Histology and histopathology最新文献

{"title":"Mechanism of lncRNA PLACT1 in regulating the proliferation of pancreatic adenocarcinoma cells through the KLF2/KIAA1522 axis.","authors":"Fei Wang, Xiaoli Hou, Shutao Wu, Wei Sun, Yixia Wang, Yasen Cao, Hong Cheng","doi":"10.14670/HH-25-011","DOIUrl":"10.14670/HH-25-011","url":null,"abstract":"<p><strong>Background: </strong>Pancreatic adenocarcinoma (PAAD) is among the most common cancers worldwide. This study aims to investigate the role of long noncoding RNA pancreatic cancer-associated transcript 1 (LncRNA PLACT1) in PAAD cell proliferation.</p><p><strong>Methods: </strong>PAAD and normal cells were cultured. The levels of PLACT1, Krüppel-like factor 2 (KLF2), and KIAA1522 were detected. After PLACT1 expression was interfered with, cell proliferation was detected using the cell counting kit-8, clone formation assay, and 5-ethynyl-2-deoxyuridine (EdU) staining. The binding of PLACT1 to euchromatic histone lysine methyltransferase 2 (EHMT2) was analyzed. The enrichment of EHMT2 and histone H3 lysine 9 dimethylation (H3K9me2) on the KLF2 promoter was analyzed by chromatin immunoprecipitation. KLF2 expression was detected after EHMT2 intervention. The binding of KLF2 to the KIAA1522 promoter was analyzed. The nude mouse xenograft model was constructed to detect the role of PLACT1 <i>in vivo</i>.</p><p><strong>Results: </strong>PLACT1 and KIAA1522 were highly expressed, and KLF2 was poorly expressed in PAAD cells. Silencing PLACT1 decreased cell proliferation, the number of cell clones, and EdU-positive cells. Mechanistically, PLACT1 inhibited KLF2 expression by recruiting EHMT2 to induce H3K9me2 in the KLF2 promoter region, resulting in reduced KLF2 enrichment at the KIAA1522 promoter and increased KIAA1522 expression. KLF2 downregulation or KIAA1522 overexpression alleviated the inhibitory effect of PLACT1 silencing on PAAD cell proliferation. PLACT1 silencing prevented PAAD tumorigenesis by regulating the KLF2/KIAA1522 pathway.</p><p><strong>Conclusion: </strong>PLACT1 silencing inhibited PAAD by inhibiting KLF2 and promoting KIAA1522 expression, suggesting the therapeutic effect of PLACT1 silencing on PAAD.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1081-1092"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145400667","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":"Downregulation of PDCD10 mitigates the malignant biological behavior and increases the sensitivity of esophageal squamous cell carcinoma cells to radiotherapy by inhibiting the PI3K/AKT pathway.","authors":"Junkai Xu, Qisong Chen, Qing Gao","doi":"10.14670/HH-25-010","DOIUrl":"10.14670/HH-25-010","url":null,"abstract":"<p><p>The intensification of radiotherapy is an effective way to improve the therapeutic efficacy of radiation-sensitive malignancies such as esophageal cancer (EC). Esophageal squamous cell carcinoma (ESCC) accounts for 85% of all EC cases worldwide, with a relatively higher incidence and mortality in East Asia. In this study, we explored the functions and mechanisms of programmed cell death 10 (PDCD10) in the malignancy and radiotherapy sensitivity of ESCC cells. We observed that PDCD10 is highly expressed in ESCC tissues and is correlated with a poor prognosis in patients with ESCC. PDCD10 downregulation suppressed ESCC cell proliferation, migration, and invasion but promoted apoptosis. In addition, it enhanced ionizing radiation (IR)-induced ESCC cell damage, whereas PDCD10 overexpression had the opposite effect. Mechanistically, PDCD10 increased the phosphorylation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) in ESCC cell lines. The administration of LY294002, a PI3K inhibitor, significantly inhibited the oncogenic functions of PDCD10, leading to an increase in IR-induced cell damage. These findings establish PDCD10 as a critical intrinsic regulator of the sensitivity of ESCC cells to IR through the modulation of the PI3K/AKT pathway.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1065-1079"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145389083","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":"Stimulator of interferon genes (STING) in renal tumors: Biological bases, diagnostic relevance, and predictive potential.","authors":"Stefano Marletta, Anna Caliò, Lisa Marcolini, Lavinia Stefanizzi, Filippo Maria Martelli, Cinzia Giacometti, Guido Martignoni","doi":"10.14670/HH-25-027","DOIUrl":"10.14670/HH-25-027","url":null,"abstract":"<p><p>Renal tumors encompass a diverse group of neoplasms with distinct morphological and molecular features. Recent research has highlighted the stimulator of interferon genes (STING) pathway as a key player in tumorigenesis, immune modulation, and autophagy across various renal tumor histotypes. This review explores the biological, diagnostic, prognostic, and therapeutic implications of STING in both epithelial and mesenchymal renal neoplasms. In clear cell renal cell carcinoma, STING expression correlates with aggressive histological features and poor clinical outcomes, suggesting a role in immune evasion and tumor progression. Similarly, in fumarate hydratase-deficient renal cell carcinoma, STING activation, driven by mitochondrial dysfunction and fumarate accumulation, aligns with PD-L1 expression and tumoral inflammatory infiltrate, supporting its potential function as a predictive biomarker of immunotherapy response. In renal perivascular epithelioid cell (PEC) proliferations, widespread STING expression is linked to autophagy regulation and mTOR pathway interaction, offering novel therapeutic insights. The dual role of STING in promoting or suppressing inflammation underscores the therapeutic potential of both agonists and antagonists of this pathway, depending on the specific tumor entity. Moreover, STING's interplay with interferons and cytokines, such as IL-6 and IFNγ, further supports its relevance in modulating immune responses and treatment efficacy. Despite current limitations, accumulating evidence places STING as a promising biomarker and therapeutic target in numerous renal tumors. Future studies are warranted to clarify its mechanistic roles and optimize its clinical application across renal tumor subtypes.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"979-993"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145819150","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":"Overview of joint tissue alterations in femoroacetabular impingement: What we know through laboratory analyses.","authors":"Giorgia Borciani, Michela Battistelli, Eleonora Olivotto","doi":"10.14670/HH-25-019","DOIUrl":"10.14670/HH-25-019","url":null,"abstract":"<p><p>Hip osteoarthritis (HOA) is the most common hip joint disorder, accounting for approximately 27.9% of all cases of osteoarthritis (OA), often leading to total hip replacement (THR). In the last decades, femoroacetabular impingement (FAI) has been addressed as a significant etiological factor in the development of early-onset HOA, especially in young adults with non-dysplastic hips. FAI has been found to cause damage to all joint tissues, cartilage, labrum, and subchondral bone, thus underlining the importance of an early diagnosis and intervention to prevent progression to end-stage disease. This review aims to provide a comprehensive overview of the biochemical, morphological, and cellular alterations occurring in hip joint tissues in the presence of FAI. Understanding the early pathological changes is of crucial importance as they often precede radiographic signs of disease and may serve as valuable biomarkers for early detection and management of FAI and peri-arthritic conditions to delay or prevent the need for THR in younger populations.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"937-952"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145603914","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":"Immunohistochemical localization of D-β-aspartic acid and periostin in benign parotid gland tumors.","authors":"Yutaka Tateda, Takahiro Suzuki, Teruyuki Sato, Kenji Izuhara, Kazue Ise, Hiroki Shimada, Keigo Murakami, Kazuhiro Murakami, Yasuhiro Nakamura, Nobuo Ohta","doi":"10.14670/HH-25-013","DOIUrl":"10.14670/HH-25-013","url":null,"abstract":"<p><p>Periostin is involved in airway remodeling, salivary tumors, and various otolaryngological diseases. D-β-aspartic acid is the major isomer of D-aspartic acid found in the tissues of elderly individuals. In this study, we investigated the expression and role of D-β-aspartic acid and periostin in the formation of benign parotid tumors. The data of 36 patients (16 male and 20 female) who underwent parotid tumor resection between April 2017 and March 2022 and were clinically and pathologically diagnosed as having benign parotid tumors were included in this study. The mean age of the patients was 59.2 (range 26-82) years. Tumors were histologically classified as pleomorphic adenomas, Warthin's tumors, basal cell adenomas, oncocytomas, and myoepitheliomas. Increased D-β-aspartic acid expression was observed in the epithelium and stroma of benign parotid tumors. In the epithelium, D-β-aspartic acid was found in 35 of 38 samples (92.1%). In the stroma, it was found in 19 of 38 samples (50.0%). In the stroma of benign parotid tumors, increased expression of periostin was found in 32 of 38 samples (84.2%). Four periostin expression patterns were observed in benign parotid tumors: negative, superficial, infiltrative, and diffuse. Statistically significant differences were found between the expression pattern of D-β-aspartic acid in the stroma and the histological classification of benign parotid gland tumors. In addition, a statistically significant difference was found between the expression patterns of D-β-aspartic acid and periostin in the stroma. Our results suggest that D-β-aspartic acid and periostin may be involved in the pathogenesis of benign parotid gland tumors.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1019-1025"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145431292","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":"Yolkin tempers inflammatory mediator release and liver pathology in experimental endotoxemia in mice.","authors":"Michał Zimecki, Jolanta Artym, Maja Kocięba, Ewa Zaczyńska, Katarzyna Kaleta-Kuratewicz, Jan P Madej, Piotr Kuropka, Aleksandra Zambrowicz, Łukasz Bobak","doi":"10.14670/HH-25-031","DOIUrl":"10.14670/HH-25-031","url":null,"abstract":"<p><p>Yolkin is an egg yolk-derived protein with immunoregulatory properties. In this work, yolkin was evaluated as a protective agent in endotoxemic BALB/c mice. The mice were pretreated with yolkin either orally in drinking water or intraperitoneally (i.p.) before i.p. injection of <i>E. coli</i> lipopolysaccharide (LPS). Circulating blood leukocyte number, blood cell composition, serum levels of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and haptoglobin, as well as histological changes in the spleen and the liver, were examined. Yolkin differentially regulated the values of these parameters, depending on the administration protocol; however, the serum levels of TNF-α and IL-6 were generally decreased, and the level of haptoglobin, an acute-phase protein, was elevated. The pretreatment of mice with yolkin led to improved histological architecture in the investigated organs of endotoxemic mice, particularly in the liver, where yolkin diminished an increased level of vascular permeability and reversed a decreased number of Kupffer cells. These changes were independent of the route of yolkin administration. In conclusion, yolkin proved effective in the amelioration of pathogenic consequences of LPS administration and may be considered a potential protective measure for patients at risk of endotoxemia.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1027-1042"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145917554","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":"Physiological functions of seminal vesicle secretions in male fertility.","authors":"Ayumu Taira, Taichi Noda","doi":"10.14670/HH-25-028","DOIUrl":"10.14670/HH-25-028","url":null,"abstract":"<p><p>In many mammals, accessory gland secretions are ejaculated into the female reproductive tract, along with sperm, and the prostates and seminal vesicles are the main glands responsible for these secretions. Cauda epididymal sperm can efficiently fertilize eggs <i>in vitro</i>; however, we found that seminal vesicle secretions improved sperm fertilization rates <i>in vivo</i> by artificial insemination. Furthermore, using the seminal vesicle-removed mice, other studies have shown that seminal vesicle secretions contribute to embryogenesis and offspring health by regulating the environment in the female reproductive tract. These results indicate the significance of accessory gland secretions in fertilization and development <i>in vivo</i>. More than 700 proteins are present in the accessory glands, and genome editing accelerates the functional analysis of these proteins at the individual level. For example, some studies reported results from phenotypic analyses of genetically modified mice that were different from those of <i>in vitro</i> experiments. In this review, we discuss the current findings on the effects of accessory gland secretions on male fertility and the future prospects.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"995-1003"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145833920","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":"Current review on inducible nitric oxide synthase and Src tyrosine kinase inhibitors as disease-modifiers in preclinical models of epilepsy.","authors":"Suraj Sundara Vasanthi, Thimmasettappa Thippeswamy","doi":"10.14670/HH-25-022","DOIUrl":"10.14670/HH-25-022","url":null,"abstract":"<p><p>Acute exposure to seizurogenic chemicals, such as organophosphates (OPs) or domoic acid (kainate analogue), can trigger status epilepticus (SE), marked by central (seizures) and, with OPs, peripheral effects due to irreversible inhibition of acetylcholinesterase (AChE). The initial seizurogenic activity in the brain initiates a cascade of molecular and cellular changes, known as epileptogenesis, the process by which epilepsy develops. Among the several signaling pathways involved in epileptogenesis, this review discusses the roles of the Src family of tyrosine kinases (SFK), especially Fyn kinase, and inducible nitric oxide synthase (iNOS) mediated mechanisms. Both signaling molecules are upregulated following initial seizures and persist for a long time, contributing to neuroinflammation, elevated levels of reactive oxygen and nitrogen species (ROS/RNS), and proinflammatory cytokines, as well as neurodegeneration and spontaneously recurring seizures. Epilepsy is a progressive disease associated with unprovoked seizures and cognitive decline. While the current standard of care can alleviate symptoms and reduce mortality, they do not address long-term neurological consequences. In this review, we discuss preclinical testing of two CNS-targeted drugs, iNOS and SFK inhibitors 1400W and Saracatinib (SAR; AZD0530), respectively, as potential disease-modifiers.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"953-977"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145668283","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":"WuFu decoction alleviates osteoarthritis by regulating TGF-β1/Smad and ERK1/2 pathways.","authors":"Zhengcong Ye, Linghua Zhou, Jian Lin, Pengzheng Yu","doi":"10.14670/HH-25-017","DOIUrl":"10.14670/HH-25-017","url":null,"abstract":"<p><p>The age-standardized point prevalence of global osteoarthritis (OA) has increased, and OA will not only lead to disability in patients but also to a greater psychological burden. In recent years, the focus of scientists on treating OA has turned to disease prevention and treatment of early OA. Previous studies have proved that WuFu Decoction (WFD) could protect chondrocytes, and the Chinese herbs in this prescription have shown anti-inflammatory effects. In this study, we built the OA rat model by the modified Hulth method, conducted research with WFD, and set D-Glucosamine sulfate as the positive control. It is proven that WFD improved the micromorphology and tissue damage of the knee joint, decreased the score of the Mankin and OARSI system, and inhibited the IL-1β, TNF-α, MMP-13, and CTX-1 levels in serum. Additionally, WFD treatment inhibited p-ERK1/2 levels and raised the mRNA and protein levels of TGF-β1, p-Smad2, p-Smad3, type II collagen (the gene is <i>COL2A1</i>), ALP, TRACP, and BMP7. Furthermore, TGF-β1 inhibitor (Decorin) reversed the improvement effect of WFD on OA, but ERK1/2 inhibitor (PD98059) promoted this improvement effect. Silencing TGFβR2 can reverse the protective effect of WFD on primary chondrocytes. It is suggested that WFD can improve OA and chondrocytes by regulating the TGF-β1/Smad and ERK1/2 pathways. This study also identified active ingredients, such as Fumaric acid, Glycyrrhizic acid, Albiflorin, and Isoliquiritigenin. It provides a basis for the clinical application of WFD and for the promotion and development of TCM.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1101-1116"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145540705","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":"C6orf15 expression in thyroid tumors: A promising diagnostic biomarker for the classic variant of papillary thyroid carcinoma.","authors":"Aobo Xu, Pengju Zhang, Jiaxin Chai, Jiandong Wang, Pengfei Huang, Xudong Gu","doi":"10.14670/HH-25-007","DOIUrl":"10.14670/HH-25-007","url":null,"abstract":"<p><p>Although C6orf15 is highly expressed in certain human cancers, its expression pattern in papillary tumors remains unclear. In this study, we investigated C6orf15 expression in papillary tumors and assessed its potential as a diagnostic biomarker for histopathological evaluation and fine-needle aspiration cytology (FNAC). We collected a total of 87 formalin-fixed and paraffin-embedded (FFPE) thyroid tissue specimens that included: 10 cases with Hashimoto's thyroiditis (HT), 11 with follicular adenomas (FAs), two with non-invasive follicular thyroid neoplasms with papillary-like nuclear feature (NIFTP), six with follicular thyroid carcinomas (FTCs), three with invasive encapsulated follicular variant of papillary thyroid carcinomas (IEFVPTCs), three with medullary thyroid carcinomas (MTCs), and 52 with papillary thyroid carcinomas (PTCs). Additionally, 33 FNAC samples from thyroid nodules were analyzed, comprising three samples of FA, five atypia of undetermined significance (AUS), and 25 cases of PTC. Immunohistochemical (IHC) staining was performed to assess C6orf15 expression in thyroid tumor tissues and FNAC samples. We conducted <i>BRAF</i> V600E mutation analysis via Sanger sequencing and IHC and discerned that C6orf15 expression was absent in normal follicular epithelial cells, FA, NIFTP, TFC, and MTC. The positivity rates for C6orf15 in FFPE samples were as follows: 66.7% for IEFVPTC, 86.5% for PTC, and 60.0% for AUS. In FNAC samples, the positivity rate was 80.0% for PTC. A significant positive correlation was observed between C6orf15 expression and the <i>BRAF</i> V600E mutation in PTC tissues (<i>p</i><0.001), but no such association was found in FNAC samples (<i>p</i>=0.230). C6orf15 exhibited high expression levels in the majority of IEFVPTC (66.7%), PTC tissues (86.5%), and FNAC samples (80.0%). These findings suggest that C6orf15 constitutes a promising diagnostic biomarker for the classic variant of PTC and is applicable to histopathological assessment and FNAC-based diagnosis.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"1055-1063"},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145336756","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}