Analytical Cellular Pathology最新文献

{"title":"The Clinical and Pathological Effects of Serum C3 Level and Mesangial C3 Intensity in Patients with IgA Nephropathy","authors":"Xiaoyue Hou, Yanan Liang, Weiwei Zhang, Rong Li","doi":"10.1155/2024/8889306","DOIUrl":"https://doi.org/10.1155/2024/8889306","url":null,"abstract":"<i>Objective</i>. To investigate the clinical and pathological effects of serum C3 level, mesangial C3 deposition intensity and blood lipid on IgA nephropathy. <i>Methods</i>. According to the deposition intensity of immunofluorescence (IF) complement C3 in mesangial region, a total of 151 patients were divided into: (1) negative group (65 cases), (2) weak positive group (51 cases), and (3) strong positive group (35 cases). According to the level of serum C3, the patients were divided into two groups: (1) 33 patients with decreased serum C3 (<85 mg/dL); (2) 118 patients with normal serum C3. The clinicopathological data of the patients were analyzed retrospectively according to the groups. <i>Results</i>. (1) With the increase of C3 deposition in mesangial region, the mean value of serum C3 level decreased, and the difference was statistically significant (<span><svg height=\"8.8423pt\" style=\"vertical-align:-0.2064009pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.6359 19.289 8.8423\" width=\"19.289pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,0,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,11.658,0)\"></path></g></svg><span></span><span><svg height=\"8.8423pt\" style=\"vertical-align:-0.2064009pt\" version=\"1.1\" viewbox=\"22.8711838 -8.6359 28.182 8.8423\" width=\"28.182pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,22.921,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,29.161,0)\"></path></g><g transform=\"matrix(.013,0,0,-0.013,32.125,0)\"><use xlink:href=\"#g113-49\"></use></g><g transform=\"matrix(.013,0,0,-0.013,38.365,0)\"><use xlink:href=\"#g113-49\"></use></g><g transform=\"matrix(.013,0,0,-0.013,44.605,0)\"></path></g></svg>).</span></span> (2) Compared with the normal serum C3 group, the blood urea nitrogen (BUN), serum creatinine (Scr), and albumin (Alb) in the serum C3 decreased group were higher, and the differences were statistically significant (<span><svg height=\"9.2729pt\" style=\"vertical-align:-0.6370001pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.6359 19.289 9.2729\" width=\"19.289pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,0,0)\"><use xlink:href=\"#g113-81\"></use></g><g transform=\"matrix(.013,0,0,-0.013,11.658,0)\"></path></g></svg><span></span><span><svg height=\"9.2729pt\" style=\"vertical-align:-0.6370001pt\" version=\"1.1\" viewbox=\"22.8711838 -8.6359 21.918 9.2729\" width=\"21.918pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"><g transform=\"matrix(.013,0,0,-0.013,22.921,0)\"><use xlink:href=\"#g113-49\"></use></g><g transform=\"matrix(.013,0,0,-0.013,29.161,0)\"><use xlink:href=\"#g113-47\"></use></g><g transform=\"matrix(.013,0,0,-0.013,32.125,0)\"><use xlink:href=\"#g113-49\"></use></g><g transform=\"matrix(.013,0,0,-0.013,38.365,0)\"></path></g></svg>),</span></span> while the fasting blood glucose (FBG), low-densi","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"1 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139078014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNM3OS Enhances the Apoptosis and Senescence of Spermatogonia Associated with Nonobstructive Azoospermia by Providing miR-214-5p and Decreasing E2F2 Expression","authors":"Rui Hua, Qingjun Chu, Feiyan Guo, Qinjie Chen, Maocai Li, Xuan Zhou, Yongtong Zhu","doi":"10.1155/2023/1477658","DOIUrl":"https://doi.org/10.1155/2023/1477658","url":null,"abstract":"<i>Background</i>. Nonobstructive azoospermia (NOA) is a complex disease characterized by the spermatogenic dysfunction of testicular tissues. The roles played by long noncoding RNAs (lncRNAs) in NOA pathogenesis have not been extensively studied. <i>Methods</i>. Microarray assays were performed on samples of testicular biopsy tissue obtained from patients with NOA for the purpose of identifying differentially expressed lncRNAs and messenger RNA (mRNA) transcripts, and the results were verified by quantitative real-time polymerase chain reaction. Mouse-derived GC-1 spermatogonia (spg) cells undergoing treatment with Adriamycin (ADR) were used to investigate the biological functions of the selected lncRNAs <i>in vitro</i>. The target microRNAs (miRNAs) of lncRNAs and the target mRNAs of miRNAs were predicted by a bioinformatics analysis. Functional studies performed using the CCK-8 assay, EdU incorporation assay, apoptosis detection, and senescence-associated <i>β</i>-galactosidase (SA-<i>β</i>-Gal) staining were conducted using GC-1 spg cells. <i>Results</i>. Totals of 2,652 lncRNAs and 2,625 mRNAs were found to be differentially expressed in the testicular tissue of NOA patients when compared with patients in a control group. Dynamin 3 opposite strand (DNM3OS) was a provider of pe-miR-214-5p that positively regulates miR-214-5p expression in GC-1 spg cells. The E2 factor (E2F) family of transcription factor 2 (E2F2) was initially predicted and subsequently verified to be a downstream gene of miR-214-5p. E2F2 expression was upregulated after DNM3OS knockdown in ADR-treated GC-1 spg cells. Moreover, knockdown of either DNM3OS or miR-214-5p significantly alleviated ADR-induced decreases in cellular activity and proliferation, as well as increases in apoptosis and senescence of mouse spermatogonial GC-1 spg cells. <i>Conclusions</i>. DNM3OS was found to regulate the apoptosis and senescence of spermatogonia by providing miR-214-5p and decreasing E2F2 expression, suggesting it as a novel target for gene therapy of male infertility.","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"39 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2023-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138820506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Luteolin Pretreatment Ameliorates Myocardial Ischemia/Reperfusion Injury by lncRNA-JPX/miR-146b Axis","authors":"Tongda Xu, Yuanyuan Zhang, Gege Liao, Haochen Xuan, Jie Yin, Jieli Bao, Yang Liu, Dongye Li","doi":"10.1155/2023/4500810","DOIUrl":"https://doi.org/10.1155/2023/4500810","url":null,"abstract":"&lt;i&gt;Background&lt;/i&gt;. In the present study, we aimed to find out whether luteolin (Lut) pretreatment could ameliorate myocardial ischemia/reperfusion (I/R) injury by regulating the lncRNA just proximal to XIST (JPX)/microRNA-146b (miR-146b) axis. &lt;i&gt;Methods&lt;/i&gt;. We established the models &lt;i&gt;in vitro&lt;/i&gt; (HL-1 cells) and &lt;i&gt;in vivo&lt;/i&gt; (C57BL/6J mice) to certify the protection mechanism of Lut pretreatment on myocardial I/R injury. Dual luciferase reporter gene assay was utilized for validating that JPX could bind to miR-146b. JPX and miR-146b expression levels were determined by RT-qPCR. Western blot was utilized to examine apoptosis-related protein expression levels, including cleaved caspase-9, caspase-9, cleaved caspase-3, caspase-3, Bcl-2, Bax, and BAG-1. Apoptosis was analyzed by Annexin V-APC/7-AAD dualstaining, Hoechst 33342 staining, as well as flow cytometry. Animal echocardiography was used to measure cardiac function (ejection fraction (EF) and fractional shortening (FS) indicators). &lt;i&gt;Results&lt;/i&gt;. miR-146b was demonstrated to bind and recognize the JPX sequence site by dual luciferase reporter gene assay. The expression level of miR-146b was corroborated to be enhanced by H/R using RT-qPCR (&lt;span&gt;&lt;svg height=\"9.2729pt\" style=\"vertical-align:-0.6370001pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.6359 19.289 9.2729\" width=\"19.289pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,0,0)\"&gt;&lt;/path&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,11.658,0)\"&gt;&lt;/path&gt;&lt;/g&gt;&lt;/svg&gt;&lt;span&gt;&lt;/span&gt;&lt;svg height=\"9.2729pt\" style=\"vertical-align:-0.6370001pt\" version=\"1.1\" viewbox=\"22.8711838 -8.6359 28.182 9.2729\" width=\"28.182pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,22.921,0)\"&gt;&lt;/path&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,29.161,0)\"&gt;&lt;/path&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,32.125,0)\"&gt;&lt;use xlink:href=\"#g113-49\"&gt;&lt;/use&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,38.365,0)\"&gt;&lt;use xlink:href=\"#g113-49\"&gt;&lt;/use&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,44.605,0)\"&gt;&lt;/path&gt;&lt;/g&gt;&lt;/svg&gt;&lt;/span&gt; vs. Con). Moreover, JPX could reduce the expression of miR-146b, whereas inhibiting JPX could reverse the alteration (&lt;span&gt;&lt;svg height=\"9.2729pt\" style=\"vertical-align:-0.6370001pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.6359 19.289 9.2729\" width=\"19.289pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,0,0)\"&gt;&lt;use xlink:href=\"#g113-81\"&gt;&lt;/use&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,11.658,0)\"&gt;&lt;use xlink:href=\"#g117-91\"&gt;&lt;/use&gt;&lt;/g&gt;&lt;/svg&gt;&lt;span&gt;&lt;/span&gt;&lt;svg height=\"9.2729pt\" style=\"vertical-align:-0.6370001pt\" version=\"1.1\" viewbox=\"22.8711838 -8.6359 28.182 9.2729\" width=\"28.182pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,22.921,0)\"&gt;&lt;use xlink:href=\"#g113-49\"&gt;&lt;/use&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,29.161,","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"9 11","pages":""},"PeriodicalIF":3.2,"publicationDate":"2023-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138508950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Depletion of lncRNA MEG3 Ameliorates Imatinib-Induced Injury of Cardiomyocytes via Regulating miR-129-5p/HMGB1 Axis.","authors":"Peng Tang, Jinjian Zhou, Huagang Liu, Shenglan Mei, Kai Wang, Hao Ming","doi":"10.1155/2023/1108280","DOIUrl":"https://doi.org/10.1155/2023/1108280","url":null,"abstract":"<p><p>Imatinib is a classical targeted drug to treat chronic myeloid leukemia (CML). However, it shows cardiotoxicity, which limits its clinical application. Long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) shows proapoptotic properties in human cells. This study is performed to investigate whether targeting MEG3 can attenuate imatinib-mediated cardiotoxicity to cardiomyocytes. In this work, H9c2 cells were divided into four groups: control group, hypoxia group, hypoxia + imatinib, and hypoxia + imatinib + MEG3 knockdown group. MEG3 and microRNA-129-5p (miR-129-5p) expression levels were detected by the quantitative real-time PCR (qRT-PCR). The viability and apoptosis of H9c2 cells were then evaluated by cell counting kit-8 (CCK-8), flow cytometry, and TUNEL assays. The targeting relationships between MEG3 and miR-129-5p, between miR-129-5p and high-mobility group box 1 (HMBG1), were validated by dual-luciferase reporter assay and RNA Immunoprecipitation (RIP) assay. The protein expression level of HMGB1 was detected by western blot. It was revealed that, Imatinib-inhibited cell viability and aggravated the apoptosis of H9c2 cells cultured in hypoxic condition, and MEG3 knockdown significantly counteracted this effect. MiR-129-5p was a downstream target of MEG3 and it directly targeted HMGB1, and knockdown of MEG3 inhibited HMGB1 expression in H9c2 cells. In conclusion, targeting MEG3 ameliorates imatinib-induced injury of cardiomyocytes via regulating miR-129-5p/HMGB1 axis.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2023 ","pages":"1108280"},"PeriodicalIF":3.2,"publicationDate":"2023-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10673670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138463948","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":"Inhibitory Effect of β-Sitosterol on the Ang II-Induced Proliferation of A7r5 Aortic Smooth Muscle Cells","authors":"Yuankun Chen, Shumiao He, Ao Zeng, Siqing He, Xiaobao Jin, Chunmei Li, Wenjie Mei, Qun Lu","doi":"10.1155/2023/2677020","DOIUrl":"https://doi.org/10.1155/2023/2677020","url":null,"abstract":"Context. Excessive proliferation of vascular smooth muscle cells (VSMCs) plays a critical role in the development of cardiovascular diseases. β-Sitosterol exerts protective effects against the cardiovascular disease. However, whether β-sitosterol protects against the excessive proliferation of VSMCs remain unclear. Objective. To explore the effects of β-sitosterol on VSMC proliferation. Materials and Methods. A7r5 cells were pretreated with 2 µM angiotensin II (Ang II) for 24 hr to establish an excessive VSMC proliferation model, followed by treatment with β-sitosterol for 24 hr. Cells were divided into five groups: control, Ang II, and Ang II + β-sitosterol (2, 4, 8 µM). CCK-8 assay, flow cytometry, and Ad-mCherry-GFP-LC3B assay analyzed cell proliferation, cell cycle, cell apoptosis, and autophagic flux. Additionally, the expression of proteins was detected by the western blotting. Results. β-Sitosterol effectively inhibited Ang II-induced A7r5 cell proliferation (IC50 : 6.841 µM at 24 hr). It achieved this by arresting cell cycle progression, promoting apoptosis, inhibiting autophagy, and suppressing the contractile–synthetic phenotypic switch. Mechanistically, β-sitosterol downregulated PCNA, Cyclin D1, and Bcl-2, while upregulating pro-caspase 3, cleaved-caspase 3, and Bax to induce cell cycle arrest and apoptosis. Additionally, it suppressed the contractile–synthetic phenotypic transformation by downregulating OPN and upregulating α-SMA. The Ad-mCherry-GFP-LC3B Assay and western blotting revealed β-sitosterol’s autophagy inhibitory effects by downregulating LC3, ULK1, and Beclin-1 while upregulating P62 expression. Discussion and Conclusion. This study found for the first time that β-sitosterol could inhibit the proliferation of A7r5 cells induced by Ang II. β-Sitosterol treatment may be recommended as a therapeutic strategy to prevent the cardiovascular diseases.","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"37 11","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135432768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL16 Inhibits the Malignant Progression of Epithelial Ovarian Cancer through the lncRNA MALAT1/<i>β</i>-Catenin Axis.","authors":"Changshu Li,&nbsp;Ji Liu,&nbsp;Yuanyuan Lyu,&nbsp;Shizhang Ling,&nbsp;Yonghong Luo","doi":"10.1155/2023/9952234","DOIUrl":"https://doi.org/10.1155/2023/9952234","url":null,"abstract":"<p><p>Epithelial ovarian cancer (EOC) ranks third in the incidence of gynecological malignancies. m6A methylation as RNA modification plays a crucial role in the evolution, migration, and invasion of various tumors. However, the role of m6A methylation in ovarian cancer (OC) only recently has begun to be appreciated. Therefore, we used various bioinformatic methods to screen the public GEO datasets of epithelial ovarian cancer (EOC) for m6A methylation-related regulators. We identified methyltransferase 16 (METTL16) that was dramatically downregulated in EOC as such a regulator. We also identified metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a known target lncRNA of METTL16, in these five GEO datasets. RT-qPCR and immunohistochemical staining confirmed that compared with the normal ovarian tissues and cells, METTL16 was significantly downregulated, while lncRNA MALAT1 was significantly upregulated, in 30 EOC tissues of our own validation cohorts and EOC cell lines, revealing a negative correlation between METTL16 and lncRNA MALAT1. Moreover, our analysis unveiled a correlation between downregulated METTL16 and the known adverse prognostic factors of EOC patients in our own cohorts. The CCK-8, EdU, scratch wound healing, and transwell invasion assays revealed that METTL16 significantly suppressed the proliferating, migrating, and invading abilities of OC cells. The inhibitory effects of METTL16 on the in vivo tumor growth of EOC cells were measured by subcutaneous tumor formation assay in mice. Furthermore, the RIP, RNA stability assay, western blotting, and cytoimmunofluorescence staining showed that METTL16 hindered the growth of EOC cells through promoting the degradation of MALAT1 by binding that, in turn, upregulates <i>β</i>-catenin protein and promotes nuclear transport of <i>β</i>-catenin protein in EOC cells. This study suggests that METTL16 acts as a tumor suppressor gene of EOC by achieving its inhibitory function on the malignant progression of EOC through the METTL16/MALAT1/<i>β</i>-catenin axis that are new targets for EOC diagnosis and therapy.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2023 ","pages":"9952234"},"PeriodicalIF":3.2,"publicationDate":"2023-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10625488/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71488003","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":"Comprehensive Pan-Cancer Analysis Reveals the Potential Biological, Immunological, and Prognostic Value of NKG2A","authors":"Yao Rong, Yongfeng Wang, Mingzheng Tang, Guiqian Zhang, Yuan Yuan, Fengyuan Dong, Zhihang Wu, Guorong Ma, Songhua Liu, Xiashuang Zhao, Hui Cai","doi":"10.1155/2023/2211942","DOIUrl":"https://doi.org/10.1155/2023/2211942","url":null,"abstract":"Background. NKG2A (KLRC1) belongs to the NKG2 family, which has been shown to affect the activity of natural killer (NK) cells and CD8T cells. However, a comprehensive biological analysis and exploration of NKG2A in different cancers is lacking and this needs to be further investigated. Methods. A comprehensive pan-cancer analysis of NKG2A was performed based on multiple databases. The Cancer Genome Atlas (TCGA) and Genotype–Tissue Expression (GTEx) databases were used to analyze the expression profile of NKG2A in pan-cancer. The relevance of NKG2A to the prognosis of different cancers was assessed using Kaplan–Meier survival analysis. In addition, we explored the correlation between NKG2A expression and gene mutations, pathological staging, tumor-infiltrating immune cells (TIICs), DNA methyltransferase (DNMT) genes, tumor mutation burden (TMB), microsatellite instability (MSI), mismatch repair (MMR), and immune checkpoints (ICPs). Finally, the expression levels of NKG2A in several cancer cell lines were verified by qRT-PCR. Results. Pan-cancer comprehensive analysis showed that NKG2A expression levels were significantly different between multiple cancers and corresponding normal tissues. The differential expression of NKG2A was related to the prognosis and pathological staging of patients with multiple cancers, and was closely related to the excessive infiltration of immune cells and the regulation of ICP genes in the tumor microenvironment (TME). In addition, TMB, MSI, MMR, and DNMT genes in many cancer types are also affected by NKG2A expression. Gene set enrichment analysis (GSEA) showed that NKG2A was associated with multiple immune-related functions and pathways in malignant tumors. qRT-PCR results showed that NKG2A was underexpressed in liver, gastric, and colon cancer cell lines compared to normal cells, which was consistent with bioinformatics analysis. Conclusion. The present study suggests that NKG2A may be a potential predictive biomarker for cancer immune response and prognosis.","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"76 0","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"135510908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Low-Density Lipoprotein Contributes to Endometrial Carcinoma Cell Proliferation, Migration, and Invasion by Activating the JAK-STAT Signaling Pathway.","authors":"Lifan Shen,&nbsp;Chen Zhang,&nbsp;Kaiying Cui,&nbsp;Xin Liang,&nbsp;Genhai Zhu","doi":"10.1155/2023/4015167","DOIUrl":"https://doi.org/10.1155/2023/4015167","url":null,"abstract":"<p><strong>Background: </strong>Cholesterol-rich low-density lipoprotein (LDL) particles have been demonstrated to regulate breast cancer cell proliferation and migration, but their biological function and relevant mechanisms in endometrial carcinoma (EC) remain unclear.</p><p><strong>Methods: </strong>Serum and tissue samples were collected from EC patients (<i>n</i> = 50) and patients with benign endometrial hyperplasia (<i>n</i> = 50). Ishikawa and RL95-2 cells were stimulated with different concentrations of LDL, followed by treatment with a JAK2 inhibitor (SD-1029). LDL concentrations were determined by ELISA. The <i>in vitro</i> biological behavior of cells was examined using the CCK-8 assay, EdU staining, and Transwell assay. The tumorigenicity of LDL <i>in vivo</i> was examined using a xenograft mouse model. western blotting, immunofluorescence, and immunohistochemistry studies were performed to measure related protein expression.</p><p><strong>Results: </strong>The LDL concentrations and levels of p-JAK2 and p-STAT3 expression were elevated in the clinical samples. Similar trends in expression were detected in EC cells after LDL stimulation. LDL treatment significantly promoted EC cell proliferation, migration, and invasion, and also upregulated p-JAK2 and p-STAT3 expression in a dose-dependent manner. Moreover, SD-1029 dramatically blocked the LDL-mediated effects on EC cells. Intravenous injection of LDLs promoted tumor growth in the xenograft nude mice, and also increased p-JAK2, p-STAT3, and Ki-67 expression, and downregulated caspase-3 expression.</p><p><strong>Conclusions: </strong>These findings indicate that LDLs exert an oncogenic effect in EC cells by activating the JAK/STAT signaling pathway, and also suggest the JAK/STAT pathway as a possible therapeutic target for EC.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2023 ","pages":"4015167"},"PeriodicalIF":3.2,"publicationDate":"2023-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10611539/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71414977","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":"Comprehensive Analysis of METTLs (METTL1/13/18/21A/23/25/2A/2B/5/6/9) and Associated mRNA Risk Signature in Hepatocellular Carcinoma","authors":"Haoyu Wang, Shangshang Hu, Junjie Nie, Xiaodan Qin, Xu Zhang, Qian Wang, John Zhong Li","doi":"10.1155/2023/6007431","DOIUrl":"https://doi.org/10.1155/2023/6007431","url":null,"abstract":"Currently, 80%–90% of liver cancers are hepatocellular carcinomas (HCC). HCC patients develop insidiously and have an inferior prognosis. The methyltransferase-like (METTL) family principal members are strongly associated with epigenetic and tumor progression. The present study mainly analyzed the value of METTLs (METTL1/13/18/21A/23/25/2A/2B/5/6/9) and associated mRNA risk signature for HCC. METTLs expression is upregulated in HCC and is a poor prognostic factor in HCC. METTLs were upregulated in patients older than 60 and associated with grade. Except for METTL25, the remaining 10 genes were associated with the HCC stage, invasion depth (T). In addition, METTLs showed an overall alteration rate of 50%. Except for METTL13/2A/25/9, the expression of the other seven genes was significantly associated with overall survival, disease-specific survival, and progression-free survival. Multivariate studies have shown that METTL21A/6 can be an independent prognostic marker in HCC. A total of 664 mRNAs were selected based on Pearson correlation coefficient (R &gt; 0.5), unsupervised consensus clustering, weighted coexpression network analysis, and univariate Cox analysis. These mRNAs were significantly associated with METTLs and were poor prognostic factors in HCC patients. The least absolute shrinkage and selection operator (lasso) was used to construct the best METTLs associated with mRNA risk signature. The mRNA risk signature was significantly associated with age, stage, and t grade. The mRNA high-risk group had higher TP53 and RB1 mutations. This study constructed a nomogram with the mRNA risk profile and clinicopathological features, which could better predict the OS of individuals with HCC. We also analyzed associations between METTLs and mRNA risk signatures in epithelial-mesenchymal transition, immune checkpoints, immune cell infiltration, tumor mutational burden, microsatellite instability, cancer stem cells, tumor pathways, and drug sensitivity. In addition, this study constructed a protein interaction network network including METTLs and mRNA risk signature genes related to tumor microenvironment remodeling based on single-cell sequencing. In conclusion, this study provides a theoretical basis for the mechanism, biomarker screening, and treatment of HCC.","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"177 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136014384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine Learning Developed a Programmed Cell Death Signature for Predicting Prognosis, Ecosystem, and Drug Sensitivity in Ovarian Cancer.","authors":"Le Wang,&nbsp;Xi Chen,&nbsp;Lei Song,&nbsp;Hua Zou","doi":"10.1155/2023/7365503","DOIUrl":"10.1155/2023/7365503","url":null,"abstract":"<p><strong>Background: </strong>Ovarian cancer (OC) is the leading cause of gynecological cancer death and the fifth most common cause of cancer-related death in women in America. Programmed cell death played a vital role in tumor progression and immunotherapy response in cancer.</p><p><strong>Methods: </strong>The prognostic cell death signature (CDS) was constructed with an integrative machine learning procedure, including 10 methods, using TCGA, GSE14764, GSE26193, GSE26712, GSE63885, and GSE140082 datasets. Several methods and single-cell analysis were used to explore the correlation between CDS and the ecosystem and therapy response of OC patients.</p><p><strong>Results: </strong>The prognostic CDS constructed by the combination of StepCox (<i>n</i> = both) + Enet (alpha = 0.2) acted as an independent risk factor for the overall survival (OS) of OC patients and showed stable and powerful performance in predicting the OS rate of OC patients. Compared with tumor grade, clinical stage, and many developed signatures, the CDS had a higher C-index. OC patients with low CDS score had a higher level of CD8+ cytotoxic T, B cell, and M1-like macrophage, representing a related immunoactivated ecosystem. A low CDS score indicated a higher PD1 and CTLA4 immunophenoscore, higher tumor mutation burden score, lower tumor immune dysfunction and exclusion score, and lower tumor escape score in OC, demonstrating a better immunotherapy response. OC patients with high CDS score had a higher gene set score of cancer-related hallmarks, including angiogenesis, epithelial-mesenchymal transition, hypoxia, glycolysis, and notch signaling.</p><p><strong>Conclusion: </strong>The current study constructed a novel CDS for OC, which could serve as an indicator for predicting the prognosis, ecosystem, and immunotherapy benefits of OC patients.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2023 ","pages":"7365503"},"PeriodicalIF":3.2,"publicationDate":"2023-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10586435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49693392","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}