Cytojournal最新文献

{"title":"Targeting the Ajuba/Notch axis increases the sensitivity of colon cancer cells to 5-fluorouracil.","authors":"Xinghua Liang, Xuelian Liu, Long Zhang, Junhao Liu, Rong Yan, Haiyan Li, Xiancheng Zeng, Hong Wang","doi":"10.25259/Cytojournal_44_2024","DOIUrl":"10.25259/Cytojournal_44_2024","url":null,"abstract":"<p><strong>Objective: </strong>Colorectal cancer is severely challenging because of the insufficient understanding of the mechanism underlying its resistance to clinical chemotherapy. The purpose of our study is to investigate the role of the LIM protein Ajuba (JUB) in the chemoresistance of colon cancer and its potential effect on clinical treatment.</p><p><strong>Material and methods: </strong>The protein levels of JUB in colon cancer tissues were evaluated using Western blot analysis and immunohistochemistry assays. The correlation between JUB and the prognosis of patients with colorectal cancer was determined using Kaplan-Meier plot analysis. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assays were employed to determine the 50% inhibitory concentration of 5-fluorouracil (5-FU) and thus assess the effect of JUB on the effectiveness of 5-FU. In addition, the rate of cellular apoptosis was measured using fluorescence-activated cell sorting assays. Side population and sphere formation analyses were conducted to determine the role of JUB in promoting the stem cell-like traits of colon cancer cells. <i>In vivo</i> assays were performed and detect whether the downregulation of JUB induces 5-FU sensitivity. Moreover, luciferase and Western blot assays were employed to uncover the mechanism through which JUB promotes chemoresistance in colon cancer.</p><p><strong>Results: </strong>JUB expression was upregulated in chemoresistant colon cancer (<i>P</i> < 0.001) and correlated with relapse-free survival (<i>P</i> = 0.000002). Functionally, the upregulation of JUB conferred 5-FU resistance to colon cancer cells <i>in vitro</i>, whereas the downregulation of JUB induced 5-FU sensitivity in colon cancer cells <i>in vivo</i>. The high expression of JUB promoted the tumorigenic capability of colon cancer cells. Furthermore, the increased expression of JUB activated multiple downstream genes of the Notch signaling pathway with increased expression in JUB-overexpressing cells but reduced expression in JUB-silenced cells. Importantly, the inhibition of Notch signaling using a small-molecule inhibitor significantly suppressed JUB-induced chemoresistance.</p><p><strong>Conclusion: </strong>Results suggest that JUB plays an important role and may serve as a biomarker for the clinical treatment of patients with 5-FU-resistant colon cancer.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"44"},"PeriodicalIF":2.5,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907774","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":"Midkine promotes thyroid cancer cell migration and invasion by activating the phosphatidylinositol 3 kinase/protein kinase B/mammalian target of rapamycin pathway.","authors":"Li Yuan, Ping Zhou, Wengang Liu, Liqing Jiang, Mengwen Xia, Yongfeng Zhao","doi":"10.25259/Cytojournal_47_2024","DOIUrl":"10.25259/Cytojournal_47_2024","url":null,"abstract":"<p><strong>Objective: </strong>Thyroid cancer (TC) therapy, which is routinely used at present, can improve patients' survival rates. However, lymph node metastasis results in a higher degree of TC malignancy in patients who experience recurrence and/or death. The elucidation of new mechanisms of TC metastasis can help identify new therapeutic targets. Midkine (MDK) is expressed aberrantly in various cancers. However, the regulatory mechanisms of MDK in TC remain largely unknown. Hence, this study mainly explores the effect and molecular function of MDK in TC.</p><p><strong>Material and methods: </strong>MDK gene expression and protein levels were analyzed using the Gene Expression Profiling Interactive Analysis and the Human Protein Atlas online databases. MDK messenger RNA (mRNA) in TC was analyzed by quantitative real-time polymerase chain reaction. MDK, phosphatidylinositol 3 kinase (PI3K), phosphorylated AKT (p-AKT), and phosphorylated mammalian target of rapamycin (p-mTOR) protein in TC were analyzed by Western blotting. Transwell and wound healing assays were performed to evaluate TC cell metastasis.</p><p><strong>Results: </strong>MDK mRNA was significantly highly expressed in most patients with TC (<i>P <</i> 0.05). Moreover, MDK gene expression levels correlated with different TC stages. MDK protein was negative in normal tissues and positive in TC tissues. MDK mRNA and protein were significantly highly expressed in TC cells (<i>P <</i> 0.01). Compared with metastasis in the control group, that in the MDK group is significantly suppressed by MDK knockdown (<i>P</i> < 0.001). MDK knockdown also significantly inhibited PI3K, p-AKT, and p-mTOR protein expression in TPC-1 and K1 cells (<i>P <</i> 0.001). The activation of PAmT-P significantly enhanced the PI3K, p-AKT, and p-mTOR protein expression in TPC-1 and K1 cells (<i>P <</i> 0.001) and promoted metastasis (<i>P <</i> 0.001), thereby disrupting the inhibitory effect of the MDK knockdown.</p><p><strong>Conclusion: </strong>Our findings confirmed that MDK promotes TC migration and invasion by activating PAmT-P. MDK is a novel molecular target for the treatment of patients with metastatic TC.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"41"},"PeriodicalIF":2.5,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907835","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":"Increased caveolin 1 by human antigen R exacerbates <i>Porphyromonas gingivali</i>-induced atherosclerosis by modulating oxidative stress and inflammatory responses.","authors":"Fang Miao, Yangyang Lei, Yunfei Guo, Yongxia Ma, Ye Zhang, Binbin Jia","doi":"10.25259/Cytojournal_76_2024","DOIUrl":"10.25259/Cytojournal_76_2024","url":null,"abstract":"<p><strong>Objective: </strong>Many different types of infectious oral diseases have been identified clinically, including chronic periodontitis. <i>Porphyromonas gingivalis</i> is the main pathogen causing chronic periodontitis, which is closely related to atherosclerosis (AS) and can promote the expression levels of caveolin 1 (Cav-1) and induced ribonucleic acid (RNA)-binding protein human antigen R (HuR). However, the roles of Cav-1 and its relationship with HuR in <i>P. gingivalis</i>-mediated AS progression remain largely unknown. Here, we aimed to detect the role and molecular mechanisms of Cav-1 in <i>P. gingivalis</i>-mediated AS.</p><p><strong>Material and methods: </strong>To investigate the role of Cav-1 in <i>P. gingivalis</i>-mediated AS, we infected human umbilical vein endothelial cells (HUVECs) with <i>P. gingivalis</i> at a multiplicity of infection of 100:1 for 6, 12, and 24 h to simulate <i>P. gingivalis-</i>induced AS models <i>in vitro</i> and then transfected them with Cav-1 small interfering RNA to silence Cav-1. Combining molecular biology experimental techniques such as cell counting kit-8 assay, enzyme-linked immunosorbent assay, immunofluorescence staining, flow cytometry, Western blotting, and Oil Red O staining, and apolipoprotein E-deficient AS model mice, the impacts of Cav-1 on cell viability, inflammation, oxidative stress, apoptosis, Cav-1 and intercellular cell adhesion molecule-1 (ICAM-1) levels, and atherosclerotic plaque formation were investigated. Then, the relationship between Cav-1 and HuR was investigated through biotin pull-down and RNA immunoprecipitation assays, reverse transcription quantitative polymerase chain reaction, and Western blot.</p><p><strong>Results: </strong><i>P. gingivalis</i> can induce Cav-1 expression in a time- and dose-dependent manner (<i>P</i> < 0.05). This effect can inhibit the proliferation of HUVECs (<i>P</i> < 0.05). Cav-1 interference repressed inflammatory response, reactive oxygen species (ROS) and ICAM-1 levels, and apoptosis in the HUVECs (<i>P</i> < 0.05). Cav-1 messenger RNA was stabilized by HuR, which can bind to the 3' untranslated region of Cav-1. Increase in HuR level reversed the effects of Cav-1 silencing on ROS and ICAM-1 levels and apoptosis in the HUVECs (<i>P</i> < 0.05). In addition, the levels of inflammatory response, oxidative stress, and atherosclerotic plaque formation induced by <i>P. gingivalis</i> in the mouse model were significantly reduced after Cav-1 expression was inhibited (<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>HuR-activated Cav-1 may promote atherosclerotic plaque formation by modulating inflammatory response and oxidative stress, leading to AS.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"42"},"PeriodicalIF":2.5,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11683369/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142907830","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":"Single-cell RNA sequencing analysis reveals the role of TXNDC5 in keloid formation.","authors":"Zhikun Liu, Lining Xian, Jianmin Li, Shudan Zheng, Hongju Xie","doi":"10.25259/Cytojournal_58_2024","DOIUrl":"10.25259/Cytojournal_58_2024","url":null,"abstract":"<p><strong>Objective: </strong>Thioredoxin domain-containing protein 5 (TXNDC5) is associated with fibrosis in a variety of organs, but its mechanism of action in keloid is unclear. In this study, we aimed to investigate the mechanism of TXNDC5 in keloid.</p><p><strong>Material and methods: </strong>Single-cell RNA sequencing data of keloid and normal scar samples obtained from public databases were normalized and clustered using the Seurat package. Pathway enrich analysis was conducted using biological process enrichment analysis and Gene Set Enrichment Analysis (GSEA). In addition, TXNDC5 expression and its effects on migration and invasion of keloid fibroblasts (KFs) were validated based on cell function experiments.</p><p><strong>Results: </strong>A total of five cell types were obtained. The KF clusters were further clustered into two fibroblast subtypes (Fibroblast cells 1 and Fibroblast cells 2). Biological process enrichment analysis showed that transforming growth factor beta (TGF-β) signaling pathway was enriched in the two fibroblast subtypes. GSEA analysis demonstrated that genes in TGF-β signaling pathway were mainly enriched in Fibroblast cells 1, and that genes involved in cell proliferation, migration, and the TGF-β signaling pathway were all high-expressed in fibroblast cells 1. TXNDC5 was positively correlated with fibroblast proliferation, migration and TGF-β signaling pathway, and AUCell score. The cellular experiment confirmed that the messenger RNA and protein levels of TXNDC5 and TGF-β1 were high-expressed in KFs cells (<i>P</i><0.001), and that knockdown of TXNDC5 downregulated TGF-β1 expression and inhibited migration and invasion of KFs (<i>P</i><0.0001).</p><p><strong>Conclusion: </strong>Our study indicated that TGF-β signaling pathway was enriched in fibroblast cells, and TXNDC5 was positively correlated with proliferation, migration, and TGF-β signaling pathway. Cellular experiment demonstrated that knocking down TXNDC5 downregulated TGF-β1 expression, and suppressed migration and invasion of KFs. The current discoveries provided a new therapeutic strategy for the treatment of keloid.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"40"},"PeriodicalIF":2.5,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574684/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142677631","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":"Newcastle disease virus promotes pyroptosis in medulloblastoma cells by regulating interferon-gamma-mediated guanylate-binding protein 1 expression and activating caspase-4.","authors":"Pengwu Ren, Jiayan Yu, Dongxiang Wang, Lijuan Zeng, Xianqiang Zhang, Xiaohe Liu, Yongfu Cao, Zijian Hu, Xiaoyong Zhao, Kongbin Yang","doi":"10.25259/Cytojournal_39_2024","DOIUrl":"10.25259/Cytojournal_39_2024","url":null,"abstract":"<p><strong>Objective: </strong>The literature has reported that Newcastle disease virus (NDV) can have inhibitory effects on various tumors. This study aims to investigate the mechanism by which NDV induces pyroptosis in medulloblastoma (MB) cells.</p><p><strong>Material and methods: </strong>We treated MB cell lines Daoy and D283 with NDV or recombinant interferon-gamma (IFN-g) proteins. Guanylate-binding proteins (GBPs) were measured using real-time quantitative polymerase chain reaction. Small interfering RNA-specific targeting <i>GBP1</i> was transfected into MB cells. Apoptosis was assessed using Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nucleoside nick end labeling and flow cytometry assays. Pyroptosis-related proteins, including caspase-4, caspase-1, and gasdermin D (GSDMD), were detected using Western blotting.</p><p><strong>Results: </strong>Bioinformatics analysis revealed that GBP family genes and interferon-related genes might be responsive to NDV stimulation in MB cells. Treatment with NDV resulted in increased IFN-g levels and upregulated GBP expression, particularly <i>GBP1</i>. In addition, IFN-g treatment induced <i>GBP1</i> expression and enhanced cell apoptosis. <i>GBP1</i> knockdown attenuated the decreased cell proliferation and increased cell apoptosis induced by NDV in MB cells. <i>GBP1</i> overexpression upregulated the expression of pyroptosis-related proteins, including caspase-4, caspase-1, and GSDMD, subsequently leading to inhibition of cell proliferation and an increase in cell apoptosis levels. The silencing of caspase-4 confirmed the regulatory role of <i>GBP1</i> in MB cell pyroptosis.</p><p><strong>Conclusion: </strong>Our findings suggest that NDV elevates IFN-g and <i>GBP1</i> expression in MB cells, potentially contributing to caspase-4-mediated pyroptosis activation.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"39"},"PeriodicalIF":2.5,"publicationDate":"2024-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574683/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142677630","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":"Gray zone Bethesda category III - Atypia of undetermined significance lesions of the thyroid: Potential diagnostic issues and image morphometry as a useful adjunct to cytomorphology.","authors":"Tarunpreet Saini, Reetu Kundu, Manish Rohilla, Parikshaa Gupta, Nalini Gupta, Radhika Srinivasan, Uma Nahar Saikia, Pranab Dey","doi":"10.25259/Cytojournal_86_2023","DOIUrl":"10.25259/Cytojournal_86_2023","url":null,"abstract":"<p><strong>Objective: </strong>Atypia of undetermined significance (AUS) is an indeterminate category which presents a significant challenge for pathologists and clinicians. The management options are dependent on the rate of malignancy for a given populace.</p><p><strong>Material and methods: </strong>This is a retrospective analysis of 61 cases of the AUS Bethesda category III with grouping into neoplastic and non-neoplastic according to the histopathology data and clinical follow-up. Detailed cytomorphological features were analyzed and image morphometry was done using image J software. Student's <i>t</i>-test was used.</p><p><strong>Results: </strong>Out of the total 61 cases, 35 were neoplastic cases of AUS (histopathology proven), and 26 were non-neoplastic (on follow-up) cases. The risk of neoplasia and risk of malignancy observed were 57.4% and 47.5%, respectively. Neoplastic cases displayed prominent intranuclear inclusions (54%) and pseudopapillary clusters (20%). Majority of non-neoplastic cases revealed fine chromatin (96%) and pale chromatin (4%) while among neoplastic cases, 14% showed pale chromatin. Neoplastic cases showed moderate to marked nuclear pleomorphism (20%) compared to non-neoplastic cases which were monomorphic to mildly pleomorphic. None of the non-neoplastic cases exhibited frequent nuclear overlapping, nuclear grooving, or nucleoli which emphasizes the need for scrutiny of smears for these features. On image morphometry, cases with malignant outcome had larger nuclear area, perimeter, diameter, and nuclear density which were statistically significant.</p><p><strong>Conclusion: </strong>The study illustrates the importance of identifying subtle cytomorphological features and usefulness of image morphometry as an adjunctive objective tool in AUS cases. This helps in making an accurate cytological diagnosis which guides the treating clinician regarding surgical management or need for clinical follow-up.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"38"},"PeriodicalIF":2.5,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142677629","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":"Effect of 5-Aza-2'-deoxycytidine on T-cell acute lymphoblastic leukemia cell biological behaviors and PTEN expression.","authors":"Yan Li, Zhenwei Jia, Xiaoyang Kong, Hongbo Zhao, Xiaoyan Liu, Guirong Cui, Jianmin Luo","doi":"10.25259/Cytojournal_31_2024","DOIUrl":"10.25259/Cytojournal_31_2024","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Objective: &lt;/strong&gt;We currently face a sharp increase of T-cell acute lymphoblastic leukemia (T-ALL) incidence and a challenge of unmasking its complex etiology. The deoxycytidine analog 5-Aza-2'-deoxycytidine (5-Aza-dC) is currently the most common nucleoside methyltransferase inhibitor. The objective of this study was to clarify the role of 5-Aza-dC in T-ALL cell biological behaviors and phosphatase and tensin homolog deleted on chromosome ten (PTEN) expression.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Material and methods: &lt;/strong&gt;T-ALL cell lines were divided into the experimental group with 5-Aza-dC solution treatment, and the control group without treatment. PTEN methylation was detected using methylation-specific polymerase chain reaction (MS-PCR). Following the measurement of cell proliferation, viability, apoptosis, invasion, migration, etc., quantitative reverse transcription-polymerase chain reaction (PCR) was conducted to detect PTEN, DNA methyl-transferases (DNMT1), DNMT3a, MBD2, and MeCP2 expressions; Western blot to detect PTEN, PI3K, AKT, and mTOR protein expressions. In addition, rescue experiments to inhibit and restore the expression of PTEN in different groups were performed for further identification of the results in the former parts.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;MS-PCR results showed that in Jurkat cells, the target band was amplified using methylated primers for the PTEN gene promoter region; moreover, at 10 μmol/L of 5-Aza-dC for 24 h, PTEN methylation was completely removed without any un-methylated band observed. The experimental group had significantly lower cell proliferation and viability rates, higher apoptosis rates, decreased cell proportion in S phase, reduced invasion and migration; increased PTEN expression, decreased DNMT1, DNMT3a, MBD2, and MeCP2 mRNA expressions; and decreased PI3K, AKT, and mTOR protein expressions than those in the control group (all &lt;i&gt;P&lt;/i&gt; &lt; 0.05). Furthermore, according to the rescue experiment, silenced PTEN expression weakened the beneficial roles of 5-Aza-dC treatment, and resulted in significantly higher cell proliferation and viability rates, lower apoptosis rates, increased cell proportion in S phase, increased cell invasion and migration; decreased PTEN expression, elevated DNMT1, DNMT3a, MBD2, and MeCP2 mRNA expressions, and higher PI3K, AKT, and mTOR protein expressions (all &lt;i&gt;P&lt;/i&gt; &lt; 0.05). While restored PTEN expression enhanced functions of 5-Aza-dC treatment, leading to obviously lower cell proliferation and viability rates, higher apoptosis rates, increased cell proportion in G1 phase, and reduced cell invasion and migration; as well as increased PTEN expression, decreased DNMT1, DNMT3a, MBD2, and MeCP2 mRNA expressions, and lower PI3K, AKT, and mTOR protein expressions (all &lt;i&gt;P&lt;/i&gt; &lt; 0.05).&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;Demethylation treatment with 5-Aza-dC can inhibit T-ALL cell malignant biological behaviors and enhance the sensitivity to chemotherapy agents possibly, whic","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"36"},"PeriodicalIF":2.5,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142677521","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":"Development of a clinical prediction model for pathological upgrading in low-grade squamous intraepithelial lesions following cervical conization.","authors":"Xinrui Peng, Jiayuan Wan, Yafei Wang, Liqun Wang","doi":"10.25259/Cytojournal_7_2024","DOIUrl":"10.25259/Cytojournal_7_2024","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to identify key factors influencing post-operative pathologic escalation in Chinese women with histologic cervical low-grade squamous intraepithelial lesions (LSILs) undergoing cervical conization and construct a predictive nomogram model.</p><p><strong>Material and methods: </strong>A retrospective analysis was conducted on 107 patients with LSIL from Bengbu City, Anhui Province, China, who underwent cervical conization at the First Affiliated Hospital of Bengbu Medical College from January 2019 to January 2023. Patients were categorized into groups based on post-operative pathological upgrade. Univariate and multivariate logistic regression analyses identified independent risk factors. A nomogram model was developed and evaluated for clinical predictive ability using calibration curves, the Hosmer-Lemeshow test, and decision curve analysis (DCA).</p><p><strong>Results: </strong>Post-operative pathological upgrades were experienced by 39.3% of patients with LSIL. Independent risk factors for escalation included positive human papillomavirus (HPV)16/18/52/53/58 high-risk types (<i>P</i> < 0.05, OR = 4.95, 95% CI = 1.32-18.46), ThinPrep Cytology Test (TCT) results indicating high-grade squamous intraepithelial lesion (HSIL)/atypical squamous cells, cannot exclude a high-grade squamous intraepithelial lesion (ASC-H)/atypical glandular cells ( AGC) (<i>P</i> < 0.01, OR = 13.12, 95% CI = 3.10-55.50), and cervical transformation zone (TZ) type III (<i>P</i> < 0.05, OR = 6.10, 95% CI = 1.65-22.56). Based on these factors, the nomogram demonstrated good differentiation and calibration (area under the curve [AUC]: 0.744, 95% CI: 0.674-0.839). DCA indicated high clinical predictive value.</p><p><strong>Conclusion: </strong>HPV16/18/52/53/58 high-risk types, TCT HSIL/ASC-H/AGC, and colposcopic cervical TZ type III are independent risk factors for post-operative pathologic escalation in LSIL. Consideration of pre-operative HPV, TCT results, and cervical TZ type is crucial for effective triage and patient management. The constructed nomogram provides a practical tool for risk assessment of patients with LSIL undergoing cervical conization.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"37"},"PeriodicalIF":2.5,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574685/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142677558","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 of basaloid scalp lesion: Potential diagnostic pitfall.","authors":"Casem Ballouk, Sama Alazawi, Mir Yousufuddin Ali Khan, Vinod B Shidham","doi":"10.25259/Cytojournal_81_2023","DOIUrl":"10.25259/Cytojournal_81_2023","url":null,"abstract":"","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"35"},"PeriodicalIF":2.5,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574682/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142677628","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 mechanism of L1 cell adhesion molecule interacting with protein tyrosine kinase 2 to regulate the focal adhesion kinase-growth factor receptor-bound protein 2-son of sevenless-rat sarcoma pathway in the identification and treatment of type I high-risk endometrial cancer.","authors":"Wei He, Wei Liu, Xiumei Liu, Wenhua Tan","doi":"10.25259/Cytojournal_50_2024","DOIUrl":"10.25259/Cytojournal_50_2024","url":null,"abstract":"<p><strong>Objective: </strong>The objective of this study was to investigate how L1 cell adhesion molecule (L1CAM) interacting with protein tyrosine kinase 2 (PTK2) affects endometrial cancer (EC) progression and determine its association with the focal adhesion kinase (FAK)-growth factor receptor-bound protein 2 (GRB2)-son of sevenless (SOS)-rat sarcoma (RAS) pathway. EC is a female cancer of major concern in the world, and its incidence has increased rapidly in recent years. L1CAM is considered a reliable marker of poor prognosis in patients with EC.</p><p><strong>Material and methods: </strong>A single-center and prospective study was conducted using data from the Cancer Genome Atlas and samples from normal and EC tissues to explore the differential expression of L1CAM. Additional experimental models included human immortalized endometrial epithelium cells (hEECs) and EC cell lines such as KLE, RL95-2, and Ishikawa. L1CAM expression was regulated using lentiviruses designed for either overexpression or interference, and PTK2/focal adhesion kinase (FAK) signaling was inhibited with PF431396. Transfected KLE cells were injected into mice, and tumor growth was monitored over 14 days. Cellular proliferation and survival were assessed using cell counting kit, colony formation, and terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate (dUTP) nick-end labeling assays. Metastatic behavior was evaluated through Transwell assays for cell migration and invasion. The expression levels of matrix metallopeptidase (MMP) 2 and MMP9 were determined by Western blot. In addition, the activation of the FAK-GRB2-SOS-RAS pathway was examined by assessing the protein levels of FAK, GRB2, SOS, and RAS.</p><p><strong>Results: </strong>There was a significant difference in L1CAM expression between EC tumor tissues and normal tissues, and L1CAM messenger RNA (1.85-fold) and L1CAM protein (2.59-fold) were significantly more expressed in EC tissues (<i>P</i> < 0.01) than in normal tissues. The tumor growth of L1CAM overexpressing EC cells was faster than that of negative control EC cells (6.43 fold; <i>P</i> < 0.001). L1CAM promoted the expression of FAK (1.43-2.72-fold; <i>P</i> < 0.001); enhanced EC cell proliferation (<i>P</i> < 0.01), survival and motility (<i>P</i> < 0.001), migration (<i>P</i> < 0.001), and invasion (<i>P</i> < 0.001); and activated the FAK-GRB2-SOS-RAS pathway, all of which were reversed when FAK expression was not upregulated (<i>P</i> < 0.001).</p><p><strong>Conclusion: </strong>By upregulating PTK2 and its encoded protein FAK, L1CAM was found to promote tumor progression and increase the activation of the FAK-GRB2-SOS-RAS pathway. These findings establish L1CAM and PTK2 as reference genes for poor prognostic prediction in EC and as targets for EC therapy, providing a valuable basis for distinguishing between benign and malignant endometrial conditions and justifying the necessity of targeted therapeutic approaches.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"21 ","pages":"34"},"PeriodicalIF":2.5,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11574687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142677632","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}