Histology and histopathology最新文献

{"title":"Therapeutic potential of CD73⁺ mesenchymal stem cells for myocardial infarction and beyond.","authors":"Huifang Hou, Miaoyun Zheng, Kai Pan, Guodong Wang, Zongjin Li, Qiong Li","doi":"10.14670/HH-18-859","DOIUrl":"https://doi.org/10.14670/HH-18-859","url":null,"abstract":"<p><p>Extracellular adenine nucleotides serve as crucial signaling molecules and influence a broad spectrum of physiological and pathological processes. CD73, the rate-limiting enzyme in the metabolism of extracellular adenine nucleotides, is ubiquitously expressed on various cell types, particularly stem cells. CD73⁺ mesenchymal stem cells (MSCs) have emerged as promising candidates for therapeutic applications due to their immunomodulatory and pro-regenerative properties. Numerous studies have highlighted the crucial role of CD73 in mediating tissue protection in myocardial infarction (MI). In this review, a brief overview of the cell type-specific expression, regulatory effects of CD73 on MSCs, and proangiogenic and immunomodulatory mechanisms is provided, with a focus on current findings concerning the protective functions of CD73 in the context of MI within the framework of stem cell therapy.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18859"},"PeriodicalIF":2.5,"publicationDate":"2024-12-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142881898","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":"Gradual expression of MMP9 and MT1-MMP at the tumor-stroma interface in head and neck squamous cell carcinoma.","authors":"Stefan Rusu, Vincent Nuyens, Alexandre Rousseau, Philippe Lothaire, Nathalie Nagy, Karim Zouaoui Boudjeltia, Pierrick Uzureau","doi":"10.14670/HH-18-858","DOIUrl":"https://doi.org/10.14670/HH-18-858","url":null,"abstract":"<p><p>Due to the late-stage diagnosis of head and neck squamous cell carcinoma (HNSCC), treatment remains a significant clinical challenge. The metalloproteinases MMP-9 and MT1-MMP play a pivotal role in extracellular matrix remodeling, thereby facilitating tumor growth and metastasis. Tumor progression requires the degradation of the basement membrane. The principal components of this structure, namely collagen IV and laminin, are the main targets of both MMP-9 and MT1-MMP. However, they can also exert influence over the expression of these enzymes. Oxidative stress plays an instrumental role in tumor development, functioning as a key inducer of metalloproteinase expression. The present study investigates the distribution of MMP-9 and MT1-MMP within tumor nests and along the basement membrane, comparing these with the distributions of collagen IV, laminin-332, and the antioxidant MnSOD. Biopsies from 12 patients with HNSCC and poor prognostic factors were subjected to immunofluorescence analysis. MMP-9 and MT1-MMP were found to be predominantly present in tumor cells, with a significant decrease in expression from the periphery to the center of tumor nests. Co-localization studies with laminin-332 and collagen IV, revealed substantial overlap, in accordance with the role of MMPs in basal membrane degradation. The cellular expression of laminin-332 associated with MMP-9 expression suggests an intricate relationship between metalloproteinases and their targets. While the previously observed pattern of glutathione-producing enzyme was similar to the metalloproteinases pattern, MnSOD expression was homogeneously distributed within tumor nests. Our findings reveal various distribution patterns of oxidative stress regulators, suggesting a complicated interplay in the development of HNSCC.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18858"},"PeriodicalIF":2.5,"publicationDate":"2024-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876496","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":"HM13 is a predictive biomarker of metastasis and neutrophil infiltration in colorectal cancer.","authors":"Yanbing Ren, Ying Mao, Xiao Yuan","doi":"10.14670/HH-18-857","DOIUrl":"https://doi.org/10.14670/HH-18-857","url":null,"abstract":"<p><strong>Background: </strong>High levels of histocompatibility minor 13 (HM13) have been related to the progression of several cancers. Here, we investigated the function of HM13 in colorectal cancer (CRC).</p><p><strong>Methods: </strong>HM13 expression, clinicopathology analysis, and its influence on survival were analyzed in multiple public databases (TCGA, TIMER2.0, and GEPIA). HM13 mRNA and protein levels in CRC cells were examined by qRT-PCR and western blot, respectively. CCK-8, Transwell, wound-healing, and adhesion assays were used to measure cell proliferation, migration, invasion, and adhesion in HM13-overexpressed and -silenced cells. The relationship between HM13 expression and neutrophil infiltration was also analyzed. CRC xenograft mouse models were used for <i>in vivo</i> verification of HM13 function.</p><p><strong>Results: </strong>In this study, TCGA dataset analysis revealed that elevated HM13 levels correlated with malignant progression and worse survival outcomes in CRC. Cell migration, proliferation, invasion, and adhesion were suppressed through the knockdown of sh-HM13 and enhanced through HM13 overexpression. Additionally, HM13 expression significantly correlated with the infiltration level of neutrophils in CRC in TCGA and TIMER analyses. HM13 levels were also positively correlated with myeloperoxidase (MPO) levels. In addition, <i>in vivo</i> studies further confirmed that MPO overexpression partially abolished the inhibition of tumor growth by sh-HM13 in CRC.</p><p><strong>Conclusion: </strong>The results suggested that high HM13 expression in CRC could promote tumor growth and metastasis by reducing neutrophil infiltration and may serve as a useful target in the treatment of metastatic CRC.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18857"},"PeriodicalIF":2.5,"publicationDate":"2024-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864113","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":"S100A2 upregulates GLUT1 expression to promote glycolysis in the progression of nasopharyngeal carcinoma.","authors":"Ying Peng, Jing Xia, Dinggang Zhou, Zhongchun Yang, Ruifang Zeng, Min Xu, Hongwei Peng","doi":"10.14670/HH-18-778","DOIUrl":"10.14670/HH-18-778","url":null,"abstract":"<p><p>Nasopharyngeal carcinoma (NPC) is a malignant epithelial tumor. Among the S100 protein family members, the imbalance of S100 calcium-binding protein A2 (S100A2) was related to the pathogenesis of several types of cancer, and S100A2 has been reported to be upregulated in the plasma of NPC patients; however, its specific role in NPC pathogenesis remains unclear. Thus, this study aims to determine the potential role of S100A2 in NPC to provide novel insights into NPC management. C666-1 and NPC/HK-1 cells were transfected with S100A2 silencing/overexpression (si/oe) constructs. For <i>in vivo</i> investigations, NPC/HK-1 cells were transfected with si/oe-S100A2 to induce tumor formation in nude mice. Cellular viability and apoptosis were assessed using the CCK8 assay, colony-forming assay, and flow cytometry. Glucose uptake and lactate production levels were quantified using biochemical assays. S100A2 expression was measured via RT-qPCR, Western blot, immunohistochemistry, and immunofluorescence were performed to determine the levels of S100A2, PI3K, AKT, p-PI3K, p-AKT, GLUT1, HK-2, LDHA, and ki-67 proteins. S100A2 expression levels were significantly higher in NPC cancer tissues than in adjacent tissues. Similarly, C666-1 and NPC/HK-1 cells exhibited increased S100A2 expression, and silencing S100A2 significantly inhibited NPC cell viability, proliferation, glucose uptake, and lactate production, and induced apoptosis and decreased the protein levels of GLUT1, LDHA, and HK2 in NPC cells. Conversely, S100A2 overexpression enhanced these characteristics in NPC cells but could be mitigated by the PI3K/AKT inhibitor (LY294002). Silencing S100A2 suppressed the tumor formation of NPC/HK-1 cells, while S100A2 overexpression promoted tumor formation and could be hindered by a GLUT1 inhibitor (WZB117). S100A2 is upregulated in cancer tissues of NPC patients and was found to promote proliferation, glycolysis, and tumor formation in NPC cells through its interaction with GLUT1.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1669-1683"},"PeriodicalIF":4.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141467532","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":"Qualitative evaluations of reactive microglial heterogeneity in cultured porcine retina.","authors":"Kjell Johansson, Camilla Mohlin","doi":"10.14670/HH-18-772","DOIUrl":"10.14670/HH-18-772","url":null,"abstract":"<p><p>A late stage of several retinal disorders is retinal detachment, a complication that results in rapid photoreceptor degeneration and synaptic damage. The porcine retina is a favorable <i>in vitro</i> model for studies of the degenerative processes that follow retinal detachment. Photoreceptor degeneration and synaptic injuries develop rapidly in the cultured porcine retina and correlate with resident microglial cell transition into a reactive phenotype. In this <i>in vitro</i> study, we used retinas cultured for five days and analyzed reactive CD11b and Iba1 immunoreactive microglia that localized close to/within the synaptic outer plexiform layer (OPL) and in the outer nuclear layer (ONL). A subpopulation of the CD11b and Iba1immunoreactive microglia also expressed CD68 immunoreactivity on lysosomal membranes or as a diffuse cytoplasmic stain. Some CD68 immunoreactive microglia were juxtaposed to L/M-opsin immunoreactive cone photoreceptors in the ONL. CD11b and Iba immunoelectron microscopy further suggests the presence of a dark microglial phenotype in the degenerating cultured porcine retina. For immunoelectron microscopy, nickel-enhanced diaminobenzidine (DAB) staining resulted in clearly distinguished reaction products in the cytosol of dark microglia.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1611-1620"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141300574","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":"Effect of 3D printing technology-assisted TKA on cartilage tissue in rabbit with knee osteoarthritis.","authors":"Guoliang Wang, Feng Cheng, Jianxun Cui, Nan Chen, Qing Li","doi":"10.14670/HH-18-743","DOIUrl":"https://doi.org/10.14670/HH-18-743","url":null,"abstract":"<p><strong>Background: </strong>Knee osteoarthritis (KOA) is a common chronic degenerative joint disease. 3D printing technology has become one of the important directions of medical development along with individualized precision treatment in orthopedics.</p><p><strong>Objective: </strong>To investigate the effect of 3D printing technology-assisted total knee arthroplasty (TKA) on cartilage in rabbits with KOA.</p><p><strong>Methods: </strong>A rabbit model of KOA was established and treated by TKA or 3D printing-assisted TKA. Four weeks after treatment, radiological evaluation of rabbit knees was performed by X-ray examination, in order to observe the severity of osteoarthritic lesions. Then the knee joints of rabbits were collected for Hematoxylin-eosin, Toluidine blue, and Safranin O-Fast green staining. The expressions of cartilage matrix metabolism-related and apoptosis-related genes were scrutinized by real-time quantitative reverse transcription-polymerase chain reaction, Western blot, and immunohistochemistry. The levels of inflammatory-related factors in the cartilage tissues of rabbits were tested by enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>In rabbits with KOA, 3D printing technology-assisted TKA alleviated the inflammation and bone remodeling of the knee joint, relieved synovial hyperplasia and inflammatory cell infiltration in the articular cartilage, reduced articular cartilage degradation, suppressed cartilage matrix metabolism, and mitigated the inflammatory response and apoptosis of cartilage cells.</p><p><strong>Conclusion: </strong>3D printing technology-assisted TKA exhibits a good treatment effect in rabbit KOA. This study provides an important basis for the clinical application of 3D printing technology-assisted TKA in KOA treatment.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":"39 12","pages":"1631-1641"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142647430","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":"Brain endothelial cell activation and dysfunction associate with and contribute to the development of enlarged perivascular spaces and cerebral small vessel disease.","authors":"Melvin Ray Hayden","doi":"10.14670/HH-18-792","DOIUrl":"10.14670/HH-18-792","url":null,"abstract":"<p><p>Multiple injurious stimuli to the brain's endothelium results in brain endothelial cell activation and dysfunction (BECact/dys) with upregulation of inflammatory signaling cascades and a decrease in bioavailable nitric oxide respectively. These injurious stimuli initiate a brain injury and a response to injury wound healing genetically programed cascade of events, which result in cellular remodeling of the neurovascular unit and blood-brain barrier with increased inflammation and permeability. These remodeling changes also include the perivascular spaces that become dilated to form enlarged perivascular spaces (EPVS) that may be identified noninvasively by magnetic resonance imaging. These EPVS are associated with and considered to be a biomarker for cerebral small vessel disease (SVD) and a dysfunctional glymphatic system with impaired removal of neurotoxic waste, which ultimately results in neurodegeneration with impaired cognition and dementia. The penultimate section discusses the understudied role of venous cerebral circulation in relation to EPVS, SVD, and the vascular contribution to cognitive impairment (VCID). The focus of this review will be primarily on BEC<i>act/dys</i> that associates with and contributes to the development of EPVS, SVD, and impaired glymphatic system efflux. Importantly, BEC<i>act/dys</i> may be a key piece of the puzzle to unlock this complicated story of EPVS and SVD. Multiple transmission electron micrographs and illustrations will be utilized to depict anatomical ultrastructure and allow for the discussion of multiple functional molecular cascades.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1565-1586"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141758418","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":"Correlation of NAT10 expression with clinical data and survival profiles in esophageal squamous cell carcinoma patients, and its impact on cell proliferation and apoptosis.","authors":"Wei Sun, Xiaoying Shen, Xinyi Wang, Xiaoyan Zhang, Yongling Ji, Jin Wang","doi":"10.14670/HH-18-752","DOIUrl":"10.14670/HH-18-752","url":null,"abstract":"<p><strong>Background: </strong>This study investigates the association between NAT10 expression and clinical parameters while assessing prognostic outcomes in esophageal squamous cell carcinoma (ESCC) patients. Furthermore, the study seeks to elucidate the functional role of NAT10 in neoplastic cell proliferation and apoptosis.</p><p><strong>Materials and methods: </strong>NAT10 expression was assessed in ESCC tissue microarrays through immunohistochemistry (IHC) tests. We employed SPSS software to analyze the correlation between NAT10 staining data, clinical indicators, and their implications for patient prognosis. Small interference RNA (siRNA) was utilized to inhibit NAT10 expression in two esophageal cancer cell lines, TE-1 and KYSE150. Subsequently, we meticulously quantified and compared cellular proliferation and apoptotic ratios among experimental groups. NAT10, Ki67, and Caspase3 expression levels in different groups were evaluated using quantitative polymerase chain reaction (qPCR) and Western blot (WB) assays. Statistical analyses were conducted using GraphPad Prism software, with significance at <i>P</i><0.05.</p><p><strong>Results: </strong>Our findings indicate that NAT10 is overexpressed in ESCC tissues and exhibits a significant correlation with tumor diameter and overall patient survival. Decreasing NAT10 expression led to the inhibition of tumor cell proliferation and the promotion of apoptosis. Furthermore, siRNA-mediated NAT10 inhibition resulted in the downregulation of Ki67 expression and the concomitant upregulation of Caspase3.</p><p><strong>Conclusion: </strong>The observed overexpression of NAT10 in ESCC tissues is associated with larger tumor diameters and reduced patient survival. NAT10 appears to play a pivotal role in the progression of esophageal cancer by influencing cell proliferation and apoptosis. These findings suggest potential clinical implications, with Ki67 and Caspase3 potentially participating in this intricate molecular biological process.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1659-1667"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140876276","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":"Oridonin alleviates inflammation and endoplasmic reticulum stress in pediatric pneumonia via regulating the SIRT1-mediated Wnt/β-catenin signaling pathway.","authors":"Weijuan Han, Chen Qian, Peipei Fu, Junmei Xu","doi":"10.14670/HH-18-795","DOIUrl":"10.14670/HH-18-795","url":null,"abstract":"<p><strong>Background: </strong>Pediatric pneumonia is a prevalent and significant health concern worldwide, with elevated morbidity and mortality rates among affected children. This study was designed to elucidate the therapeutic impact of Oridonin (Ori) on pediatric pneumonia and unravel the underlying mechanisms involved.</p><p><strong>Methods: </strong>A pediatric infantile pneumonia model was established in mice through intratracheal administration of LPS. Additionally, a cell damage model was created in WI-38 cells by administering LPS. Protein levels were assessed via western blotting, and cell viability was measured with CCK-8. Inflammatory cytokines were quantified through ELISA, and specific assays were employed to evaluate oxidative stress markers. Flow cytometry was utilized to assess cell apoptosis.</p><p><strong>Results: </strong>Ori alleviated lung inflammation, oxidative stress, apoptosis, and endoplasmic reticulum stress (ERS) in LPS-induced pneumonia mice. In addition, Ori increased the viability of LPS-induced pneumonia cells but decreased cell apoptosis. Furthermore, Ori reduced oxidative stress, inflammation, and ERS in LPS-induced pneumonia cells by enhancing SIRT1 to activate the Wnt/β-catenin pathway.</p><p><strong>Conclusion: </strong>This study suggested that Ori inhibited pediatric pneumonia by dampening the inflammatory response, oxidative stress, cell apoptosis, and ERS via the SIRT1/Wnt/β-catenin pathway.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1685-1693"},"PeriodicalIF":4.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141733977","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":"TRIM22 mechanism promoting KAT2A ubiquitination degradation to regulate ferroptosis in hepatocellular carcinoma cell invasion and metastasis.","authors":"Xiaoshan Chen, Wei Wang, Wei Wei","doi":"10.14670/HH-18-856","DOIUrl":"https://doi.org/10.14670/HH-18-856","url":null,"abstract":"<p><strong>Objective: </strong>Hepatocellular carcinoma (HCC) is a highly fatal cancer. This study aims to investigate the underlying mechanism of tripartite motif-containing 22 (TRIM22) in HCC cell invasion and metastasis through the K (lysine) acetyltransferase 2A (KAT2A)/glutathione peroxidase 4 (GPX4) axis.</p><p><strong>Methods: </strong>Human HCC cells BEL7405 were cultured <i>in vitro</i> and treated with MG-132, Ferrostain-1, pcDNA3.1-TRIM22, pcDNA3.1-KAT2A, or pcDNA3.1-NC. TRIM22-KAT2A interaction and KAT2A ubiquitination level, cell proliferation, invasion, migration, and histone H3 lysine 9 acetylation (H3K9ac) enrichment level on the GPX4 promoter were assessed by Co-IP, CCK-8, Transwell, and ChIP-qPCR assays. Mice were injected subcutaneously with Lv-oe-NC or Lv-oe-TRIM22 BEL7405 cells via the tail vein. Tumor proliferation and levels of TRIM22, KAT2A, GPX4, Fe²⁺, malondialdehyde (MDA), reactive oxygen species (ROS), and glutathione (GSH) in tissues and cells were evaluated by immunohistochemistry, RT-qPCR, western blot, and kits.</p><p><strong>Results: </strong>oe-TRIM22-treated BEL7405 cells exhibited increased TRIM22 expression, and abated KAT2A protein expression and malignant cell biological behaviors, which were partially reversed by upregulating KAT2A or suppressing ferroptosis. TRIM22 interacted with KAT2A, which was ubiquitinated to regulate GPX4 histone acetylation. TRIM22 overexpression elevated Fe²⁺, MDA, and ROS levels and cell death, and diminished GSH, GPX4, and H3K9ac enrichment levels, whereas further overexpression of KAT2A brought about opposite trends. TRIM22 suppressed HCC growth and metastasis by mediating ferroptosis through the KAT2A/GPX4 axis.</p><p><strong>Conclusions: </strong>TRIM22 promoted KAT2A ubiquitination degradation to reduce H3K9ac enrichment levels in the GPX4 promoter region, and facilitated ferroptosis, thereby inhibiting HCC cell invasion and metastasis and <i>in vivo</i> growth and metastasis.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18856"},"PeriodicalIF":2.5,"publicationDate":"2024-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142852978","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}