Acta histochemica最新文献

{"title":"Neurochemical heterogeneity of ChAT-immunoreactive neurons in the basal forebrain cholinergic nuclei and striatum in reference to CGRP, CCK, and calcium-binding proteins","authors":"Mirza Mienur Meher ,&nbsp;Marya Afrin ,&nbsp;Mir Rubayet Jahan ,&nbsp;Kanako Nozaki ,&nbsp;Koh-hei Masumoto ,&nbsp;Akie Yanai ,&nbsp;Md Nabiul Islam","doi":"10.1016/j.acthis.2025.152291","DOIUrl":"10.1016/j.acthis.2025.152291","url":null,"abstract":"<div><div>Cholinergic neurons in the basal forebrain cholinergic nuclei (BFCN) and neostriatum (CPu) play key roles in learning, attention, and motor control. The loss of cholinergic neurons causes major neurodegenerative diseases such as Alzheimer’s disease. This study aimed to elucidate the molecular diversity of choline acetyltransferase immunoreactive (ChAT-ir) neurons in these brain regions. We performed immunohistochemistry to determine the co-expression of ChAT-ir neurons with two neuropeptides, calcitonin gene-related peptide (CGRP) and cholecystokinin (CCK), as well as three calcium-binding proteins, such as calbindin, calretinin, and parvalbumin, in the adult mouse brain. The results showed that ChAT, calbindin, CGRP and CCK were strongly expressed in the BFCN, including medial septal nucleus (MS), nucleus of vertical limb and horizontal limb of the diagonal band of Broca (VDB and HDB), substantia innominata basal part (SIB), and in the caudate putamen (CPu). CGRP and CCK showed a high immunoreactive co-expression with ChAT, especially in the HDB and CPu. Calbindin immunoreactivity was widely present and coincided with ChAT in the VDB, HDB, and CPu. However, calretinin immunoreactivity showed a selective co-expression with ChAT in the VDB, SIB, and CPu. Although parvalbumin immunoreactivity was observed throughout the BFCN and CPu, but there was no co-expression between ChAT and parvalbumin. The neurochemical diversity of ChAT-ir neurons in the BFCN and neostriatum suggests the specialized functions of cholinergic neurons across different circuits, especially by modulating CGRP, CCK, or calbindin. These results could provide new insight into cholinergic modulation throughout the BFCN and striatum.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"127 4","pages":"Article 152291"},"PeriodicalIF":2.4,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145009844","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":"Neuroprotective effect of Urolithin A via downregulating VDAC1-mediated autophagy in Alzheimer's disease","authors":"Bensi Zhang ,&nbsp;Xiujun Zhang ,&nbsp;Waleephan Treebupachatsakul ,&nbsp;Rungusa Pantan ,&nbsp;Natnicha Kampan ,&nbsp;Manussabhorn Phatsara ,&nbsp;Chun Shi ,&nbsp;Suteera Narakornsak","doi":"10.1016/j.acthis.2025.152290","DOIUrl":"10.1016/j.acthis.2025.152290","url":null,"abstract":"<div><h3>Background</h3><div>Amyloid β (Aβ) accumulation in the brains of patients with Alzheimer's disease (AD) contributes to cognitive impairment and neuronal damage. Urolithin A (UA), a gut microbiota–derived metabolite of ellagic acid, has been reported to cross the blood-brain barrier to exert anti-inflammatory and anti-oxidation effects in the brain. However, the molecular mechanisms of UA in AD were still unclear. This study aims to explore the neuroprotective effect and mechanism of UA on APP/PS1 mice and Aβ_1–42-injured N2a and PC12 cells.</div></div><div><h3>Methods</h3><div>In this study, Morris water maze was used to detect the cognitive function. Immunofluorescence was used to detect the deposition of Aβ and the expression of voltage-dependent anion channel 1 (VDAC1) in the brains of APP/PS1 mice. Western blotting was used to detect the expression of VDAC1, AMPK pathway, PI3K pathway and autophagy-related proteins. CCK8 was used to detect the viability of Aβ_1–42-injured cells.</div></div><div><h3>Results</h3><div>In this research, we found that UA improved cognitive dysfunction and reduced Aβ deposition in APP/PS1 mice. Furthermore, UA activated autophagy and upregulated the levels of autophagy-related proteins in both APP/PS1 mice and Aβ_1–42-injured N2a and PC12 cells. At the same time, UA down-regulated the phosphorylation level of PI3K/AKT/mTOR and up-regulated the phosphorylation level of AMPK in APP/PS1 mice and Aβ_1–42-injured N2a cells and PC12 cells. In addition, UA down-regulated VDAC1, consistent with the effect of VDAC1 antagonist DIDS (4′-diisothiocyano-2,2′-disulfonic acid stilbene). Importantly, the UA-induced activation of autophagy and modulation of the PI3K and AMPK pathways were reversed by VDAC1 overexpression.</div></div><div><h3>Conclusion</h3><div>These findings demonstrated that UA down-regulated VDAC1 played a key neuroprotective role on AD by inhibiting the PI3K/AKT/mTOR pathway and activating the AMPK pathway to promote autophagy.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"127 4","pages":"Article 152290"},"PeriodicalIF":2.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144921397","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":"USP22-mediated PNMA5 deubiquitination promotes proliferation, migration and invasion of prostate cancer cells.","authors":"Hong Zhi, Tana, Nigemutu Bai, Wuenbilige Bai, Bowen Bai, Suo Liu","doi":"10.1016/j.acthis.2025.152279","DOIUrl":"10.1016/j.acthis.2025.152279","url":null,"abstract":"<p><strong>Background: </strong>Prostate cancer (PCa) stands as one of the primary contributors to cancer-related mortality among men globally. It is reported that USP22 functions as an oncogene, while PNMA5 exhibits a significant pro-metastatic effect. This research investigation centered on examining the interplay between USP22 and PNMA5 and their collaborative role in enhancing PCa progression.</p><p><strong>Methods: </strong>The expression of USP22 and PNMA5 in tissue was determined by IHC. The differential expression of cellular USP22 and PNMA5 were detected using qPCR and immunoblotting, respectively. Cell viability and proliferation were assessed by MTT and sphere-formation assay. Transwell and wound-healing assay were conducted to evaluate the metastatic ability. The interaction between USP22 and PNMA5 was detected by Co-IP and IP. A tumor-bearing mice model was established for in vivo detection.</p><p><strong>Results: </strong>USP22 and PNMA5 were highly expressed in both PCa tumor tissues and cells. Knocking down USP22 or PNMA5 inhibited the migration and invasion of PCa cells. USP22 mediated the deubiquitination of PNMA5. PNMA5 overexpression reversed the decrease in cell viability and proliferation rate, as well as the diminished migration and invasion ability induced by USP22 knockdown.</p><p><strong>Conclusion: </strong>USP22 promotes migration and invasion of PCa cells by regulating PNMA5 deubiquitination.</p>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"127 3","pages":"152279"},"PeriodicalIF":2.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144815475","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":"Blood transfusion mediated tumor microenvironment remodeling in breast cancer","authors":"Qinan Yin ,&nbsp;Shunshun Zhang ,&nbsp;Mouna Ouchari ,&nbsp;Pei Wang ,&nbsp;Anshun Zhao ,&nbsp;Li Zeng ,&nbsp;Jingjing Wang ,&nbsp;Kaiyuan Yao ,&nbsp;Siya Tang ,&nbsp;Haodi Ma ,&nbsp;Anne-Catherine Girondin ,&nbsp;Hecai Yang ,&nbsp;Xuewei Zheng ,&nbsp;Zhifeng Qu","doi":"10.1016/j.acthis.2025.152289","DOIUrl":"10.1016/j.acthis.2025.152289","url":null,"abstract":"<div><div>Blood transfusions play a critical role in breast cancer management, particularly in addressing perioperative blood loss and chemotherapy-induced anemia. However, emerging evidence suggests that transfusions may adversely affect oncologic outcomes by inducing transfusion-related immunomodulation (TRIM) and altering the tumor microenvironment (TME). TRIM suppresses cytotoxic immune responses, potentially facilitating tumor progression—especially in aggressive subtypes such as triple-negative breast cancer (TNBC) and HER2-positive cancers. Additionally, transfusions can paradoxically exacerbate tumor hypoxia by increasing blood viscosity and impairing microvascular perfusion, thereby reducing the effectiveness of chemotherapy, radiotherapy, and immunotherapy. This review examines the dual role of blood transfusions in breast cancer, emphasizing both their clinical benefits and potential risks. We analyze their impact on treatment resistance and tumor progression and discuss strategies to mitigate associated risks, including leukoreduction, erythropoiesis-stimulating agents (ESAs), intravenous iron supplementation, and blood conservation techniques. Furthermore, we highlight the importance of personalized transfusion approaches guided by tumor subtype, immune status, and relevant biomarkers such as tumor-infiltrating lymphocytes (TILs), PD-L1 expression, and circulating tumor DNA (ctDNA). Future research should focus on optimizing transfusion timing, implementing biomarker-driven protocols, and developing immune-modulating interventions to counteract TRIM. A personalized, evidence-based transfusion strategy may ultimately enhance treatment efficacy and improve long-term outcomes in breast cancer care.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"127 4","pages":"Article 152289"},"PeriodicalIF":2.4,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144889220","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":"Corrigendum to \"Inducible gankyrin overexpression drives hepatocarcinogenesis in a liver-specific zebrafish model\" [Acta Histochem. 127 (2025) 152280].","authors":"Yuxi Sun, Zhiyuan Gong, Yueh-Min Lin, Jeng-Wei Lu","doi":"10.1016/j.acthis.2025.152281","DOIUrl":"10.1016/j.acthis.2025.152281","url":null,"abstract":"","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":" ","pages":"152281"},"PeriodicalIF":2.4,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144881816","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":"Advancing triple-negative breast cancer therapy: 3D in vitro models to unravel drug resistance mechanisms and tumor microenvironment interactions","authors":"Gomathy Baskar ,&nbsp;Thirunavukkarasu Palaniyandi","doi":"10.1016/j.acthis.2025.152282","DOIUrl":"10.1016/j.acthis.2025.152282","url":null,"abstract":"<div><div>Triple-negative breast cancer (TNBC) poses considerable clinical challenges due to its aggressive nature, early metastasis, and limited treatment options. The simplified 2D models and the physiological differences in animal models often result in inconsistent responses to anticancer drugs. To tackle these challenges, three-dimensional (3D) in vitro bioengineered models that accurately replicate the <em>in vivo</em> tumor microenvironment (TME) have been developed, offering a more reliable platform for preclinical drug testing. Recent advancements in cell culture techniques have facilitated the creation of 3D models derived from patient tissues and tumors, which effectively mimic the native tissue environment and exhibit drug sensitivity and cytotoxicity behaviors similar to those observed in vivo. It is increasingly acknowledged that the extracellular matrix and cellular diversity within the TME significantly influence the fate of cancer cells. Consequently, strategies to explore drug resistance mechanisms must account for both microenvironmental factors and genetic mutations. This review examines 3D in vitro model systems that integrate microenvironmental influences to investigate drug resistance mechanisms in breast cancer. We discussed various bioengineered models, including spheroid-based, biomaterial-based (such as polymeric scaffolds and hydrogels), patient-derived xenograft (PDX), 3D bioprinting, and microfluidic chip-based models. Additionally, we discuss the relevance of these 3D models in understanding the effects of TME signals on drug response and resistance, as well as their potential for developing strategies to overcome drug resistance and optimize treatment regimens.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"127 4","pages":"Article 152282"},"PeriodicalIF":2.4,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144858076","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":"Detection assays of mitochondrial permeability transition pore: Current status and future prospects","authors":"Dongyang Hong ,&nbsp;Jiawei Huang ,&nbsp;Sicheng Hu ,&nbsp;Yawen Zheng ,&nbsp;Yuhuan Wu ,&nbsp;Ziyang Cao ,&nbsp;Zijun Yan ,&nbsp;Hongyang Zhang ,&nbsp;Huanhuan Feng ,&nbsp;Jinxia Wang ,&nbsp;Lin Zou","doi":"10.1016/j.acthis.2025.152278","DOIUrl":"10.1016/j.acthis.2025.152278","url":null,"abstract":"<div><div>The mitochondrial permeability transition pore (mPTP) is a supramolecular entity in the inner mitochondrial membrane composed of various protein complexes, which is a critical component in maintaining mitochondrial function and cellular homeostasis. In this review, we provide a comprehensive summary of the current detection techniques for mPTP, including spectrophotometry, patch clamping, fluorescent probes, and flow cytometry, which have the potential to reveal the status of mPTP and its roles in degenerative diseases, inflammation, tumors and other diseases. Additionally, we discuss promising new methods to detect mPTP including enhancement in precision, high sensitivity, multi-parameter analysis, and technological integration. These advances highlight new possibilities of clinical diagnosis and treatment for mitochondria-related diseases.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"127 3","pages":"Article 152278"},"PeriodicalIF":2.4,"publicationDate":"2025-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144771632","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":"Inducible gankyrin overexpression drives hepatocarcinogenesis in a liver-specific zebrafish model","authors":"Zhiyuan Gong ,&nbsp;Yuxi Sun ,&nbsp;Yueh-Min Lin ,&nbsp;Jeng-Wei Lu","doi":"10.1016/j.acthis.2025.152280","DOIUrl":"10.1016/j.acthis.2025.152280","url":null,"abstract":"<div><h3>Background</h3><div>Hepatocarcinogenesis is a complex, multistep process that begins with fatty liver, progresses to fibrosis, and ultimately leads to cancer. Numerous etiological factors contribute to this progression, highlighting the importance of developing animal models to facilitate both basic and translational research aimed at discovering new therapeutic strategies. Gankyrin is a key oncoprotein involved in the genetic regulation of liver pathology.</div></div><div><h3>Material and method</h3><div>To investigate its oncogenic role without the need for cancer cell inoculation or drug treatment, we employed a Tet-On system to drive zebrafish <em>gankyrin</em> overexpression in hepatocytes under the control of the <em>fabp10a</em> promoter. <em>Results:</em> After eight weeks of induction, <em>fabp10a:eGFP-gankyrin</em> transgenic zebrafish spontaneously developed persistent hyperplasia, bile duct hyperplasia, and hepatocellular carcinoma (HCC), demonstrating the oncogenic potential of <em>gankyrin</em> in liver tumorigenesis. In this study, we demonstrate that <em>gankyrin</em> activation drives the progressive development of HCC in zebrafish. Liver-specific overexpression of <em>gankyrin</em> in wild-type zebrafish led to hyperplasia, bile duct hyperplasia, and HCC, establishing a robust zebrafish model for studying liver cancer. Our findings highlight the utility of this model for investigating the molecular mechanisms underlying tumorigenesis.</div></div><div><h3>Conclusion</h3><div>This study establishes a robust zebrafish model in which liver-specific overexpression of <em>gankyrin</em> induces spontaneous progression from hyperplasia to hepatocellular carcinoma. The model provides a valuable platform for investigating the molecular mechanisms of hepatocarcinogenesis and exploring potential therapeutic strategies.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"127 3","pages":"Article 152280"},"PeriodicalIF":2.4,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144750480","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":"HSPB1 promotes gastric cancer progression by suppressing PANoptosis","authors":"Lei Yang ,&nbsp;Miaomiao Zeng ,&nbsp;Binsheng Wang ,&nbsp;Ze Yang ,&nbsp;Bo Li ,&nbsp;Xiaoliang Zhu","doi":"10.1016/j.acthis.2025.152277","DOIUrl":"10.1016/j.acthis.2025.152277","url":null,"abstract":"<div><div>Gastric cancer (GC) remains a leading cause of cancer-related mortality worldwide, driven by molecular mechanisms that promote tumor progression and therapeutic resistance. PANoptosis, an integrated programmed cell death pathway involving apoptosis, necroptosis, and pyroptosis, has emerged as a key regulator of tumorigenesis, yet its modulation in GC is poorly understood. This study aimed to investigate the role of heat shock protein beta-1 (HSPB1) in regulating PANoptosis and its impact on GC progression, hypothesizing that HSPB1 overexpression suppresses PANoptosis to enhance tumor malignancy. We employed an integrative approach combining bioinformatics analysis of GEO (GSE54129), TCGA, and GSE15460 datasets with experimental validations. HSPB1 expression was assessed in 40 paired GC and normal tissues and multiple GC cell lines (AGS, MKN-45, NCI-N87, HGC-27, SNU-1) via qPCR, Western blot, and immunohistochemistry. Functional roles were explored by overexpressing or silencing HSPB1 in NCI-N87 and AGS cells, followed by proliferation, colony formation, migration, and apoptosis assays. In vivo effects were evaluated using a nude mouse xenograft model with shHSPB1-transfected cells, analyzing tumor growth and PANoptosis markers (P-MLKL, RIPK3, Cleaved Caspase-1, NLRP3, Cleaved Caspase-3) via Western blot, IHC, and TUNEL assays. Bioinformatics revealed HSPB1 as a PANoptosis-related prognostic biomarker, with elevated expression in GC tissues correlating with poor survival. Experimental validation confirmed HSPB1 overexpression in GC tissues and cell lines. HSPB1 overexpression enhanced proliferation, invasion, and migration while suppressing apoptosis by downregulating PANoptosis markers. Conversely, HSPB1 silencing inhibited these oncogenic traits and activated PANoptosis, significantly reducing tumor growth in vivo, accompanied by upregulated PANoptosis-related proteins and increased apoptosis.HSPB1 promotes GC progression by inhibiting PANoptosis, thereby enhancing tumor survival and aggressiveness, whereas its silencing activates these cell death pathways to suppress tumorigenesis. These findings establish HSPB1 as a critical regulator of PANoptosis in GC and a potential therapeutic target, offering new avenues for overcoming resistance and improving patient outcomes.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"127 3","pages":"Article 152277"},"PeriodicalIF":2.3,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144694552","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":"Dihydroartemisinin inhibited tongue squamous cell carcinoma progression and tongue-to-lymph node metastasis through inhibiting RalB expression","authors":"Yuman Zhang ,&nbsp;Yuting Gao ,&nbsp;Yanli Gong ,&nbsp;Yanguang Yang ,&nbsp;Yi Gong ,&nbsp;Xiaoyong Song ,&nbsp;Yajun Xiong ,&nbsp;Dan Wang ,&nbsp;Zhihan Liu ,&nbsp;Xinli Shi","doi":"10.1016/j.acthis.2025.152276","DOIUrl":"10.1016/j.acthis.2025.152276","url":null,"abstract":"<div><h3>Background</h3><div>Lymph node metastasis is a key determinant of the poor survival rate in patients with tongue squamous cell carcinoma (TSCC). Therefore, inhibiting lymph node metastasis is a primary strategy for TSCC treatment. Our previous research found that dihydroartemisinin (DHA) inhibited the migration in human tongue squamous carcinoma Cal-27 cells. However, the effect and mechanism of DHA on lymph node metastasis are unknown in TSCC.</div></div><div><h3>Methods</h3><div>The expression level of Ras related GTP binding protein B (RalB) was measured in TSCC samples by immunohistochemical staining. Wound healing, invasion, and cell adhesion assays were used to investigate cell motility. Western blot was used to investigate RalB expression level. An orthotopic nude mouse model of TSCC was established to investigate the effect and mechanism of DHA on lymph node metastasis.</div></div><div><h3>Results</h3><div>First, DHA inhibited the progression of tongue tumor and tongue-to-lymph node metastasis of TSCC. Secondly, DHA inhibited RalB expression level <em>in vitro</em> and <em>in vivo</em>. Finally, DHA inhibited tongue-to-lymph node metastasis through <em>RALB</em>.</div></div><div><h3>Conclusions</h3><div>DHA inhibited tongue-to-lymph node metastasis through <em>RALB</em>, providing a novel therapeutic strategy for TSCC metastasis.</div></div>","PeriodicalId":6961,"journal":{"name":"Acta histochemica","volume":"127 3","pages":"Article 152276"},"PeriodicalIF":2.3,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144522216","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}