Cytojournal最新文献

{"title":"Scope and limitations of intraoperative cytological methods of diagnosis of ovarian tumors.","authors":"Erna Ahsan, Saurabh Kumar Gautam, Ashok Singh, Arvind Kumar, Ravi Hari Phulware","doi":"10.25259/Cytojournal_226_2024","DOIUrl":"10.25259/Cytojournal_226_2024","url":null,"abstract":"<p><p>The mainstay of treatment for ovarian cancer is surgery. To prevent under-treatment and overtreatment and to choose the best surgical strategy for patients with ovarian tumors, intraoperative pathological assessment is essential. Frozen sections (FSs) have been historically used for intraoperative evaluation. In 1927, cytology was introduced by Dudgeon and Patrick as a new method of intraoperative pathological examination. Diagnosis can be made in minutes by making smears from the lesion, staining them quickly, and analyzing them under a microscope. Following a comprehensive search of the literature, using pertinent keywords in PubMed, and reviewing the data, it was discovered that intraoperative cytology (IOC) had been reported to have a diagnostic accuracy in ovarian lesions comparable to that of FSs. Few of the studies have confirmed that IOC has several benefits over FSs. There are drawbacks as well, which one should be mindful of. In this review, every aspect that is connected to IOC is covered in detail, along with the potential for raising the standard of IOC to make it more applicable in the present times.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"42"},"PeriodicalIF":2.5,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12134854/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zinc finger and broad-complex, tramtrack, and bric-a-brac domain containing 16 silencing attenuates bleomycin-induced pulmonary fibrosis in mice through inhibition of the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin pathway.","authors":"Xiansong Fang, Xiaoyun Wen, Liang Zhou, Yingjie Jiang, Liefeng Wang","doi":"10.25259/Cytojournal_223_2024","DOIUrl":"10.25259/Cytojournal_223_2024","url":null,"abstract":"<p><strong>Objective: </strong>Idiopathic pulmonary fibrosis (PF) is a chronic and life-threatening lung disease. This study aimed to investigate the role of zinc finger and BTB domain containing 16 (Zbtb16), a transcription factor, in the progression of PF by analyzing its expression and regulatory effects in mouse and cell models.</p><p><strong>Material and methods: </strong>The gene expression profiles in bleomycin-induced (BL-I) PF lung tissues of mice were analyzed using the gene expression omnibus database. The mouse model of BL-I PF and cell model of transforming growth factor-β1 (TGF-β1)-induced mice lung epithelial cell (LEC) fibrosis was constructed. Zbtb16 expression was evaluated by reverse transcription quantitative polymerase chain reaction, Western blot, or immunohistochemistry. Tissue sections were assessed by hematoxylin and eosin, Masson, and terminal deoxynucleotidyl transferase dUTP nick-end labeling staining. The levels of protein, inflammation factors, and albumin were measured through Western blot or enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>Bioinformatics analysis found that Zbtb16 was the highest differentially expressed marker in BL-I PF mice. Zbtb16 was highly expressed in the mice and cell model. Zbtb16 silencing could reduce lung tissues' collagen deposition, pulmonary edema, and pulmonary apoptotic cells; improve vascular permeability; and decrease fibrosis markers and inflammation factors expressed in model mice. Zbtb16 silencing could reduce fibrosis markers and inflammation factor levels in the cell model (<i>P</i> < 0.05). Kyoto encyclopedia of genes and genomes and gene set enrichment analyses suggested that Zbtb16 might regulate BL-I PF in mice through the phosphoinositide 3-kinases (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) pathway (PAmT-P). Co-immunoprecipitation showed the combination of AKT and Zbtb16. PAmT-P in the mice model and cell model was visibly activated (<i>P</i> < 0.05), and Zbtb16 silencing could inhibit it (<i>P</i> < 0.05). Moreover, the rescue experiments showed that the AKT activator SC79 could reverse the effect of TGF-β1 + small interfere RNA-Zbtb16 on LECs.</p><p><strong>Conclusion: </strong>This study identified Zbtb16 as a key regulator of PF progression, mediating its effects through the PAmT-P. Zbtb16 silencing alleviated fibrosis and inflammation <i>in vivo</i> and <i>in vitro</i>, providing a promising target for therapeutic intervention in PF.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"37"},"PeriodicalIF":2.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12134818/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227294","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":"Matrix gla protein mediates CD8⁺ T-cell exhaustion to facilitate immune evasion in intrahepatic cholangiocarcinoma.","authors":"Xiaohan Cao, Shiqian Lang, Yuchi Xie, Kai Zheng, Jun Liu","doi":"10.25259/Cytojournal_232_2024","DOIUrl":"10.25259/Cytojournal_232_2024","url":null,"abstract":"<p><strong>Objective: </strong>Matrix Gla protein (MGP) has been found to be strongly associated with cancer progression. However, its role in intrahepatic cholangiocarcinoma (ICC) remains unclear, particularly within the tumor immune microenvironment. MGP may promote immune evasion by activating the nuclear factor-kappa-light-chain-enha ncer of activated B-cells (NF-κB) signaling pathway, which increases the expression of programmed death-ligand 1 (PD-L1) and contributes to CD8⁺ T-cell exhaustion. This research mainly aims to examine the regulatory role of MGP in immune evasion in ICC.</p><p><strong>Material and methods: </strong>ICC xenograft mouse models and human ICC cell line (HuCCT1) cell models were established to evaluate MGP expression patterns. MGP knockdown or overexpression in HuCCT1 cells was co-incubated with antigen-specific CD8⁺ T cells, and flow cytometry was used to detect markers of CD8⁺ T-cell exhaustion. The effects of MGP modulation on PD-L1 expression were assessed by immunohistochemistry and immunofluorescence. Western blotting was employed to analyze the impact on NF-κB signaling. In addition, MGP overexpression and p65 knockdown in HuCCT1 cells were co-transfected to study their combined effects on PD-L1 expression and CD8⁺ T-cell exhaustion markers. Cell proliferation and apoptosis were evaluated through colony formation assays and flow cytometry.</p><p><strong>Results: </strong>Compared to adjacent tissues and human intrahepatic cholangiocellular epithelial cells, MGP was significantly overexpressed in ICC tumor tissues and HuCCT1 cells (<i>P</i> < 0.001). MGP overexpression led to NF-κB signaling phosphorylation (<i>P</i> < 0.001), elevated PD-L1 expression (<i>P</i> < 0.001), and heightened levels of CD8⁺ T-cell exhaustion markers (<i>P</i> < 0.001). Conversely, p65 knockdown mitigated the effects of MGP overexpression on HuCCT1 cell proliferation (<i>P</i> < 0.01) and CD8⁺ T-cell exhaustion (<i>P</i> < 0.01 and <i>P</i> < 0.001), while also significantly reducing PD-L1 expression (<i>P</i> < 0.01).</p><p><strong>Conclusions: </strong>MGP promotes CD8⁺ T-cell exhaustion and facilitates immune evasion in ICC through NF-κB pathway activation.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"41"},"PeriodicalIF":2.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12134819/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227362","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":"Methyltransferase 3-mediated m6A modification of Switch/sucrose non-fermenting-related matrix-associated actin-dependent regulator of chromatin subfamily a member 5 promotes mycobacterium tuberculosis-infected macrophage M1 polarization and inflammation.","authors":"Cong Chen, Hai Huang","doi":"10.25259/Cytojournal_144_2024","DOIUrl":"10.25259/Cytojournal_144_2024","url":null,"abstract":"<p><strong>Objective: </strong><i>Mycobacterium tuberculosis</i> (MTB) manipulates macrophage functions, thus mediating tuberculosis (TB) progression. Whether the switch/sucrose non-fermenting-related matrix-associated actin-dependent regulator of chromatin subfamily a member 5 (SMARCA5) mediates MTB-induced macrophage polarization remains unclear.</p><p><strong>Material and methods: </strong>Human Promyelocytic Leukemia Cell Line was induced into macrophages and then treated with MTB. Cell viability and apoptosis were tested with cell counting kit 8 assay and flow cytometry. Classically activated macrophages (M1) polarization and inflammation were measured by detecting CD86⁺ cell rate and inflammatory factor levels. The levels of SMARCA5, methyltransferase 3 (METTL3), and insulin-like growth factor 2 binding protein 1 (IGF2BP1) were assessed using quantitative real-time polymerase chain reaction or Western blot. The interaction between SMARCA5 and METTL3 or IGF2BP1 was confirmed by methylated RNA immunoprecipitation (RIP) and RIP assays. The effect of METTL3 knockdown on SMARCA5 messenger RNA (mRNA) stability was evaluated using actinomycin D treatment.</p><p><strong>Results: </strong>MTB treatment suppressed the viability and promoted the apoptosis and M1 polarization and inflammation of macrophages (<i>P</i> < 0.05), and SMARCA5 knockdown abolished these effects (<i>P</i> < 0.05). METTL3 mediated the m6A methylation of SMARCA5 to enhance the mRNA stability of the latter, and this modification was recognized by IGF2BP1. SMARCA5 upregulation reverted the si-METTL3-mediated inhibition of MTB-induced macrophage M1 polarization and inflammation (<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>METTL3-mediated SMARCA5 facilitates macrophage M1 polarization and inflammation, providing a novel target for TB treatment.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"38"},"PeriodicalIF":2.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12134857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227363","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":"Rhein-induced apoptosis in colorectal cancer cell lines: A mechanistic study of the myeloid differentiation primary response gene 88/toll-like receptor 4/nuclear factor kappa-B signaling pathway.","authors":"Xinglu Zheng, Xiaolan Zhang, Longfei Hu, Xixi Chen, Zhangshu Zhao, Liangliang Mao","doi":"10.25259/Cytojournal_257_2024","DOIUrl":"10.25259/Cytojournal_257_2024","url":null,"abstract":"<p><strong>Objective: </strong>Colorectal cancer (CRC) remains one of the leading causes of cancer-related mortality worldwide, and targeted therapies for CRC are urgently needed. This study aimed to investigate the mechanisms through which rhein induces apoptosis in CRC cells, focusing on its influence on the myeloid differentiation primary response gene 88 (MYD88)/toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) signaling pathway.</p><p><strong>Material and methods: </strong>Cell Counting Kit-8 assay was conducted, with three non-cytotoxic concentrations of rhein selected for further analysis. Cells were allocated into four groups: control, 10 μM rhein, 20 μM rhein, and 50 μM rhein. Migration ability was evaluated through wound healing assay, and invasive potential was assessed using Transwell invasion assay. Apoptotic rates were determined through terminal deoxynucleotidyl transferase dUTP nick-end labeling staining. The expression levels of apoptosis-related proteins and the key components of the MYD88/TLR4/NF-κB pathway were analyzed by quantitative reverse-transcription polymerase chain reaction and Western blotting after rhein treatment.</p><p><strong>Results: </strong>The CRC HT-29 and SW480 cells' capacity to migrate and invade was markedly reduced by rhein treatment. (<i>P</i> < 0.05) while markedly enhancing the apoptotic rates (<i>P</i> < 0.05). This finding was marked by a reduction in the expression levels of B-cell lymphoma 2 (BCL-2) protein and messenger RNA (mRNA, <i>P</i> < 0.05), along with a notable increase in the levels of Bcl-2-associated X and cysteinyl aspartate-specific protease 3 proteins and mRNAs (<i>P</i> < 0.05). The expression levels of MYD88, TLR4, and NF-κB proteins and mRNAs were substantially downregulated (<i>P</i> < 0.05). Adding the TLR4 agonist lipopolysaccharide partially reversed the inhibitory effects of rhein on this signaling pathway, thereby restoring some cellular functional behavior.</p><p><strong>Conclusion: </strong>Rhein appears to promote apoptosis in CRC cells through the MYD88/TLR4/NF-κB signaling pathway, thus inhibiting tumor initiation and progression.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"39"},"PeriodicalIF":2.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12134895/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227292","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":"Clinicopathological and molecular diagnostic features of liposarcoma: A study of 27 cases.","authors":"Yin Zhu, Dong Chen, Jingjing Yu, Shuo Wang","doi":"10.25259/Cytojournal_246_2024","DOIUrl":"10.25259/Cytojournal_246_2024","url":null,"abstract":"<p><strong>Objective: </strong>Liposarcomas are rare tumors, and it is difficult to collect cases in less densely populated areas. Therefore, we aimed to document more cases over a relatively long period to provide more data about the characteristics of liposarcomas. In this study, the clinicopathological features of liposarcomas were investigated in 27 patients.</p><p><strong>Material and methods: </strong>All cases were confirmed by diagnosis through hematoxylin and eosin staining, immunohistochemistry (IHC), and fluorescence <i>in situ</i> hybridization (FISH). Combined IHC analysis was performed for murine double minute 2 (MDM2), cyclin-dependent kinase 4 (CDK4), multiple tumor suppressor 1 (P16), and Cyclin D1. FISH was performed to detect MDM2 amplification in atypical lipomatous tumor/well-differentiated liposarcoma (ALT/WDLPS) and dedifferentiated liposarcoma (DDLPS), and DNA damage inducible transcript 3 ( DDIT3) rearrangements in myxoid liposarcoma (MLPS).</p><p><strong>Results: </strong>Seven cases of liposarcoma were located in the paratesticular region (25.9%, 7/27), 12 in the retroperitoneum (44.4%, 12/27), and eight in the limbs (29.6%, 8/27). Histological analysis showed that there were 13 cases of ALT/WDLPS (48.1%, 13/27), nine cases of DDLPS (33.3%, 9/27), three cases of MLPS (11.1%, 3/27), and two cases of pleomorphic liposarcoma (7.4%, 2/27). IHC analysis revealed that 26 cases were MDM2-positive (96.3%, 26/27), 22 were CDK4-positive (81.5%, 22/27), 26 were P16-positive (96.3%, 26/27), and 27 were cyclin D1-positive (100%, 27/27). FISH analysis revealed 20 cases of MDM2 positivity (90.9%, 20/22) and one case of DDIT3 positivity (50%, 1/2). The clinical outcomes were available for 21 patients. Four patients died (4/21, 19.0%), five experienced recurrence (5/21, 23.8%), and 12 (12/21, 57.1%) survived with no other disease.</p><p><strong>Conclusion: </strong>A combined IHC examination of the four indicators may be used to diagnose ALT/WDLPS and DDLPS, and FISH is recommended as an important supporting method.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"40"},"PeriodicalIF":2.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12134912/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227357","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":"Expression and clinical significance of programmed cell death protein 1/programmed death-ligand 1 in non-small cell lung cancer patients with rare mutations of epidermal growth factor receptor gene: A retrospective cohort study.","authors":"Yuan Du, Zeliang Zhuang, Lijun Zong, Yongxing Xu","doi":"10.25259/Cytojournal_136_2024","DOIUrl":"10.25259/Cytojournal_136_2024","url":null,"abstract":"<p><strong>Objective: </strong>Lung cancer represents a major global health issue and serves as a leading cause of cancer-related deaths, with non-small cell lung cancer (NSCLC) accounting for a considerable proportion of these cases. This study aimed to investigate the expressions and clinical importance of programmed cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1) in patients with rare mutations of the epidermal growth factor receptor (<i>EGFR</i>) gene in NSCLC.</p><p><strong>Material and methods: </strong>A retrospective analysis including 121 NSCLC patients with rare EGFR mutations was performed. Immunohistochemistry was conducted to assess PD-L1 expression, and patients were categorized into PD-L1-negative (PLN, <i>n</i> = 95) and PD-L1-positive (PLP, <i>n</i> = 26) groups. PD-1 expression was also evaluated, with patients divided into PD-1-negative (PN, <i>n</i> = 93) and PD-1-positive (PP, <i>n</i> = 25) groups. The associations among PD-L1/PD-1 expression and demographic characteristics, progression-free survival (PFS), overall survival (OS), and a 5-year survival period were analyzed.</p><p><strong>Results: </strong>Significant negative correlations were observed between PD-L1 expression and PFS (r = -0.202, R² = 0.041, <i>P</i> = 0.026) and OS (r = -0.204, R² = 0.042, <i>P</i> = 0.024). The PLN group exhibited a significantly longer PFS (13.47 ± 3.58 months) than the PLP group (11.67 ± 3.67 months; t = 2.222, <i>P</i> = 0.032) and longer OS (21.39 ± 5.69 months) compared with the PLP group (18.65 ± 4.32 months; t = 2.664, <i>P</i> = 0.010). For PD-1 expression, a negative correlation with PFS was noted (r = -0.325, R² = 0.106, <i>P</i> < 0.001). The PN group displayed longer PFS (14.36 ± 3.18 months) and OS (21.71 ± 5.82 months) compared with the PP group (PFS: 11.98 ± 3.72 months, OS: 20.01 ± 5.18 months).</p><p><strong>Conclusion: </strong>This study underscored the importance of PD-1 and PD-L1 expression as prognostic and predictive markers in NSCLC patients with uncommon EGFR mutations. These biomarkers are crucial for achieving informed treatment choices and enhancement of prognostic evaluations in this specific group.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"36"},"PeriodicalIF":2.5,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12134896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144227360","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":"A disintegrin-like and metalloproteinase 15 facilitates glioblastoma proliferation and metastasis through activation of the protease-activated receptor 1.","authors":"Rong Ren, Zuowei Li, Qiong Fang","doi":"10.25259/Cytojournal_92_2024","DOIUrl":"https://doi.org/10.25259/Cytojournal_92_2024","url":null,"abstract":"<p><strong>Objective: </strong>Glioblastoma hinders therapeutic interventions and prognostic outlooks. At the same time, a disintegrin-like and metalloproteinase 15 (ADAM15) influences cellular processes, such as adhesion and migration. Furthermore, protease-activated receptor 1 (PAR1), a vital receptor, impacts tumorigenesis and disease progression. This study aimed to investigate ADAM15 and PAR1 interaction in epithelial-mesenchymal transition (EMT) modulation in glioblastoma behavior and provide insights into therapeutic targets.</p><p><strong>Material and methods: </strong>The impacts of ADAM15 overexpression and PAR-1/2 inhibition on the proliferation, invasion, and migration of glioblastoma cells U251 and U87 were evaluated using transwell assays, EdU incorporation, clonogenic assay, Ki67 immunohistochemistry, and immunofluorescence staining. Real-time quantitative polymerase chain reaction and Western blot analysis were employed to investigate the impact of ADAM15 on PAR1 expression.</p><p><strong>Results: </strong>After analyzing the impacts of ADAM15 overexpression on the migration, invasion, and proliferation of human glioblastoma cell lines U251 and U87, the results showed that ADAM15 overexpression significantly enhanced migration (<i>P</i> < 0.001) and invasion rates (<i>P</i> < 0.001), as confirmed by scratch and transwell assays, thus indicating its tumor-promoting effects. This study revealed a significant increase in colony formation (<i>P</i> < 0.001), EdU incorporation (<i>P</i> < 0.001), and Ki67-positive cells (<i>P</i> < 0.001) in the ADAM15 overexpressed group. PAR1 and EMT markers were significantly increased in the ADAM15 overexpressed group (<i>P</i> < 0.001). Treatment with the PAR-1 antagonist SCH79797 inhibited EMT (<i>P</i> < 0.01) and suppressed cell proliferation (<i>P</i> < 0.001), migration (<i>P</i> < 0.001), and invasion (<i>P</i> < 0.001) in U251 and U87 cells overexpressing ADAM15, indicating the involvement of PAR-1 signaling in the effects of ADAM15 on cell behaviors. In comparison, the PAR-2 antagonist FSLLRY-NH2 did not show significant effects on EMT or these cell behaviors.</p><p><strong>Conclusion: </strong>ADAM15 drives glioblastoma cell lines U251 and U87 progression through PAR1.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"34"},"PeriodicalIF":2.5,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144057902","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":"Platelet-derived growth factor subunit B overexpression promotes lung cancer tumor growth and metastasis: The role of glucose metabolism.","authors":"Kai Feng, Xiaoping Cai, Gaofeng Qiao","doi":"10.25259/Cytojournal_190_2024","DOIUrl":"https://doi.org/10.25259/Cytojournal_190_2024","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;Lung cancer represents a formidable global health challenge due to its substantial prevalence and mortality rates. Metabolic reprogramming, especially the transition to aerobic glycolysis, plays a pivotal role in the progression of lung cancer by sustaining the energy demands for rapid tumor proliferation. The prominent involvement of platelet-derived growth factor subunit B (PDGFB) in promoting the growth and metastasis of lung cancer through specific signaling cascades is well established in. Nonetheless, further research is imperative to elucidate the intricate regulatory mechanisms of PDGFB in glucose metabolism and its implications for the advancement of lung cancer. Our study is dedicated to exploring the effect of PDGFB on lung cancer by modulating glucose metabolism.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Material and methods: &lt;/strong&gt;First, we determined the expression patterns of PDGFB in various lung cancer cell lines (A549, H460, HCC827, and H1975) using quantitative real-time polymerase chain reaction and Western blot analyses. We measured the expression levels of PDGFB and Ki-67 in tumor tissues from lung cancer patients through immunohistochemistry. We then transfected lung cancer cells with a PDGFB overexpression (PDGFB OE) plasmid. The effects of PDGFB OE and galactose + PDGFB OE co-treatment on cell migration and invasion characteristics were assessed using wound healing and Transwell assays. The impact of PDGFB OE and galactose + PDGFB OE co-treatment on the proliferation capacity of lung cancer cells was evaluated through colony formation and 5-ethynyl-2'-deoxyuridine staining assays. We also measured the effects of PDGFB OE on mitochondrial function and glycolytic capacity in lung cancer cells using extracellular acidification rate assay (ECAR) measurement methods.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;Elevated levels of PDGFB expression were markedly detected in various lung cancer cell lines, notably A549 and H460 (&lt;i&gt;P&lt;/i&gt; &lt; 0.001). This observation was validated by the analysis of tumor samples from patients with lung cancer who exhibited heightened PDGFB expression in tumor tissues (&lt;i&gt;P&lt;/i&gt; &lt; 0.001). Moreover, an association was found between increased levels of Ki67 expression and elevated PDGFB expression (&lt;i&gt;P&lt;/i&gt; &lt; 0.001). The upregulation of PDGFB was linked to heightened migratory (&lt;i&gt;P&lt;/i&gt; &lt; 0.001), invasive (&lt;i&gt;P&lt;/i&gt; &lt; 0.001), and proliferative (&lt;i&gt;P&lt;/i&gt; &lt; 0.001) capacities of the cells. Furthermore, an elevation in lactate levels and ECAR (&lt;i&gt;P&lt;/i&gt; &lt; 0.001) was noted in the PDGFB OE group, along with increased levels of glycolysis-related regulatory proteins. The inhibition of aerobic glycolysis with galactose effectively mitigated the PDGFB-induced enhancement of lung cancer cell proliferation and migration.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;By affecting glucose metabolism, PDGFB drives the growth and metastasis of lung cancer, underscoring its potential as a promising therapeutic target for the management o","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"33"},"PeriodicalIF":2.5,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144041640","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":"Esculin promotes skin wound healing in mice and regulates the Wnt/β-catenin signaling pathway.","authors":"Mian Xu, Mengsi Zhang, Jingjing Wu, Jinmeng Wang, Huaze Wu, Xianting Xu","doi":"10.25259/Cytojournal_184_2024","DOIUrl":"https://doi.org/10.25259/Cytojournal_184_2024","url":null,"abstract":"<p><strong>Objective: </strong>Previous studies reported that esculin could protect against renal ischemia-reperfusion injury and liver injury, but its mechanism of action in skin wound healing is unclear. The Wnt/β-catenin signaling pathway plays a positive role in the wound healing process. This study aimed to investigate the effects of esculin on the rate and quality of skin wound healing in mice and explore its regulatory role in the Wnt/b-catenin signaling pathway.</p><p><strong>Material and methods: </strong>Circular full-thickness skin wounds with a diameter of 8 mm were created on the backs of C57BL/6 mice, which were administered with 20 and 40 mg•kg^-1 esculin through gastric lavage. Wound healing was monitored, and samples collected on day 14 were analyzed through hematoxylin-eosin and Masson staining to assess granulation tissue formation and collagen deposition. Immunohistochemistry, immunofluorescence, and Western blot evaluated markers of collagen synthesis, proliferation, angiogenesis, and proteins in the Wnt/b-catenin signaling pathway. National institutes of health/3T3 cells treated with esculin (50 and 200 μM) were analyzed for proliferating cell nuclear antigen (PCNA) expression to assess proliferative activity.</p><p><strong>Results: </strong>Compared with the model group, the esculin-treated groups exhibited significantly enhanced wound healing (<i>P</i> < 0.05), increased skin epithelial thickness (<i>P</i> < 0.01), and promoted extracellular matrix formation in mice. In addition, esculin significantly raised type I collagen alpha-1 chain and type III collagen alpha-1 chain protein levels (<i>P</i> < 0.05), boosted the expression of the cell proliferation marker PCNA and the vascular marker cluster of differentiation 31 in the dermis (<i>P</i> < 0.05), and upregulated proteins related to the Wnt/b-catenin signaling pathway and increased glycogen synthase kinase 3 beta phosphorylation in skin wound and NIH/3T3 cells (<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>Esculin could upregulate and activate the Wnt/b-catenin signaling pathway to promote wound healing.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"32"},"PeriodicalIF":2.5,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12010908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144053035","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}