Acta histochemica最新文献_第3页

Neuroprotective effect of Urolithin A via downregulating VDAC1-mediated autophagy in Alzheimer's disease 尿素A通过下调vdac1介导的自噬在阿尔茨海默病中的神经保护作用

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-09-01 DOI: 10.1016/j.acthis.2025.152290

Bensi Zhang , Xiujun Zhang , Waleephan Treebupachatsakul , Rungusa Pantan , Natnicha Kampan , Manussabhorn Phatsara , Chun Shi , Suteera Narakornsak

Background

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.

Methods

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.

Results

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.

Conclusion

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.

阿尔茨海默病（AD）患者大脑中淀粉样蛋白β (Aβ)的积累有助于认知障碍和神经元损伤。尿素A （UA）是一种肠道微生物衍生的鞣花酸代谢物，据报道可以穿过血脑屏障，在大脑中发挥抗炎和抗氧化作用。然而，UA在AD中的分子机制尚不清楚。本研究旨在探讨UA对APP/PS1小鼠及a β1 - 42损伤的N2a和PC12细胞的神经保护作用及其机制。方法采用Morris水迷宫法检测大鼠认知功能。应用免疫荧光法检测APP/PS1小鼠脑内Aβ的沉积及电压依赖性阴离子通道1 （VDAC1）的表达。Western blotting检测VDAC1、AMPK通路、PI3K通路及自噬相关蛋白的表达。CCK8检测a β1 - 42损伤细胞的活力。结果本研究发现UA可改善APP/PS1小鼠的认知功能障碍，减少Aβ沉积。此外，UA在APP/PS1小鼠和a β1 - 42损伤的N2a和PC12细胞中激活自噬并上调自噬相关蛋白的水平。同时，UA下调APP/PS1小鼠及a β1 - 42损伤的N2a细胞和PC12细胞中PI3K/AKT/mTOR的磷酸化水平，上调AMPK的磷酸化水平。此外，UA下调VDAC1，与VDAC1拮抗剂DIDS（4′-二异硫氰酸-2,2′-二磺酸二苯乙烯）的作用一致。重要的是，uva诱导的自噬激活和PI3K和AMPK通路的调节被VDAC1过表达逆转。结论UA下调VDAC1通过抑制PI3K/AKT/mTOR通路，激活AMPK通路促进自噬，在AD中发挥关键的神经保护作用。

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引用次数: 0

USP22-mediated PNMA5 deubiquitination promotes proliferation, migration and invasion of prostate cancer cells. usp22介导的PNMA5去泛素化促进前列腺癌细胞的增殖、迁移和侵袭。

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-09-01 Epub Date: 2025-08-09 DOI: 10.1016/j.acthis.2025.152279

Hong Zhi, Tana, Nigemutu Bai, Wuenbilige Bai, Bowen Bai, Suo Liu

Background: 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.

Methods: 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.

Results: 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.

Conclusion: USP22 promotes migration and invasion of PCa cells by regulating PNMA5 deubiquitination.

背景：前列腺癌（PCa）是全球男性癌症相关死亡的主要原因之一。据报道，USP22作为癌基因起作用，而PNMA5表现出显著的促转移作用。本研究的重点是研究USP22和PNMA5之间的相互作用以及它们在促进前列腺癌进展中的协同作用。方法：采用免疫组化法检测组织中USP22和PNMA5的表达。分别采用qPCR和免疫印迹法检测细胞USP22和PNMA5的差异表达。MTT法和成球法检测细胞活力和增殖能力。采用Transwell法和创面愈合法评价转移能力。通过Co-IP和IP检测USP22与PNMA5的相互作用。建立荷瘤小鼠模型进行体内检测。结果：USP22和PNMA5在前列腺癌组织和细胞中均有高表达。敲低USP22或PNMA5可抑制PCa细胞的迁移和侵袭。USP22介导PNMA5的去泛素化。PNMA5过表达逆转了USP22敲低引起的细胞活力和增殖率的下降，以及迁移和侵袭能力的降低。结论：USP22通过调控PNMA5去泛素化促进PCa细胞的迁移和侵袭。

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引用次数: 0

Blood transfusion mediated tumor microenvironment remodeling in breast cancer 输血介导的乳腺癌肿瘤微环境重塑

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-08-23 DOI: 10.1016/j.acthis.2025.152289

Qinan Yin , Shunshun Zhang , Mouna Ouchari , Pei Wang , Anshun Zhao , Li Zeng , Jingjing Wang , Kaiyuan Yao , Siya Tang , Haodi Ma , Anne-Catherine Girondin , Hecai Yang , Xuewei Zheng , Zhifeng Qu

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.

输血在乳腺癌治疗中起着至关重要的作用，特别是在处理围手术期失血和化疗引起的贫血方面。然而，新出现的证据表明，输血可能通过诱导输血相关免疫调节（TRIM）和改变肿瘤微环境（TME）对肿瘤预后产生不利影响。TRIM抑制细胞毒性免疫反应，潜在地促进肿瘤进展-特别是在侵袭性亚型，如三阴性乳腺癌（TNBC）和her2阳性癌症中。此外，输血可能通过增加血液粘度和损害微血管灌注而矛盾地加剧肿瘤缺氧，从而降低化疗、放疗和免疫治疗的有效性。这篇综述探讨了输血在乳腺癌中的双重作用，强调了其临床益处和潜在风险。我们分析了它们对治疗耐药和肿瘤进展的影响，并讨论了减轻相关风险的策略，包括白细胞减少、促红细胞生成剂（esa）、静脉补铁和血液保存技术。此外，我们强调了根据肿瘤亚型、免疫状态和相关生物标志物（如肿瘤浸润淋巴细胞（TILs）、PD-L1表达和循环肿瘤DNA (ctDNA)）指导的个性化输血方法的重要性。未来的研究应侧重于优化输血时机，实施生物标志物驱动的方案，并开发免疫调节干预措施来抵消TRIM。个性化的、基于证据的输血策略可能最终提高治疗效果并改善乳腺癌护理的长期结果。

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引用次数: 0

Corrigendum to “Inducible gankyrin overexpression drives hepatocarcinogenesis in a liver-specific zebrafish model” [Acta Histochem. 127 (2025) 152280] “在肝脏特异性斑马鱼模型中诱导gankyrin过表达驱动肝癌发生”的更正[组织化学学报，127(2025)152280]。

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-08-19 DOI: 10.1016/j.acthis.2025.152281

Yuxi Sun , Zhiyuan Gong , Yueh-Min Lin , Jeng-Wei Lu

引用次数: 0

Advancing triple-negative breast cancer therapy: 3D in vitro models to unravel drug resistance mechanisms and tumor microenvironment interactions 推进三阴性乳腺癌治疗：3D体外模型揭示耐药机制和肿瘤微环境相互作用

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-08-16 DOI: 10.1016/j.acthis.2025.152282

Gomathy Baskar , Thirunavukkarasu Palaniyandi

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 in vivo 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.

三阴性乳腺癌（TNBC）由于其侵袭性、早期转移和有限的治疗选择，给临床带来了相当大的挑战。二维模型的简化和动物模型的生理差异往往导致对抗癌药物的反应不一致。为了应对这些挑战，三维（3D）体外生物工程模型已经被开发出来，可以准确地复制体内肿瘤微环境（TME），为临床前药物测试提供更可靠的平台。细胞培养技术的最新进展促进了来自患者组织和肿瘤的3D模型的创建，这些模型有效地模拟了天然组织环境，并表现出与体内观察到的相似的药物敏感性和细胞毒性行为。越来越多的人认识到，TME内的细胞外基质和细胞多样性显著影响癌细胞的命运。因此，探索耐药机制的策略必须同时考虑微环境因素和基因突变。本文综述了整合微环境影响的3D体外模型系统，以研究乳腺癌的耐药机制。我们讨论了各种生物工程模型，包括基于球体的、基于生物材料的（如聚合物支架和水凝胶）、患者来源的异种移植物（PDX）、3D生物打印和基于微流控芯片的模型。此外，我们讨论了这些3D模型在理解TME信号对药物反应和耐药性的影响方面的相关性，以及它们在制定克服耐药性和优化治疗方案的策略方面的潜力。

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引用次数: 0

Detection assays of mitochondrial permeability transition pore: Current status and future prospects 线粒体通透性过渡孔的检测方法：现状与展望

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-08-04 DOI: 10.1016/j.acthis.2025.152278

Dongyang Hong , Jiawei Huang , Sicheng Hu , Yawen Zheng , Yuhuan Wu , Ziyang Cao , Zijun Yan , Hongyang Zhang , Huanhuan Feng , Jinxia Wang , Lin Zou

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.

线粒体通透性过渡孔（mitochondrial permeability transition pore, mPTP）是线粒体内膜上由多种蛋白复合物组成的超分子实体，是维持线粒体功能和细胞稳态的关键成分。本文综述了目前mPTP的检测技术，包括分光光度法、膜片夹紧法、荧光探针法和流式细胞术等，这些技术有望揭示mPTP的状态及其在退行性疾病、炎症、肿瘤等疾病中的作用。此外，我们还讨论了有前途的检测mPTP的新方法，包括提高精度，高灵敏度，多参数分析和技术集成。这些进展突出了线粒体相关疾病的临床诊断和治疗的新可能性。

引用次数: 0

Inducible gankyrin overexpression drives hepatocarcinogenesis in a liver-specific zebrafish model 在肝脏特异性斑马鱼模型中诱导gankyrin过表达驱动肝癌发生

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-08-01 DOI: 10.1016/j.acthis.2025.152280

Zhiyuan Gong , Yuxi Sun , Yueh-Min Lin , Jeng-Wei Lu

Background

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.

Material and method

To investigate its oncogenic role without the need for cancer cell inoculation or drug treatment, we employed a Tet-On system to drive zebrafish gankyrin overexpression in hepatocytes under the control of the fabp10a promoter. Results: After eight weeks of induction, fabp10a:eGFP-gankyrin transgenic zebrafish spontaneously developed persistent hyperplasia, bile duct hyperplasia, and hepatocellular carcinoma (HCC), demonstrating the oncogenic potential of gankyrin in liver tumorigenesis. In this study, we demonstrate that gankyrin activation drives the progressive development of HCC in zebrafish. Liver-specific overexpression of gankyrin 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.

Conclusion

This study establishes a robust zebrafish model in which liver-specific overexpression of gankyrin 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.

肝癌的发生是一个复杂的多步骤过程，从脂肪肝开始，发展到纤维化，最终导致癌症。许多病因因素促成了这一进展，强调了开发动物模型以促进旨在发现新的治疗策略的基础和转化研究的重要性。Gankyrin是参与肝脏病理遗传调控的关键癌蛋白。材料和方法为了研究其在不需要癌细胞接种或药物治疗的情况下的致癌作用，我们采用Tet-On系统在fabp10a启动子的控制下驱动斑马鱼肝细胞中gankyrin的过表达。结果：诱导8周后，转基因fabp10a:eGFP-gankyrin斑马鱼自发发生持续性增生、胆管增生和肝细胞癌（HCC），显示了gankyrin在肝脏肿瘤发生中的致癌潜力。在这项研究中，我们证明了gankyrin激活推动了斑马鱼HCC的进行性发展。野生型斑马鱼肝脏特异性过表达gankyrin导致增生、胆管增生和HCC，为研究肝癌建立了稳健的斑马鱼模型。我们的研究结果强调了该模型在研究肿瘤发生的分子机制方面的实用性。结论本研究建立了一个稳健的斑马鱼模型，在该模型中肝脏特异性过表达gankyrin可诱导从增生到肝细胞癌的自发进展。该模型为研究肝癌发生的分子机制和探索潜在的治疗策略提供了一个有价值的平台。

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引用次数: 0

HSPB1 promotes gastric cancer progression by suppressing PANoptosis HSPB1通过抑制PANoptosis促进胃癌进展

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-07-24 DOI: 10.1016/j.acthis.2025.152277

Lei Yang , Miaomiao Zeng , Binsheng Wang , Ze Yang , Bo Li , Xiaoliang Zhu

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.

胃癌（GC）仍然是全球癌症相关死亡的主要原因，由促进肿瘤进展和治疗耐药的分子机制驱动。PANoptosis是一种包括凋亡、坏死和焦亡在内的综合性程序性细胞死亡途径，已成为肿瘤发生的关键调节因子，但其在GC中的调节作用尚不清楚。本研究旨在探讨热休克蛋白β -1 （HSPB1）在调节PANoptosis中的作用及其对GC进展的影响，并假设HSPB1过表达抑制PANoptosis从而增强肿瘤恶性。我们采用了一种综合方法，将GEO （GSE54129）、TCGA和GSE15460数据集的生物信息学分析与实验验证相结合。通过qPCR、Western blot和免疫组化检测40对GC和正常组织以及多个GC细胞系（AGS、MKN-45、NCI-N87、HGC-27、SNU-1）中HSPB1的表达。通过在NCI-N87和AGS细胞中过表达或沉默HSPB1，然后进行增殖、集落形成、迁移和凋亡实验，探索其功能作用。利用转染shhspb1细胞的裸鼠异种移植模型评估体内效应，通过Western blot、IHC和TUNEL分析肿瘤生长和PANoptosis标志物（P-MLKL、RIPK3、Cleaved Caspase-1、NLRP3、Cleaved Caspase-3）。生物信息学显示HSPB1是panopsis相关的预后生物标志物，在GC组织中表达升高与生存不良相关。实验证实HSPB1在GC组织和细胞系中过表达。HSPB1过表达增强细胞增殖、侵袭和迁移，同时通过下调PANoptosis标志物抑制细胞凋亡。相反，HSPB1沉默抑制这些致癌性状并激活PANoptosis，显著降低肿瘤在体内的生长，并伴有PANoptosis相关蛋白上调和细胞凋亡增加。HSPB1通过抑制PANoptosis促进GC进展，从而提高肿瘤存活和侵袭性，而其沉默激活这些细胞死亡途径以抑制肿瘤发生。这些发现表明HSPB1是胃癌PANoptosis的关键调节因子和潜在的治疗靶点，为克服耐药性和改善患者预后提供了新的途径。

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引用次数: 0

Dihydroartemisinin inhibited tongue squamous cell carcinoma progression and tongue-to-lymph node metastasis through inhibiting RalB expression 双氢青蒿素通过抑制RalB表达抑制舌鳞癌的进展和舌向淋巴结转移

IF 2.3 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-06-30 DOI: 10.1016/j.acthis.2025.152276

Yuman Zhang , Yuting Gao , Yanli Gong , Yanguang Yang , Yi Gong , Xiaoyong Song , Yajun Xiong , Dan Wang , Zhihan Liu , Xinli Shi

Background

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.

Methods

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.

Results

First, DHA inhibited the progression of tongue tumor and tongue-to-lymph node metastasis of TSCC. Secondly, DHA inhibited RalB expression level in vitro and in vivo. Finally, DHA inhibited tongue-to-lymph node metastasis through RALB.

Conclusions

DHA inhibited tongue-to-lymph node metastasis through RALB, providing a novel therapeutic strategy for TSCC metastasis.

背景：淋巴结转移是舌鳞状细胞癌（TSCC）患者生存率低的关键决定因素。因此，抑制淋巴结转移是治疗TSCC的主要策略。我们前期研究发现，双氢青蒿素（DHA）对人舌鳞癌Cal-27细胞的迁移具有抑制作用。然而，DHA对TSCC淋巴结转移的影响和机制尚不清楚。方法采用免疫组化染色法检测TSCC组织中Ras相关GTP结合蛋白B （RalB）的表达水平。伤口愈合、侵袭和细胞粘附试验用于研究细胞运动。Western blot检测RalB表达水平。建立原位裸鼠TSCC模型，探讨DHA对TSCC淋巴结转移的影响及其机制。结果首先，DHA抑制舌癌的进展和舌向淋巴结转移；其次，DHA抑制体外和体内RalB表达水平。最后，DHA通过RALB抑制舌向淋巴结转移。结论dha通过RALB抑制舌向淋巴结转移，为TSCC转移提供了新的治疗策略。

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引用次数: 0

Corrigendum to “AARS1-mediated Osterix lactylation promotes its transcriptional activity during osteoblast differentiation” [Acta Histochem. 127 (2025) 152273] “aars1介导的Osterix乳酸化促进成骨细胞分化过程中的转录活性”的更正[Acta Histochem. 127(2025) 152273]。

IF 2.4 4区生物学 Q4 CELL BIOLOGY

Acta histochemica

Pub Date : 2025-06-23 DOI: 10.1016/j.acthis.2025.152275

Feige Nian , Linfeng Guo , Zhangli Fei , Mingfeng Yang , Lihong Chen , Ye Zhang , Zhufeng Zhang , Yezhou Qian , Bin Zhang

引用次数: 0