di Na","doi":"10.25259/Cytojournal_271_2024","DOIUrl":"10.25259/Cytojournal_271_2024","url":null,"abstract":"<p><strong>Objective: </strong>The immunosuppressive tumor microenvironment (TME) limits the treatment effectiveness of immunotherapy in gastric cancer (GC). This study investigated the role of membrane-spanning four domains subfamily A member 4A (MS4A4A) in the regulation of macrophage polarization and its effect on the immune response in GC, with the aim of enhancing the effectiveness of immunotherapy by addressing the immunosuppressive TME.</p><p><strong>Material and methods: </strong>A GC ectopic tumor model was initiated in C57BL/6 mice with subcutaneous MKN-45 injection. Five groups were formed by randomly dividing the mice: model, MS4A4A recombinant protein, MS4A4A antibody, programmed cell death protein 1 (PD-1) antibody, and MS4A4A recombinant protein + PD-1 antibody groups. MKN-45 cells and bone marrow-derived macrophages (BMDMs) were cocultured with the MS4A4A protein or antibody. Macrophage polarization was analyzed through flow cytometry, gene expression through quantitative real-time polymerase chain reaction (qRT-PCR), cytokine levels through enzyme-linked immunosorbent assay, protein expression through Western blot, and tumor morphology through hematoxylin and eosin staining.</p><p><strong>Results: </strong>In the GC mouse model, the MS4A4A recombinant protein markedly enhanced tumor growth (<i>P</i> < 0.001), and the MS4A4A antibody exhibited an inhibitory effect (<i>P</i> < 0.001). MS4A4A recombinant protein decreased the levels of inflammatory cytokine concentrations and increased those of anti-inflammatory mediator concentrations (<i>P</i> < 0.001). By contrast, the MS4A4A antibody treatment group displayed the opposite effect. Inhibition of MS4A4A enhanced the accumulation of macrophages, CD4⁺ T cells, and CD8⁺ T cells in the tumor (<i>P</i> < 0.001). Flow cytometry and qRT-PCR analyses showed that MS4A4A promoted M2 macrophage polarization, and MS4A4A antibody induced M1 polarization (<i>P</i> < 0.001). MS4A4A played a key role in inhibiting nuclear factor kappa-light-chain-enhancer of activated B cells subunit p50 (p50) during M1 polarization. Furthermore, the PD-1 antibody reversed the pro-tumor effects of MS4A4A, which reestablished pro-inflammatory cytokine levels while lowering anti-inflammatory cytokines (<i>P</i> < 0.001).</p><p><strong>Conclusion: </strong>This study shows that MS4A4A promotes tumor growth by inducing M2 macrophage polarization and suppressing immune responses, while MS4A4A antibody enhances anti-tumor immunity by inducing M1 polarization. PD-1 antibody reverses MS4A4A's pro-tumor effects, restoring anti-tumor immunity. MS4A4A inhibitors or their combination with PD-1 antibodies may offer a promising strategy for GC immunotherapy.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"63"},"PeriodicalIF":3.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12514763/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145281612","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":"Preliminary investigation on the correlation between karyopherin alpha 4 and acute cerebral infarction.","authors":"Jinzhe Chu, Nannan Ren, Chunli Xie","doi":"10.25259/Cytojournal_8_2025","DOIUrl":"10.25259/Cytojournal_8_2025","url":null,"abstract":"<p><strong>Objective: </strong>Acute cerebral infarction (ACI) has a high incidence and complex etiology, so searching for specific diagnosis and therapeutic target molecules is highly important. This paper aimed to explore the mechanism of karyopherin alpha 4 (<i>KPNA4</i>) in ACI.</p><p><strong>Material and methods: </strong>Four groups were established: sham group, middle cerebral artery occlusion (MCAO) group, MCAO + small interfering negative control (si-NC group), and MCAO + si-<i>KPNA4</i> group. The Zea-Longa scoring standard was adopted to assess the neurological impairment of ACI rats. The expression of <i>KPNA4</i> was verified by real-time quantity polymerase chain reaction assay and Western blot. 2,3,5-Triphenyltetrazolium chloride and hematoxylin and eosin staining were used to examine the effects of <i>KPNA4</i> knockdown on brain injury in ACI rats. The apoptosis of oxygen-glucose deprivation (OGD)-SH-SY5Y cells was measured by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling method. Western blot analysis was performed to analyze the expression levels of apoptosis-related proteins, inflammatory factors, and nuclear factor kappa B (NF-κB) pathway-related proteins.</p><p><strong>Results: </strong><i>KPNA4</i> was overexpressed in the MCAO rat brain (<i>P</i> < 0.0001) and OGD-SH-SY5Y cells (<i>P</i> < 0.0001). Knocking down <i>KPNA4</i> significantly reduced the degree of brain damage (<i>P</i> < 0.0001) and reduced the apoptosis of OGD-SH-SY5Y cells (<i>P</i> < 0.001). <i>KPNA4</i> knockdown also significantly decreased the expression levels of inflammatory factors (interleukin [IL]-1β, tumor necrosis factor-α, and IL-18; <i>P</i> < 0.0001) and prohibited the phosphorylation of the inhibitor of NF-κB and p65 (<i>P</i> < 0.0001). However, NF-κB agonist lipopolysaccharide reversed the inhibition of <i>KPNA4</i> knockdown.</p><p><strong>Conclusion: </strong>In general, <i>KPNA4</i> knockdown can mitigate ACI-induced damage by regulating the NF-kB pathway. This finding provides a new perspective on the treatment of ACI.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"64"},"PeriodicalIF":3.1,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12514764/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145281582","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}