Histology and histopathology最新文献

{"title":"Optimizing the preparation of paraffin sections from stallion testes.","authors":"Nairag Asgenbaatar, Minna Yi, Xisheng Wang, Tseweendolmaa Ulaangerel, Yingchao Shen, Xin Wen, Ming Du, Xiaoling Dong, Yibeeltu Mengkh, Manglai Dugarjav, Gerelchimeg Bou","doi":"10.14670/HH-18-775","DOIUrl":"10.14670/HH-18-775","url":null,"abstract":"<p><p>The preparation of paraffin sections is an important experimental technique in animal histological research, and key factors that determine the quality of a section include the dehydration time, waxing time, and drying temperature of the paraffin section. Paraffin sections obtained from testis tissue of adult horses exhibited higher quality with clear tissue structure and complete cell morphology after they underwent gradient dehydration for 6 hours, were immersed in wax for 60 minutes, and were dried in a 75-degree oven for 15 minutes. The detailed, optimized procedures that are developed in the current study may simplify histological experiments and research on equine testes.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"335-342"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141563306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioinformatics study of the TNFRSF1A mechanism involved in acute liver injury in sepsis through the mTOR signaling pathway.","authors":"Zhidong Chen, Kankai Tang, Hui Zhang","doi":"10.14670/HH-18-789","DOIUrl":"10.14670/HH-18-789","url":null,"abstract":"<p><strong>Objectives: </strong>This study analyzed potential key genes involved in the mechanism of acute liver injury induced by sepsis through bioinformatics techniques, aiming to provide novel insights for the identification of early-stage sepsis-induced acute liver injury and its diagnosis.</p><p><strong>Methods: </strong>Gene chip data sets containing samples from acute liver injury induced by sepsis and control groups (GSE22009 and GSE60088) were selected from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) with |log fold change| >1 and <i>p</i><0.05 were screened with the GEO2R tool, which was also used for the selection of upregulated DEGs in the chips with <i>p</i><0.05. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, Gene Ontology, and protein-protein interaction (PPI) analyses were then conducted. Results were visualized using R language packages, including volcano plots, Venn diagrams, and boxplots. The intersection of candidate genes with relevant genes in the Comparative Toxicogenomics Database (CTD) was performed, and the clinical significance of these genes was explored through a literature review. A rat model of acute liver injury was developed by inducing sepsis with the cecum ligation and puncture method. Real-time PCR was performed to determine the gene expression in rat liver tissues.</p><p><strong>Results: </strong>A total of 646 upregulated DEGs were determined in GSE22009 and 146 in GSE60088. A Venn diagram was used to find the intersection of the upregulated DEGs between the two data sets, and 67 DEGs associated with sepsis-mediated acute liver damage were obtained. Enrichment analysis from the KEGG pathway showed that DEG upregulation was primarily associated with various pathways: TNF, NF-κB, IL-17, ferroptosis, mTOR, and JAK-STAT signaling pathways. DEGs resulted in three clusters and 15 candidate genes, as revealed by the PPI network and module analyses. Intersection with sepsis-induced acute liver injury-related genes in the CTD resulted in the identification of three significant differentially co-expressed genes: <i>CXCL1, ICAM1,</i> and <i>TNFRSF1A</i>. Sepsis-induced liver tissue indicated the overexpression of <i>CXCL1, ICAM1,</i> and <i>TNFRSF1A</i> mRNA, as compared with the control group (<i>p</i><0.05).</p><p><strong>Conclusion: </strong>The key genes identified and related signaling pathways provided insights into the molecular mechanisms of sepsis-induced acute liver injury. In vivo studies revealed the overexpression of <i>CXCL1, ICAM1</i>, and <i>TNFRSF1A</i> mRNA in sepsis-mediated injured liver tissues, providing a theoretical basis for early diagnosis and targeted treatment research.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"401-409"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141751558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intrinsically synthesized melatonin in mitochondria and factors controlling its production.","authors":"Russel J Reiter, Ramaswamy N Sharma, Luiz Gustavo de Almieda Chuffa, Danilo Grunig Humberto da Silva, Sergio Rosales-Corral","doi":"10.14670/HH-18-776","DOIUrl":"10.14670/HH-18-776","url":null,"abstract":"<p><p>The percentage of the total amount of melatonin produced in vertebrates that comes from the pineal is small (likely <5%) but, nevertheless, functionally highly noteworthy. The significance of pineal melatonin is that it is secreted cyclically such that it has a critical function in influencing not only the suprachiasmatic nucleus but clock genes that reside in perhaps every cell throughout the organism. Extrapineal melatonin, which may be synthesized in the mitochondria of all other cells in much larger amounts than that in the pineal gland has a different function than that derived from the pineal gland. Its synthesis is not circadian and it is not directly impacted by the photoperiodic environment. Also, melatonin from the extrapineal sites is not normally secreted into the blood stream; rather, it acts locally in its cell of synthesis or, possibly via paracrine mechanisms, on immediately adjacent cells. The functions of extrapineal melatonin include central roles in maintaining molecular and redox homeostasis and actions in resisting pathological processes due to its ability to directly or indirectly detoxify free radicals. The vast majority of organisms that exist on Earth lack a pineal gland so pineal-derived melatonin is unique to vertebrates. Evidence suggests that all invertebrates, protists and plants synthesized melatonin and they have no pineal homolog; thus, the production of melatonin by extrapineal cells in vertebrates should not be unexpected. While the factors that control pineal melatonin synthesis are well documented, the processes that regulate extrapineal melatonin production are undefined.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"271-282"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141450388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Risk perception of patients with ductal carcinoma <i>in situ</i> (DCIS) of the breast and their healthcare practitioners: The importance of histopathological terminology, and the gaps in our knowledge.","authors":"Julia Riggi, Christine Galant, Hilde Vernaeve, Maud Vassilieff, Martine Berlière, Mieke R Van Bockstal","doi":"10.14670/HH-18-806","DOIUrl":"10.14670/HH-18-806","url":null,"abstract":"<p><p>Despite ductal carcinoma <i>in situ</i> (DCIS) being a non-obligatory precursor of invasive breast carcinoma, its diagnosis generates substantial psychological distress. The limited knowledge about the natural history of DCIS contributes to the insufficient transmission of information about DCIS to patients and the general population. The uncertainty about the progression risk to invasive carcinoma hampers adequate communication by clinicians. Breast cancer-related mortality after a DCIS diagnosis is low. However, several studies have demonstrated that DCIS patients generally overestimate the risk of developing loco-regional recurrence or dying from breast cancer. Various factors contribute to this perceived risk. Despite the lack of infiltrative growth, DCIS is treated similarly to invasive breast cancer, with surgery, radiotherapy, and hormonal therapy. Additionally, the term 'carcinoma' in DCIS provokes anxiety. Incorrect risk perception by physicians may result in overtreatment. Here, we provide an overview of epidemiologic data on mortality after DCIS. We discuss the impact of the term \"ductal carcinoma <i>in situ</i>\" on patients' and physicians' perceptions of risk. The available evidence is mostly limited to patients within the Anglosphere. Recent studies, and European studies in particular, are scarce. We identify this as an area of interest for future large-scale European studies. We discuss the potential value of the \"ductal intraepithelial neoplasia\" (DIN) terminology, introduced in 1998. Although replacing the concept of \"DCIS\" with the DIN terminology is unlikely to solve the entire problem of risk overestimation, it could be the first step to optimize doctor-patient communication and alter the current risk perception.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"297-306"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142345765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tissue microarray validation in cervical carcinoma studies. A methodological approach.","authors":"Lucília Lovane, Carla Carrilho, Christina Karlsson","doi":"10.14670/HH-18-796","DOIUrl":"10.14670/HH-18-796","url":null,"abstract":"<p><p>Tissue microarrays (TMAs) are a cost-effective tool to study biomarkers in clinical research. Cervical cancer (CC) is one of the most prevalent in women worldwide, with the highest prevalence in low-middle-income countries due to a lack of organized screening. CC is associated with persistent high-risk human papillomavirus infection. Several biomarkers have been studied for diagnostic, therapeutic, and prognostic purposes. We aimed to evaluate and validate the effectiveness of TMA in CC compared to whole slide images (WSs). We selected and anonymized twenty cases of CC. P16, cytokeratin 5 (CK5), cytokeratin 7 (CK7), programmed death-ligand 1 (PD-L1), and CD8 expression were immunohistochemically investigated. All WS were scanned and 10 representative virtual TMA cores with 0.6 mm diameter per sample were selected. Ten random combinations of 1-5 cylinders per case were assessed for each biomarker. The agreement of scoring between TMA and WS was evaluated by kappa statistics. We found that three cores of 0.6 mm on TMA can accurately represent WS in our setting. The Kappa value between TMA and WS varied from 1 for p16 to 0.61 for PD-L1. Our study presents an approach to address TMA sampling that could be generalized to TMA-based research, regardless of the tissue and biomarkers of interest.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"317-325"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141859625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinicopathological and molecular features of genome-stable colorectal cancers.","authors":"Lingyan Jin, Hye-Yeong Jin, Younghoon Kim, Nam-Yun Cho, Jeong Mo Bae, Jung Ho Kim, Sae-Won Han, Tae-You Kim, Gyeong Hoon Kang","doi":"10.14670/HH-18-785","DOIUrl":"10.14670/HH-18-785","url":null,"abstract":"<p><p>Colorectal cancers (CRCs) are traditionally divided into those with either chromosomal instability (CIN) or microsatellite instability (MSI). By utilizing TCGA data, the Laird team found a subset of CRCs, namely, genome-stable CRCs (GS CRCs), which lack both CIN and MSI. Although the molecular features of GS CRCs have been described in detail, the clinicopathological features are not well defined. A total of 437 CRCs were analyzed for copy number variation (CNV) statuses in eight genes (<i>ARID1A, EGFR, FGFR1, KDM5B, MYBL2, MYC, SALL4,</i> and <i>SETDB1</i>) using droplet-digital PCR. CRCs that showed CNV in ≤ one gene and no MSI were defined as GS-like CRCs. Clinicopathological and molecular features of GS-like CRCs were compared with those of CIN-like CRCs. GS-like CRCs comprised 4.6% of CRCs and showed a predilection toward the proximal colon, lower nuclear optical density, <i>KRAS</i> mutation, <i>PIK3CA</i> mutation, and aberrant expression of KRT7. Survival analysis showed no significant difference between the three subgroups. Through our study, the GS-like subtype was found to comprise a minor proportion of CRCs and have proclivity toward a proximal bowel location, hypochromatic tumor nuclei, aberrant KRT7 expression, and a high frequency of <i>KRAS</i> and <i>PIK3CA</i> mutations.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"381-388"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture pretreatment inhibits ferroptosis and inflammation after middle cerebral artery occlusion in rats by activating Nrf2.","authors":"Yanpeng Pu, Jingyan Cheng, Zhenya Wang, Jingbo Zhang, Fajun Liang, Xianbao Zhang, Zhijun Zheng, Miaomiao Yin, Zhen Wang","doi":"10.14670/HH-18-780","DOIUrl":"10.14670/HH-18-780","url":null,"abstract":"<p><strong>Objective: </strong>Electroacupuncture (EA) pretreatment can effectively increase the tolerance of the brain to ischemic stroke. The mechanism of ischemic tolerance induced by EA is related to Nrf2, but its specific mechanism has not been elucidated. This paper was designed to explore the effect of EA pretreatment on brain injury and the related mechanisms.</p><p><strong>Methods: </strong>Rats were pretreated with EA before middle cerebral artery occlusion (MCAO) modeling. The symptoms of neurological deficit and the volume of cerebral infarction were measured. The levels of inflammatory factors, oxidative stress-related factors, LPO, ROS, and Fe²⁺ were evaluated by the corresponding kits. Cell apoptosis was determined through TUNEL staining. The mRNA expression of inflammatory factors was examined by RT-qPCR, and the protein expression of ferroptosis-related factors, pyroptosis-related proteins, Keap1, Nrf2, HO-1, and NQO1 by western blotting.</p><p><strong>Results: </strong>EA pretreatment improved the symptoms of neurological deficit and reduced the volume of cerebral infarction. EA pretreatment significantly inhibited oxidative stress, inflammatory response, ferroptosis, pyroptosis, and apoptosis in brain tissues of MCAO rats. Mechanistically, EA pretreatment could activate Nrf2 expression and reduce Keap1 expression.</p><p><strong>Conclusion: </strong>EA pretreatment reduced inflammation and oxidative stress and inhibited ferroptosis by activating Nrf2 expression, ultimately delaying the development of ischemic stroke.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"357-367"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141491736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinicopathologic and molecular characteristics of neuroendocrine carcinomas of the gallbladder.","authors":"Hui Tang, Xiaojun Jiang, Lili Zhu, Liming Xu, Xiaoxi Wang, Hong Li, Feifei Gao, Xinxin Liu, Chuanli Ren, Yan Zhao","doi":"10.14670/HH-18-788","DOIUrl":"10.14670/HH-18-788","url":null,"abstract":"<p><p>Gallbladder neuroendocrine carcinomas (GB-NECs) are a rare subtype of malignant gallbladder cancer (GBC). The genetic and molecular characteristics of GB-NECs are rarely reported. This study aims to assess the frequency of microsatellite instability (MSI) in GB-NECs and characterize their clinicopathologic and molecular features in comparison with gallbladder adenocarcinomas (GB-ADCs). Data from six patients with primary GB-NECs and 13 with GB-ADCs were collected and reevaluated. MSI assay, immunohistochemistry for mismatch repair proteins (MLH1, MSH2, MSH6, and PMS2), comprehensive genomic profiling (CGP) via next-generation sequencing (NGS), and evaluation of tumor mutation burden (TMB) were conducted on these samples. The six GB-NEC cases were all female, with a mean age of 62.0±9.2 years. Of these, two cases were diagnosed as large cell neuroendocrine carcinomas (LCNECs), while the remaining four were small cell neuroendocrine carcinomas (SCNECs). Microsatellite states observed in both GB-NECs and GB-ADCs were consistently microsatellite stable (MSS). Notably, <i>TP53</i> (100%, 6/6) and <i>RB1</i> (100%, 6/6) exhibited the highest mutation frequency in GB-NECs, followed by <i>SMAD4</i> (50%, 3/6), <i>GNAS</i> (50%, 3/6), and <i>RICTOR</i> (33%, 2/6), with <i>RB1, GNAS,</i> and <i>RICTOR</i> specifically present in GB-NECs. Immunohistochemical (IHC) assays of p53 and Rb in the six GB-NECs were highly consistent with genetic mutations detected by targeted NGS. Moreover, no statistical difference was observed in TMB between GB-NECs and GB-ADCs (<i>p</i>=0.864). Although overall survival in GB-NEC patients tended to be worse than in GB-ADC patients, this difference did not reach statistical significance (<i>p</i>=0.119). This study has identified the microsatellite states and molecular mutation features of GB-NECs, suggesting that co-mutations in <i>TP53</i> and <i>RB1</i> may signify a neuroendocrine inclination in GB-NECs. The IHC assay provides an effective complement to targeted NGS for determining the functional status of p53 and Rb in clinical practice.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"389-400"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141748014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of acupuncture in improving the outcome of sepsis-induced lung injury.","authors":"Peng Li, Fangfang Li, Si Chen, Qiulei Ma, Jie Wang, Bingquan Ma, Jin Xu","doi":"10.14670/HH-18-781","DOIUrl":"10.14670/HH-18-781","url":null,"abstract":"<p><strong>Objective: </strong>The purpose of this study was to investigate the effect of serum exosomes of mice after acupuncture (acu-exo) on acute lung injury (ALI) in sepsis <i>in vitro</i> and <i>in vivo</i>.</p><p><strong>Methods: </strong>Serum exosomes (acu-exo) of normal mice were prepared after acupuncture. Lipopolysaccharide (LPS) was used to establish the model of ALI <i>in vivo</i> and <i>in vitro</i>. Immunohistochemistry, western blot, and immunofluorescence were used to evaluate the mechanism of acu-exo on ALI. P2X7 knockout mice and P2X7 siRNA were used to verify the mechanism.</p><p><strong>Results: </strong>Compared with normal mice, serum exosomes were significantly increased in normal mice after acupuncture. The results showed that P2X7 was increased in the lung of septic mice as compared with the WT group. It was also found that the increase in NLRP3 and NF-κB was accompanied by the activation of P2X7. Increased P2X7 led to activation of the P2X7 receptor causing mitochondrial dysfunctions in lung tissue of septic mice. Knockout of P2X7 or silenced P2X7 markedly decreased NLRP3 and NF-κB and led to mitochondrial function recovery in lung tissue of sepsis. At the same time, acu-exo significantly restored the above changes in the lung tissue of septic mice.</p><p><strong>Conclusions: </strong>Inhibition of P2X7 led to mitochondrial function recovery of lung tissue by inhibiting NLRP3 and NF-κB. At the same time, acu-exo could improve ALI by decreasing NLRP3 and NF-κB activation.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"369-380"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141497877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"EFNA4 deletion suppresses the migration, invasion, stemness, and angiogenesis of gastric cancer cells through the inactivation of Pygo2/Wnt signaling.","authors":"Xian Wang, Tiran Zhang, Rong Yu","doi":"10.14670/HH-18-779","DOIUrl":"10.14670/HH-18-779","url":null,"abstract":"<p><p>Gastric cancer represents an aggressive malignancy and a leading contributor to cancer death. Ephrin-A4 (EFNA4) has been proposed to be related to the immune microenvironment and prognosis of gastric cancer. This study was undertaken to discuss the participation and mechanism of EFNA4 in the development of gastric cancer. RT-qPCR and western blot examined EFNA4 and Pygopus2 (Pygo2) expression in gastric cancer cells. After transfection of EFNA4 interference plasmids or co-transfection of EFNA4 interference plasmids and Pygo2 overexpression plasmids, cell proliferation was detected by the CCK-8 method and EDU staining. Wound healing, Transwell, TUNEL, and endothelial cell tube formation assays detected cell migration, invasion, apoptosis, and angiogenesis, respectively. Western blot examined the expression of metastasis-, apoptosis-, angiogenesis-, and Wnt signaling-associated proteins. Cell stemness was estimated by the sphere formation assay, RT-qPCR, and western blot. Through the experimental data, it was noticed that EFNA4 expression was increased in gastric cancer cells. Knockdown of EFNA4 suppressed the proliferation, migration, invasion, angiogenesis as well as stemness while aggravating the apoptosis of gastric cancer cells. Also, EFNA4 depletion reduced Pygo2 protein expression and then inactivated Wnt/β-catenin signaling. Further elevation of Pygo2 reversed the impacts of EFNA4 silencing on Wnt/β-catenin signaling, cell proliferation, apoptosis, migration, invasion, angiogenesis as well as stemness in gastric cancer. Accordingly, the knockdown of EFNA4 might downregulate Pygo2 and inactivate Wnt/β-catenin signaling to exert protective effects against gastric cancer.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"343-356"},"PeriodicalIF":2.5,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141491735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}