Analytical Cellular Pathology最新文献

{"title":"Shock Wave Therapy Alleviates Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury by Inhibiting Both Apoptosis and Ferroptosis.","authors":"Jiannan Wang, Na Jia, Kaiyi Zhu, Kun Xu, Mingjing Yan, Ming Lan, Junmeng Liu, Bing Liu, Tao Shen, Qing He","doi":"10.1155/2024/8753898","DOIUrl":"10.1155/2024/8753898","url":null,"abstract":"<p><p>Shock wave therapy (SWT) is a new alternative therapy for patients with severe coronary artery disease that improves myocardial ischemic symptoms by delivering low-energy shock wave stimulation to ischaemic myocardium with low-energy pulsed waves. However, the specific mechanism of its protective effect is not fully understood, especially for the protective mechanism in cardiomyocytes after hypoxia/reoxygenation (H/R). We selected a rat H9c2 cardiomyocyte cell line to establish a stable H/R cardiomyocyte injury model by hypoxia/reoxygenation, and then used SWT for therapeutic intervention to explore its cardiomyocyte protective mechanisms. The results showed that SWT significantly increased cell viability and GSH levels while decreasing LDH levels, ROS levels, and MDA levels. SWT also improved mitochondrial morphology and function of cells after H/R. Meanwhile, we found that SWT could increase the expression of GPX4, xCT, and Bcl-2, while decreasing the expression of Bax and cleaved caspase-3, and inhibiting cardiomyocyte apoptosis and ferroptosis. Moreover, this protective effect of SWT on cardiomyocytes could be significantly reversed by knockdown of xCT, a key regulator protein of ferroptosis. In conclusion, our study shows that SWT can attenuate hypoxia-reoxygenation-induced myocardial injury and protect cardiomyocyte function by inhibiting H/R-induced apoptosis and ferroptosis, and this therapy may have important applications in the treatment of clinical myocardial ischemic diseases.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2024 ","pages":"8753898"},"PeriodicalIF":2.6,"publicationDate":"2024-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11338664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142019292","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":"Role of miR-93-5p and Its Opposing Effect of Ionizing Radiation in Non-Small Cell Lung Cancer.","authors":"Qingtao Ni, Kai Sang, Jian Zhou, Chi Pan","doi":"10.1155/2024/4218464","DOIUrl":"10.1155/2024/4218464","url":null,"abstract":"<p><strong>Background: </strong>Radiation therapy is an effective local therapy for lung cancer. However, the interaction between genes and radiotherapy is multifaceted and intricate. Therefore, we explored the role of miR-93-5p in the proliferation, apoptosis, and migration abilities of A549 cells. Simultaneously, we also investigated the interactions between miR-93-5p and ionizing radiation (IR).</p><p><strong>Methods: </strong>Cell Counting Kit-8, transwell, and apoptotic assay were performed to measure the proliferation, migration, and apoptosis abilities. The expression levels of miR-93-5p and its target gene in lung cancer were predicted using starBase v3.0. Then, data were validated using qPCR and western blot.</p><p><strong>Results: </strong>miR-93-5p significantly promoted the proliferation (<i>P</i> < 0.01) and migration abilities (<i>P</i> < 0.001) of A549 cells. Gasdermin E (GSDME) was identified to be a putative target of miR-93-5p and had a negative correlation with miR-93-5p (<i>P</i> < 0.001). Overexpression of miR-93-5p significantly decreased GSDME in A549 (<i>P</i> < 0.001). Interestingly, miR-93-5p decreased cell proliferation (<i>P</i> < 0.01) and cell migration (<i>P</i> < 0.01) and increased apoptosis (<i>P</i> < 0.01) in A549 cells after exposure to IR.</p><p><strong>Conclusions: </strong>miR-93-5p is presumed to play an oncogenic role in lung cancer by enhancing A549 cell proliferation and migration. It can enhance the sensitivity of radiotherapy under IR conditions. We speculate that the miR-93-5p/GSDME pathway was inhibited, activating the GSDME-related pyroptosis pathway when the cells were exposed to IR. Therefore, miR-93-5p can overcome resistance to radiotherapy and improve the efficacy of radiotherapy.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2024 ","pages":"4218464"},"PeriodicalIF":2.6,"publicationDate":"2024-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11330335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142001132","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":"Immunohistochemical Profile of p62/SQSTM1/Sequestosome-1 in Human Low- and High-Grade Intracranial Meningiomas.","authors":"Antonio Ieni, Cristina Pizzimenti, Vincenzo Fiorentino, Mariausilia Franchina, Antonino Germanò, Giovanni Raffa, Maurizio Martini, Guido Fadda, Giovanni Tuccari","doi":"10.1155/2024/5573892","DOIUrl":"10.1155/2024/5573892","url":null,"abstract":"<p><p>Among autophagic-related proteins, p62/SQSTM1/Sequestosome-1 represents a relevant actor in cellular proliferation and neoplastic growth. Although, recently, p62 expression has been analyzed in different neurodegenerative and glial neoplastic diseases, no available information have been reported in meningiomas, which have an high epidemiological relevance being the second most common category of intracranial tumors after gliomas. Generally meningiomas have a benign behavior, but their recurrence is not uncommon mainly when atypical or anaplastic varieties occur. However, intranuclear vacuoles have been ultrastructurally observed in meningiomas, and they were labelled by p62 antibodies. Therefore, in the present study, we have investigated p62 immunohistochemical pattern in a cohort of 133 cases representative of low- and high-grade meningiomas, to verify if p62 expression may be related to clinicopathological data, thus achieving a potential prognostic role. The p62 immunoexpression was frequently found in the nucleus and cytoplasm of neoplastic elements, and utilizing an intensity-distribution score, 55 (41.3%) cases were considered as high expressors while 78 (58.7%) cases were instead recorded as low expressors. Fifteen cases exhibited recurrences of the disease, 14 of which were codified as high expressors. Moreover, a direct relationship between p62 and Mib-1 immunoexpression as well as between p62 and neoplastic grade have been documented. Finally, we suggest that impaired autophagic flux with an increase in p62 expression may be involved in the activation of NRF2 also contributing in the development of recurrence in meningioma patients.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2024 ","pages":"5573892"},"PeriodicalIF":2.6,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11315968/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141917844","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":"Construction and Identification of Eukaryotic Expression Vector pEGFP-N1-MIC-1 for Mouse MIC-1 Gene and Its Effect on Gastric Cancer Cells.","authors":"HuiPeng Zhang, Zhongyu Qin, ShuaiShuai Shi, YunFei Li, Yang Song, YiQiang Zhang","doi":"10.1155/2024/2165242","DOIUrl":"10.1155/2024/2165242","url":null,"abstract":"<p><p>This study aimed to construct an eukaryotic expression vector, pEGFP-N1-MIC-1, for overexpressing the mouse macrophage inhibitory cytokine-1 (MIC-1) gene. Additionally, we transfected the MFC cell line to observe the upregulation of MIC-1 gene expression and assess its impact on macrophage phenotype conversion. Enzyme digestion and DNA sequencing confirmed the successful construction of the pEGFP-N1-MIC-1 vector. The transfected MFC cells exhibited a significant increase in MIC-1 protein expression levels. Furthermore, transfection with pEGFP-N1-MIC-1 increased the migration and colony formation capabilities of MFC cells. These results may contribute to future research and the development of therapeutic interventions targeting MIC-1 in macrophages, particularly in the context of gastric cancer.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2024 ","pages":"2165242"},"PeriodicalIF":2.6,"publicationDate":"2024-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11265941/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141753146","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":"Synergistic Effects of Icariin and Extracellular Vesicles Derived from Rabbit Synovial Membrane-Derived Mesenchymal Stem Cells on Osteochondral Repair via the Wnt/<i>β</i>-Catenin Pathway.","authors":"Dongming Tang, Wang Tang, Huanqing Chen, Donghua Liu, Feng Jiao","doi":"10.1155/2024/1083143","DOIUrl":"10.1155/2024/1083143","url":null,"abstract":"<p><strong>Objectives: </strong>Osteochondral defects (OCDs) are localized areas of damaged cartilage and underlying subchondral bone that can produce pain and seriously impair joint function. Literature reports indicated that icariin (ICA) has the effect of promoting cartilage repair. However, its mechanism remains unclear. Here, we explored the effects of icariin and extracellular vesicles (EVs) from rabbit synovial-derived mesenchymal stem cells (rSMSCs) on repairing of OCDs.</p><p><strong>Materials and methods: </strong>Rabbit primary genicular chondrocytes (rPGCs), knee skeletal muscle cells (rSMCKs), and rSMSCs, and extracellular vesicles derived from the latter two cells (rSMCK-EVs and rSMSC-EVs) were isolated and identified. The rPGCs were stimulated with ICA, rSMSC-EVs either separately or in combination. The rSMCK-EVs were used as a control. After stimulation, chondrogenic-related markers were analyzed by quantitative RT-PCR and western blotting. Cell proliferation was determined by the CCK-8 assay. The preventative effects of ICA and SMSC-EVs <i>in vivo</i> were determined by H&E and toluidine blue staining. Immunohistochemical analyses were performed to evaluate the levels of COL2A1 and <i>β</i>-catenin <i>in vivo</i>. <i>Results. In vitro</i>, the proliferation of rPGCs was markedly increased by ICA treatment in a dose-dependent manner. When compared with ICA or rSMSC-EVs treatment alone, combined treatment with ICA and SMSC-EVs produced stronger stimulative effects on cell proliferation. Moreover, combined treatment with ICA and rSMSC-EVs promoted the expression of chondrogenic-related gene, including COL2A1, SOX-9, and RUNX2, which may be via the activation of the Wnt/<i>β</i>-catenin pathway. <i>In vivo</i>, combined treatment with rSMSC-EVs and ICA promoted cartilage repair in joint bone defects. Results also showed that ICA or rSMSC-EVs both promoted the COL2A1 and <i>β</i>-catenin protein accumulation in articular cartilage, and that was further enhanced by combined treatment with rSMSC-EVs and ICA.</p><p><strong>Conclusion: </strong>Our findings highlight the promising potential of using combined treatment with ICA and rSMSC-EVs for promoting osteochondral repair.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2024 ","pages":"1083143"},"PeriodicalIF":2.6,"publicationDate":"2024-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11214593/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141471950","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":"Combination of Pirfenidone and Andrographolide Ameliorates Hepatic Stellate Cell Activation and Liver Fibrosis by Mediating TGF-<i>β</i>/Smad Signaling Pathway.","authors":"Guang Xu, Tidong Ma, Chonggao Zhou, Fan Zhao, Kun Peng, Bixiang Li","doi":"10.1155/2024/2751280","DOIUrl":"10.1155/2024/2751280","url":null,"abstract":"<p><strong>Background: </strong>Biliary atresia (BA) is a devastating congenital disease characterized by inflammation and progressive liver fibrosis. Activation of hepatic stellate cells (HSCs) plays a central role in the pathogenesis of hepatic fibrosis. Our study aimed to investigate the pharmacological effect and potential mechanism of pirfenidone (PFD) and andrographolide (AGP) separately and together on liver fibrosis of BA.</p><p><strong>Materials and methods: </strong>The bile ducts of male C57BL/6J mice were ligated or had the sham operation. The <i>in vivo</i> effects of PFD and/or AGP on liver fibrosis of BA were evaluated. Human hepatic stellate cells (LX-2) were also treated with PFD and/or AGP <i>in vitro</i>.</p><p><strong>Results: </strong>PFD and/or AGP ameliorates liver fibrosis and inflammation in the mice model of BA, as evidenced by significant downregulated in the accumulation of collagen fibers, hepatic fibrosis markers (<i>α</i>-SMA, collagen I, and collagen IV), and inflammatory markers (IL-1<i>β</i>, IL-6, and TNF-<i>α</i>). Moreover, compared with monotherapy, these changes are more obvious in the combined treatment of PFD and AGP. Consistent with animal experiments, hepatic fibrosis markers (<i>α</i>-SMA, collagen I, and CTGF) and inflammatory markers (IL-1<i>β</i>, IL-6, and TNF-<i>α</i>) were significantly decreased in activated LX-2 cells after PFD and/or AGP treatment. In addition, PFD and/or AGP inhibited the activation of HSCs by blocking the TGF-<i>β</i>/Smad signaling pathway, and the combined treatment of PFD and AGP synergistically inhibited the phosphorylation of Smad2 and Smad3.</p><p><strong>Conclusion: </strong>The combined application of PFD and AGP exerted superior inhibitive effects on HSC activation and liver fibrosis by mediating the TGF-<i>β</i>/Smad signaling pathway as compared to monotherapy. Therefore, the combination of PFD and AGP may be a promising treatment strategy for liver fibrosis in BA.</p>","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"2024 ","pages":"2751280"},"PeriodicalIF":2.6,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11213636/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141471949","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":"N-Acetylcysteine Treats Spinal Cord Injury by Inhibiting Astrocyte Proliferation","authors":"Dong Zhang, Chaoxi Qin, Fei Meng, Xiaopeng Han, Xing Guo","doi":"10.1155/2024/6624283","DOIUrl":"https://doi.org/10.1155/2024/6624283","url":null,"abstract":"Astrocyte proliferation commonly occurs after spinal cord injury (SCI). N-Acetylcysteine (NAC) has a regulatory effect on many diseases. In this study, we investigated the effect and underlying mechanism of NAC on astrocytes in SCI. We isolated rat primary astrocytes and stimulated with lipopolysaccharide to induce cell proliferation and degeneration. A rat model of SCI was also established, and the Basso–Beattie–Bresnahan score was determined. The localization of glial fibrillary acidic protein in the cells and tissues was determined using TUNEL staining and immunofluorescence, while that of connexin 43 was assessed via immunofluorescence. Pathological changes associated with SCI were detected using hematoxylin and eosin staining, and inflammatory factors were detected using enzyme-linked immunosorbent assay. Additionally, JAK/STAT expression was evaluated using western blotting and quantitative reverse transcription polymerase chain reaction. NAC downregulated the glial fibrillary acidic protein abundance and connexin 43 in reactive astrocytes and SCI rat models while inhibiting the abundance of secreted proteins DSPG, HSPG, KSPG, tenascin C, vimentin, CSPG, ephrin-B2, and nestin. NAC also regulated the JAK/STAT signaling pathway by downregulating the expression of JAK2, STAT5, STAT3, STAT1, PIM1, NFATc1, COL1, COL3, TGF-<i>β</i>, SMAD1, CTGF, CyCD1, and CDK4, thus alleviating SCI. Finally, NAC exhibited durable effects, with no SCI recurrence within 60 days. Therefore, NAC relieves SCI by inhibiting the proliferation of reactive astrocytes and suppressing the expression of secretory and JAK/STAT pathway proteins.","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"20 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141194280","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":"Identification of circRNA Expression Profile and Potential Systemic Immune Imbalance Modulation in Premature Rupture of Membranes","authors":"Dongni Huang, Yuxin Ran, Ruixin Chen, Jie He, Nanlin Yin, Hongbo Qi","doi":"10.1155/2024/6724914","DOIUrl":"https://doi.org/10.1155/2024/6724914","url":null,"abstract":"Premature rupture of membrane (PROM) refers to the rupture of membranes before the onset of labor which increases the risk of perinatal morbidity and mortality. Recently, circular RNAs (circRNAs) have emerged as promising regulators of diverse diseases. However, the circRNA expression profiles and potential circRNA–miRNA–mRNA regulatory mechanisms in PROM remain enigmatic. In this study, we displayed the expression profiles of circRNAs and mRNAs in plasma and fetal membranes of PROM and normal control (NC) groups based on circRNA microarray, the Gene Expression Omnibus database, and NCBI’s Sequence Read Archive. A total of 1,459 differentially expressed circRNAs (DECs) in PROM were identified, with 406 upregulated and 1,053 downregulated. Then, we constructed the circRNA–miRNA–mRNA network in PROM, encompassing 22 circRNA–miRNA pairs and 128 miRNA–mRNA pairs. Based on the analysis of gene ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway and gene set enrichment analysis (GSEA), DECs were implicated in immune-related pathways, with certain alterations persisting even postpartum. Notably, 11 host genes shared by DECs of fetal membrane tissue and prenatal plasma in PROM were significantly implicated in inflammatory processes and extracellular matrix regulation. Our results suggest that structurally stable circRNAs may predispose to PROM by mediating systemic immune imbalances, including peripheral leukocyte disorganization, local immune imbalance at the maternal–fetal interface, and local collagen disruption. This is the first time to decipher a landscape on circRNAs of PROM, reveals the pathogenic cause of PROM from the perspective of circRNA, and opens up a new direction for the diagnosis and treatment of PROM.","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"68 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141149258","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":"Regulation of Cancer-Associated miRNAs Expression under Hypoxic Conditions","authors":"Jesús Valencia-Cervantes, Martha Patricia Sierra-Vargas","doi":"10.1155/2024/5523283","DOIUrl":"https://doi.org/10.1155/2024/5523283","url":null,"abstract":"Solid tumors frequently experience hypoxia or low O₂ levels. In these conditions, hypoxia-inducible factor 1 alpha (HIF-1<i>α</i>) is activated and acts as a transcription factor that regulates cancer cell adaptation to O₂ and nutrient deprivation. HIF-1<i>α</i> controls gene expression associated with various signaling pathways that promote cancer cell proliferation and survival. MicroRNAs (miRNAs) are 22-nucleotide noncoding RNAs that play a role in various biological processes essential for cancer progression. This review presents an overview of how hypoxia regulates the expression of multiple miRNAs in the progression of cancer cells.","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"132 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140933832","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":"Hsa_circ_0051908 Promotes Hepatocellular Carcinoma Progression by Regulating the Epithelial–Mesenchymal Transition Process","authors":"Yinbing Wu, Huafei Tang, Shuzhong Cui, Quanxing Liao, Lisi Zeng, Yinuo Tu","doi":"10.1155/2024/8645534","DOIUrl":"https://doi.org/10.1155/2024/8645534","url":null,"abstract":"<i>Background/Aims</i>. Circular RNAs (circRNAs) are often used for tumor diagnosis and treatment owing to their high stability, high expression abundance, and strong tissue specificity. The role of hsa_circ_0051908, a newly reported circRNA, in the development of hepatocellular carcinoma (HCC) is unknown. <i>Materials and Methods</i>. Hsa_circ_0051908 expression was determined using RT-qPCR. HCC cell proliferation, apoptosis, invasion, and migration were assessed using CCK-8 assay, EdU staining, TUNEL staining, flow cytometry, and transwell assay. The molecular mechanism was analyzed using western blotting. In addition, the role of hsa_circ_0051908 in tumor growth was evaluated <i>in vivo</i>. <i>Results</i>. Hsa_circ_0051908 expression was increased in both HCC tissues and cell lines. The proliferation, migration, and invasion of HCC cells were significantly decreased after hsa_circ_0051908 knockdown, while cell apoptosis was notably increased. Furthermore, we found that hsa_circ_0051908 silencing downregulated vimentin and Snail and upregulated E-cadherin. <i>In vivo</i>, hsa_circ_0051908 silencing significantly inhibited the growth of the tumor. <i>Conclusions</i>. Our data provide evidence that hsa_circ_0051908 promotes HCC progression partially by mediating the epithelial–mesenchymal transition process, and it may be used for HCC treatment.","PeriodicalId":49326,"journal":{"name":"Analytical Cellular Pathology","volume":"27 1","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140831719","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}