Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology最新文献

{"title":"MicroRNA-17-5p and MicroRNA-130b-3p Promote Radioresistance of Glioma Stem Cells by Targeting PTEN/AKT/HIF-1α Pathway-Controlled Phosphopentose Metabolism","authors":"T. Xie, Yu Ding, J. Dong, Xi-An Fu","doi":"10.1155/2023/6660072","DOIUrl":"https://doi.org/10.1155/2023/6660072","url":null,"abstract":"Background. The radioresistance of glioma stem cells (GSCs) is related to some microRNAs (miRs) generated by radiation. This study aimed to investigate the effects of miR-17-5p and miR-130b-3p on the radiosensitivity of GSCs. Methods. miR-17-5p and miR-130b-3p expressions in SU3 and SU3-5R cells were determined. SU3 cells transfected with miR-17-5p or miR-130b-3p mimics or inhibitors were used to determine cell viability after irradiation as well as to examine changes of supernatant glucose, intracellular glucose 6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6-PGDH), reduced nicotinamide adenine dinucleotide phosphate (NADPH), reduced glutathione (GSH), glutathione peroxidase (GSH-Px), phosphatase and tensin homolog (PTEN), hypoxia-inducible factor-1α (HIF-1α), glucose transporter (GLUT)-1/3, protein kinase B (AKT), and p-AKT levels. The target gene of the two miRs was verified by luciferase reporter gene assay. Results. miR-17-5p and miR-130b-3p expressions in the radiation-resistant SU3-5R cells or 8 Gy irradiation-treated SU3 cells were high. After transfection of SU3 cells with miR-17-5p or miR-130b-3p mimics, cell viability, intracellular HIF-1α, GLUT-1/3, AKT, and p-AKT protein expressions, and intracellular G6PDH, 6-PGDH, NADPH, GSH-Px, and GSH levels were high, whereas intracellular PTEN expression and supernatant glucose were low. The opposite effects were also observed in the two miR inhibitors-transfected SU3 cells. Further study confirmed that miR-17-5p or miR-130b-3p could directly bind with the PTEN. Conclusion. Radiation-induced miR-17-5p and miR-130b-3p might cause the radioresistance of GSCs, and the mechanisms were associated with the enhancement of antioxidant production, which was from the increments of AKT/HIF-1α signaling pathway-controlled glucose transmembrane transport and phosphopentose metabolism by targeting PTEN.","PeriodicalId":76996,"journal":{"name":"Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41307700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINC01614 Promotes Colorectal Cancer Cell Growth and Migration by Regulating miR-217-5p/HMGA1 Axis.","authors":"Jiwei Jia, Pei Guo, Li Zhang, Wenqing Kong, Fangfang Wang","doi":"10.1155/2023/6833987","DOIUrl":"10.1155/2023/6833987","url":null,"abstract":"<p><p>Colorectal cancer (CRC) substantially contributes to cancer-related deaths worldwide. Recently, a long non-coding RNA (lncRNA), LINC01614, has emerged as a vital gene regulator in cancer progression. Yet, how LINC01614 affects CRC progression remains enigmatic. Here, we defined LINC01614 expression in CRC, investigated the performance of CRC cells lacking LINC01614, and elucidated the underpinning mechanism. We observed that LINC01614 was upregulated in both CRC tissues and cell lines. LINC01614 knockdown repressed the proliferation and metastasis capacity of CRC cell lines. Consistently, an <i>in vivo</i> LINC01614 deficiency model exhibited slow tumor growth rate. Moreover, luciferase reporter assay, RNA pull-down, and immunoprecipitation confirmed that LINC01614 targeted miR-217-5p. LINC01614 knockdown reduced the expression of HMGA1 and N-cadherin, while increasing that of E-cadherin, resulting in decreased viability, proliferation, migration, and invasion capacity of CRC cells. Our results demonstrate that LINC01614 regulates CRC progression by modulating the miR-217-5p/HMGA1 axis, thus holding great potential as a prognostic biomarker for CRC diagnosis and treatment.</p>","PeriodicalId":76996,"journal":{"name":"Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology","volume":" ","pages":"6833987"},"PeriodicalIF":0.0,"publicationDate":"2023-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11401691/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"45306802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Construction of a Cuproptosis-Related lncRNA Prognostic Model for Bladder Urothelial Carcinoma and Screening of Potential Drugs","authors":"Xuzhan Ma, Libin Sun","doi":"10.1155/2023/1761398","DOIUrl":"https://doi.org/10.1155/2023/1761398","url":null,"abstract":"Objective. This study aimed to analyze the cuproptosis-related long non-coding RNA (lncRNA) in patients with bladder urothelial carcinoma (BLCA), construct a prognostic model, and screen its potential drugs. Methods. The transcriptome expression and clinical and mutation burden data related to BLCA were downloaded from The Cancer Genome Atlas database. The prognostic lncRNAs were screened using univariate Cox and Lasso regression analyses, and then included in the multifactor risk ratio model. The risk score of each sample was calculated based on the prognostic model formula, and the patients were divided into high- and low-risk groups for survival difference analysis. Clinically relevant receiver operating characteristic (ROC) curve, C-index principal component analysis, and clinical data statistics were used to evaluate the predictive power of the model. The risk-differential lncRNAs were functionally enriched. We calculated the tumor mutation burden of risk lncRNAs, and survival and the Tumor Immune Dysfunction and Exclusion analyses for high- and low-risk groups. Finally, immunocorrelation analysis and potential drug screening were performed. Results. Eleven lncRNAs with independent prognostic significance were screened out to construct the prognostic model. Survival analysis showed a significant difference in survival between the high- and low-risk groups. The areas under the ROC curve at 1, 3, and 5 years were 0.711, 0.679, and 0.713, respectively. The discrimination between the lncRNA high- and low-risk groups in the constructed model was the most obvious. The risk-differential lncRNAs were closely related to immunity. The treatment drugs with high sensitivity were screened based on the IC50 value. Conclusion. The 11 cuproptosis-related lncRNAs may serve as molecular biomarkers and therapeutic targets for BLCA.","PeriodicalId":76996,"journal":{"name":"Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43526187","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between CHFR and PARP-1, and Their Roles in Regulation of Proliferation and Apoptosis of B Cell Lymphoma","authors":"Xiaodan Liu, Nian-Ju Zheng, Liang Song, Hua Pan, Aiqin Song","doi":"10.1155/2023/7940316","DOIUrl":"https://doi.org/10.1155/2023/7940316","url":null,"abstract":"Background. Aberrant methylation of checkpoint with forkhead and ring finger domains (CHFR) was found in B-cell non-Hodgkin lymphoma (NHL), whereas its role in carcinogenesis is not clear. CHFR can control poly (ADP-ribose) polymerase levels by causing its degradation. The study was aimed to explore the roles and mechanisms of CHFR in the pathogenesis of B-cell NHL. Methods. Short hairpin ribonucleic acid (ShRNAs) targeting CHFR and poly (ADP-ribose) polymerase 1 (PARP-1) were transduced into Raji cells, and real-time polymerase chain reaction (PCR) and western blotting were carried out to determine their expression. Afterwards, the CCK-8 assay and flow cytometry were used to evaluate the cell growth and apoptosis. Tumor size and weight were determined using a xenograft model, and decitabine (5-Aza-dC) was used to further determine the methylation status of CHFR through a methylation specificity-PCR assay. Results. 5-Aza-dC-treatment promoted the expression of CHFR and decreased the expression of PARP-1 at both messenger ribonucleic acid (mRNA) and protein levels. 5-Aza-dC also accelerated Raji-cell apoptosis and restrained its growth in vitro and in vivo (\u0000 \u0000 P\u0000 <\u0000 0.05\u0000 \u0000 ). These results were contrary to those observed in the shRNA-CHFR group but consistent with those observed in the shRNA-PARP-1 group. The expression profiles of CHFR and PARP-1 in the xenograft model were consistent with those in the cellular model. Treatment with 5-Aza-dC led to demethylation of CHFR in nude mice. Besides, there may be a negative correlation between CHFR and PARP-1 in B-cell NHL cells. Conclusion. Our findings indicated that 5-Aza-dC could lead to the demethylation of the CHFR promoter and suppress Raji cell growth.","PeriodicalId":76996,"journal":{"name":"Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47324675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia-Induced GST1 Exerts Protective Effects on Trophoblasts via Inhibiting Reactive Oxygen Species (ROS) Accumulation","authors":"Lingjuan Chen, Gaoli Chen, Lixuan Guo, Yaping Wang, Chengjin Ai","doi":"10.1155/2023/9391252","DOIUrl":"https://doi.org/10.1155/2023/9391252","url":null,"abstract":"Hypoxic conditions are a typical extrinsic factor for the modification of trophoblast biological functions, including cell proliferation, migration, and invasion. Hypoxia-induced reactive oxygen species (ROS) accumulation causes chronic trophoblast injury and contributes to preeclampsia (PE). Glutathione-S-transferase P (GSTP1) is a main regulator of ROS. However, it is still unknown whether GSTP1 is involved in ROS regulation under hypoxic conditions. Here, we investigated the expression level of GSTP1 in first-trimester villi placentas compared with full-term placentas and the effect of hypoxic conditions on GSTP1. GSTP1 expression in first-trimester villi placentas was much higher than that in full-term placentas. After hypoxia exposure, GSTP1 was significantly upregulated in JEG3 cells, a trophoblast-like cell line. Hypoxic-induced GSTP1 scavenged ROS accumulated by hypoxia exposure, potentially by promoting GST activity. The inhibitory effects of hypoxia exposure on cell proliferation, migration, and invasion induced by hypoxia exposure were obviously reversed by overexpression of GSTP1. Hypoxia-induced cell apoptosis was also reversed by GSTP1 overexpression, indicating the protective effects of GSTP1 against ROS-induced cell injury. Moreover, overexpressed GSTP1 markedly promoted the cell proliferation, migration, invasion, and colony formation abilities in JEG3 cells, demonstrating that GSP1 also exerts promoting effects under normoxic conditions. These data show that hypoxia-induced GSTP1 expression facilitates trophoblast cell proliferation, migration, and invasion and exerts protective effects under hypoxic conditions, which may play an important role during the increase in PE.","PeriodicalId":76996,"journal":{"name":"Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43410227","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of a Novel KCNN4-Related ceRNA Network and Prognostic Model for Renal Clear Cell Carcinoma.","authors":"Hengtao Bu, Qiang Song, Jiexiu Zhang, Yuang Wei, Bianjiang Liu","doi":"10.1155/2023/2533992","DOIUrl":"10.1155/2023/2533992","url":null,"abstract":"<p><strong>Background: </strong>Clear cell renal cell carcinoma (ccRCC) accounts for more than 80% of renal cell carcinomas. Yet, it has not been fully understood about the derivation and progression of the tumor, as well as the long-term benefits from multimodality therapy. Therefore, reliable and applicable molecular markers are urgently needed for the prediction of diagnosis and prognosis of ccRCC patients.</p><p><strong>Methods: </strong>Genetic and clinical information of 533 ccRCC patients from The Cancer Genome Atlas database was collected for comprehensive bioinformatic analyses. UALCAN was used to detect gene expression in paired tumor samples. Two data sets from Gene Expression Omnibus database were analyzed to identify differentially expressed genes (DEGs), and Gene Set Enrichment Analysis was applied for the functional enrichment of DEGs. Tumor Immune Single Cell Hub and Tumor IMmune Estimation Resource databases were separately used for analyses of single-immune cell and immune cell infiltration. Encyclopedia of RNA Interactomes database was explored to predict targeted microRNAs (miRNAs) and corresponding long non-coding RNAs (lncRNAs). Cox regression analysis was performed for the construction of risk signature and prognosis model. Finally, quantitative real-time polymerase chain reaction and western blot were conducted for KCNN4 expression detection in cell lines and clinical samples. Small interfering RNA was employed to knock down KCNN4, and corresponding functional experiments were conducted on ccRCC cells as well.</p><p><strong>Results: </strong>KCNN4 showed elevated expression in tumors and prominent clinical correlation in ccRCC. In total, 41 KCNN4-related genes were enriched, and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses showed they were intimately related to immune-related signaling pathways. Spearman's analysis revealed the significantly positive correlation of KCNN4 with immune cell infiltration. By integrating hub miRNA-let-7e-5p and four critical lncRNA, a competitive endogenous RNA network-based risk signature was constructed. The prognosis model derived from it showed considerable predictive value for survival of ccRCC patients. Finally, in vitro experiments confirmed the remarkable tumor-promoting role of KCNN4 in ccRCC cells.</p><p><strong>Conclusion: </strong>KCNN4 significantly affected the immune status of tumor microenvironment and immunotherapy elements, through which it promoted tumor progression in ccRCC, and it could be a potential biomarker for prognosis and immunotherapy effects of ccRCC patients.</p>","PeriodicalId":76996,"journal":{"name":"Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology","volume":" ","pages":"2533992"},"PeriodicalIF":0.0,"publicationDate":"2023-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11401688/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42848340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selected bibliography.","authors":"W. R. N. D. Errera","doi":"10.1080/00185868.1974.9952351","DOIUrl":"https://doi.org/10.1080/00185868.1974.9952351","url":null,"abstract":"","PeriodicalId":76996,"journal":{"name":"Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology","volume":"1 1","pages":"388-91"},"PeriodicalIF":0.0,"publicationDate":"2019-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88633024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selected bibliography.","authors":"Pradeep Kumar","doi":"10.7591/9781501701061-010","DOIUrl":"https://doi.org/10.7591/9781501701061-010","url":null,"abstract":"","PeriodicalId":76996,"journal":{"name":"Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology","volume":"78 1","pages":"323-6"},"PeriodicalIF":0.0,"publicationDate":"2019-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90604971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selected bibliography.","authors":"","doi":"10.1017/9781108567992.009","DOIUrl":"https://doi.org/10.1017/9781108567992.009","url":null,"abstract":"","PeriodicalId":76996,"journal":{"name":"Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology","volume":"26 1","pages":"320-2"},"PeriodicalIF":0.0,"publicationDate":"2017-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78116160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical operation of high throughput digital microscope system: The impact of the condenser on cytogenetic image quality","authors":"L. Ren, Zheng Li, Yuhua Li, B. Zheng, Shibo Li, Xiaodong Chen, Hong Liu","doi":"10.3233/ACP-130076","DOIUrl":"https://doi.org/10.3233/ACP-130076","url":null,"abstract":"","PeriodicalId":76996,"journal":{"name":"Analytical cellular pathology : the journal of the European Society for Analytical Cellular Pathology","volume":"1 1","pages":"1-14"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/ACP-130076","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"69722914","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}