European Journal of Histochemistry最新文献_第3页

Knockdown of miR-411-3p induces M2 macrophage polarization and promotes colorectal cancer progression by regulation of MMP7. 敲低miR-411-3p可诱导M2巨噬细胞极化，通过调控MMP7促进结直肠癌进展。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-05-05 DOI: 10.4081/ejh.2025.4178

Tianliang Bai, Ping Li, Yabin Liu, Bindan Cai, Gang Li, Wenbin Wang, Rui Yan, Xiangkui Zheng, Shangkun Du

{"title":"Knockdown of miR-411-3p induces M2 macrophage polarization and promotes colorectal cancer progression by regulation of MMP7.","authors":"Tianliang Bai, Ping Li, Yabin Liu, Bindan Cai, Gang Li, Wenbin Wang, Rui Yan, Xiangkui Zheng, Shangkun Du","doi":"10.4081/ejh.2025.4178","DOIUrl":"10.4081/ejh.2025.4178","url":null,"abstract":"Colorectal cancer (CRC) is prone to metastasis, leading to a poor prognosis. miR-411-3p exhibits a tumor-suppressive function in CRC, but its exact mechanism is unclear. The malignant biological properties of CRC cells were detected by Carboxyfluorescein diacetate succinimidyl ester (CFSE) staining, scratch-wound and transwell assay. Levels of markers associated with macrophage polarization were evaluated by flow cytometry and ELISA kits. Bioinformatics analysis to screen whether the downstream target mRNA of miR-411-3p is matrix metalloproteinase 7 (MMP7), and Dual-Luciferase reporter assay verified the targeting relationship between the two. qRT-PCR tested miR-411-3p and MMP7 levels. MMP7 level was quantified by Western blot. Additionally, a nude mouse subcutaneous graft tumor model was constructed, Ki-67 expression was detected by immunohistochemistry, and the impact of miR-411-3p/MMP7 on the polarization of M2 macrophages was explored. miR-411-3p expression is downregulated in CRC. Knockdown of miR-411-3p elevated the amount of CFSE-positive, migrating, and invading cells, decreased apoptosis, and elevated the levels of M2 macrophage polarization markers. After overexpression of miR-411-3p, all of the above metrics were reversed in CRC cells. miR-411-3p targeted negative regulation of MMP7 expression, and MMP7 overexpression further enhanced the promotional effect of knockdown of miR-411-3p on the malignant progression of CRC and M2 macrophage polarization. Furthermore, knockdown of miR-411-3p upregulated the MMP7 level, elevated Ki-67-positive cells count, and induced M2 macrophage polarization in vivo. Knockdown of miR-411-3p upregulates MMP7 and induces M2 macrophage polarization, which in turn promotes malignant biological progression of CRC.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12086358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144057418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MiR-122-5p inhibits the epithelial mesenchymal transition of liver cancer cells by inducing hiPSCs to differentiate into hepatocyte-like cells. MiR-122-5p通过诱导hiPSCs向肝细胞样细胞分化，抑制肝癌细胞上皮间充质转化。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-05-06 DOI: 10.4081/ejh.2025.4190

Qianzhe Xing, Yanjie Xu, Ying Luo, Chenglong Li, Peng Wang, Bin Kang, Chengjun Lu

{"title":"MiR-122-5p inhibits the epithelial mesenchymal transition of liver cancer cells by inducing hiPSCs to differentiate into hepatocyte-like cells.","authors":"Qianzhe Xing, Yanjie Xu, Ying Luo, Chenglong Li, Peng Wang, Bin Kang, Chengjun Lu","doi":"10.4081/ejh.2025.4190","DOIUrl":"10.4081/ejh.2025.4190","url":null,"abstract":"Epithelial-mesenchymal transition (EMT) is closely linked to liver cancer prognosis, invasiveness, and aggressiveness. One promising treatment for liver cancer is cell therapy, where stem cells are stimulated to develop into functional liver cells. This study aimed to investigate the effect of miR-122-5p on the differentiation of human induced pluripotent stem cells (hiPSCs) into hepatocyte-like cells and its impact on the EMT process in liver cancer cells. MiR-122-5p was overexpressed or silenced in hiPSCs to analyze the expression of liver-specific markers, including AFP, ALB and ASGPR, to confirm hepatocyte-like differentiation. A co-culture system with HepG2 liver cancer cells was also used to evaluate the effect of miR-122-5p-overexpressing hiPSCs or miR-122-5p-silencing hiPSCs on the expression of EMT markers. Results revealed that overexpression of miR-122-5p in hiPSCs induced hepatocyte-like characteristics, as evidenced by increased levels of AFP, ALB, and ASGPR. However, knockdown of miR-122-5p had the opposite effect. In the co-culture system, hiPSCs overexpressing miR-122-5p inhibited the EMT process of HepG2 cells, resulting in increased levels of mesenchymal markers and decreased levels of epithelial markers. Taken together, miR-122-5p promotes the differentiation of hiPSCs into hepatocyte-like cells and inhibits EMT process of liver cancer cells. Targeting miR-122-5p may be a novel approach to prevent liver cancer progression through cell therapy.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12086357/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144057217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

E-cadherin inhibits the proliferation and migration of human colorectal cancer cells through Hippo signaling pathway. E-cadherin通过Hippo信号通路抑制人结直肠癌细胞的增殖和迁移。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-05-26 DOI: 10.4081/ejh.2025.4196

Zhijing Wang, Xiaohua Qin, Shanshan Liu, Yilei Wen, Bikan Lan, Hantao Liao, Haixian Wei

{"title":"E-cadherin inhibits the proliferation and migration of human colorectal cancer cells through Hippo signaling pathway.","authors":"Zhijing Wang, Xiaohua Qin, Shanshan Liu, Yilei Wen, Bikan Lan, Hantao Liao, Haixian Wei","doi":"10.4081/ejh.2025.4196","DOIUrl":"10.4081/ejh.2025.4196","url":null,"abstract":"E-cadherin (E-cad) is a crucial regulatory factor in rescue Epithelial-mesenchymal transition and is involved in the occurrence of various malignant tumor. However, the mechanisms by which E-cadherin regulates tumor metastasis in CRC remain unclear. We established sh-E-cad (silenced by short hairpin RNA) and rescue-E-cad (overexpressed by E-cad plasmid transfection) CRC cell lines to investigate the role of E-cad in CRC in vitro. Immunohistochemistry, clonogenic assays, scratch wound healing assays, CCK-8 assays, flow cytometry, Transwell assay, real time-PCR and Western blot were employed to investigate the underlying mechanisms by which E-cad involve the progression of CRC. In CRC tissues, E-cad expression was significantly reduced, while YAP expression was markedly elevated. Silencing E-cad induced a significant increase of clonogenic ability in CRC cells, which was reduced upon rescue of E-cad expression. Transwell assays indicate that low expression of E-cad enhances the cell migration, a finding corroborated by scratch wound healing experiments. CCK-8 results demonstrate that silencing E-cad promotes the proliferation of CRC cells. Importantly, we found that E-cad influences apoptosis rather than the cell cycle. Analysis of Hippo signaling pathway-related factors revealed that silencing E-cad resulted in significantly decreased expression of MST1/2 and LATS1/2, as well as reduced phosphorylation levels of YAP, while YAP expression was significantly increased. Additionally, immunofluorescence confirmed the nuclear translocation of YAP. Our study indicates that E-cad regulates the malignant progression of CRC via the Hippo signaling pathway, offering a potential new strategy for CRC treatment.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12172619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144152759","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

miR-627-5p inhibits malignant progression of cervical cancer by targeting ANGPTL4. miR-627-5p 通过靶向 ANGPTL4 抑制宫颈癌的恶性进展

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 DOI: 10.4081/ejh.2025.4161

Xinghua Wu, Kai Lin, Chen Gao, Yinfang Ni, Li Zhang, Tailai Yang, Jinguo Chen

{"title":"miR-627-5p inhibits malignant progression of cervical cancer by targeting ANGPTL4.","authors":"Xinghua Wu, Kai Lin, Chen Gao, Yinfang Ni, Li Zhang, Tailai Yang, Jinguo Chen","doi":"10.4081/ejh.2025.4161","DOIUrl":"10.4081/ejh.2025.4161","url":null,"abstract":"In recent years, accumulating evidence has highlighted the critical role of miR-627-5p in the occurrence and progression of various cancers. However, its specific role and mechanism in cervical cancer (CC) remain unclear. This study aimed to elucidate the mechanism by which miR-627-5p inhibits the malignant progression of CC and assess its potential clinical implications. In C33A cells, the mRNA expression levels of ANGPTL4 and miR-627-5p were analyzed using qRT-PCR. The miR-627-5p mimics and their control (miR-NC) were transfected into C33A cells to determine whether miR-627-5p directly regulates ANGPTL4 expression. A comprehensive suite of assays, including CCK-8, migration, transwell, flow cytometry, and Western blotting, was conducted to evaluate how miR-627-5p modulates the malignant biological behavior of CC cells. Rescue experiments were performed by overexpressing ANGPTL4. In C33A cells, miR-627-5p expression was reduced, whereas ANGPTL4 expression was elevated. Further analysis confirmed that miR-627-5p negatively regulates ANGPTL4 by directly targeting its 3'-UTR. Functional assays demonstrated that miR-627-5p inhibits proliferation, invasion, migration, and epithelial-mesenchymal transition (EMT) while promoting apoptosis and S-phase arrest in C33A cells, effects that were reversed by ANGPTL4 overexpression. These findings highlight the potential of miR-627-5p as both a biomarker and a therapeutic target for CC. By inhibiting EMT and regulating ANGPTL4 expression, miR-627-5p may provide a novel avenue for improving therapeutic strategies, particularly in advanced or metastatic CC. Moreover, miRNA-based therapies, supported by advanced delivery systems such as nanoparticle carriers, could enhance the stability and precision of miR-627-5p applications. This study lays the groundwork for future research integrating miR-627-5p into precision medicine approaches for CC treatment.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12038335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143796858","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Anatomical insights into the proximal aponeurosis of the long head of the biceps femoris. 股二头肌长头近端腱膜的解剖学观察。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-05-13 DOI: 10.4081/ejh.2025.4165

Carmela Julia Mantecón-Tagarro, Eri Nanizawa, Munekazu Naito, Shun Otsuka, Huub Maas, Yasuo Kawakami

{"title":"Anatomical insights into the proximal aponeurosis of the long head of the biceps femoris.","authors":"Carmela Julia Mantecón-Tagarro, Eri Nanizawa, Munekazu Naito, Shun Otsuka, Huub Maas, Yasuo Kawakami","doi":"10.4081/ejh.2025.4165","DOIUrl":"10.4081/ejh.2025.4165","url":null,"abstract":"The biceps femoris long head (BFlh) is prone to strain injuries, but its reasons remain unclear. This study analyzed the BFlh proximal intramuscular aponeurosis in donor samples (n=4) through morphometric, microscopic, and histological methods. Cross-sections were taken every 5% of the muscle belly to differentiate connective, adipose, and muscle tissues. The aponeurosis extended from the muscle surface, becoming intramuscular from 40-70% of the muscle belly, and ended distally. Quantitative analysis revealed significant reductions of size in both the cross-sectional area (CSA) and width of the aponeurosis at 50% of muscle length, with CSA ranging from 4.9 mm² to 13.4 mm² and widths from 6.8 mm to 12.4 mm across subjects. Dense connective tissue bundles were separated by adipose or loose connective tissues. The aponeurosis shape varied along the muscle, with T- and hook-shaped configurations, and small branches were observed distally. These findings reveal the BFlh proximal aponeurosis as a complex structure, potentially influencing its injury susceptibility.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12117529/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Independent and interactive roles of hirudin and HMGB1 interference in protecting renal function by regulating autophagy, apoptosis, and kidney injury in chronic kidney disease. 水蛭素和 HMGB1 通过调节慢性肾病患者的自噬、细胞凋亡和肾损伤，在保护肾功能方面发挥独立和交互作用。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 DOI: 10.4081/ejh.2025.4182

Ying Li, Xuan Gao, Yao Chen, Huihui Li, Jing Tang, Wei Sun

{"title":"Independent and interactive roles of hirudin and HMGB1 interference in protecting renal function by regulating autophagy, apoptosis, and kidney injury in chronic kidney disease.","authors":"Ying Li, Xuan Gao, Yao Chen, Huihui Li, Jing Tang, Wei Sun","doi":"10.4081/ejh.2025.4182","DOIUrl":"10.4081/ejh.2025.4182","url":null,"abstract":"Chronic kidney disease (CKD) is a progressive disorder characterized by renal fibrosis, inflammation, and dysregulated autophagy and apoptosis. High-mobility group box 1 (HMGB1) plays a crucial role in regulating autophagy in CKD. Hirudin, a potent thrombin inhibitor, has demonstrated antifibrotic and anti-inflammatory properties, but its effects on autophagy and apoptosis in CKD remain unclear. In this study, a rat model of renal interstitial fibrosis (RIF) and an HK-2 cell culture model were established to assess the effects of varying doses of hirudin and HMGB1 interference. Molecular and histological analyses, including RTqPCR, Western blot, TUNEL staining, hematoxylin-eosin (H&E) staining, immunofluorescence, and immunohistochemistry (IHC), were performed to assess renal injury, fibrosis, apoptosis, and autophagy-related markers. Hirudin treatment significantly reduced the expression of LC3, ATG12, ATG5, α-SMA, COL1A1, caspase-3, and caspase-9 while increasing P62 levels (p<0.05). It also lowered the renal coefficient (p<0.001) and apoptosis levels. The optimal effective concentration of hirudin in vitro was determined to be 4.8 ATU/mL (p<0.001). HMGB1 interference suppressed autophagy and apoptosis, as indicated by decreased LC3-II/LC3-I, ATG12, ATG5, caspase-3, and caspase-9 levels, increased P62 expression (p<0.001), and reduced apoptosis. However, simultaneous HMGB1 interference in hirudin-treated cells weakened the therapeutic effects of hirudin, leading to increased autophagy and apoptosis markers, decreased P62 levels, and a higher renal coefficient. These findings indicate that hirudin exerts protective effects in CKD by modulating autophagy and apoptosis, potentially through HMGB1 regulation. These findings highlight the therapeutic potential of targeting these mechanisms in renal dysfunction and underscore the necessity for further research to support clinical applications.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12038336/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143796691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Erratum - Effect of CDX2 on proliferation, invasion, migration, and apoptosis of duodenal cancer cells. CDX2对十二指肠癌细胞增殖、侵袭、迁移和凋亡的影响。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-05-20 DOI: 10.4081/ejh.2025.4235

Jun Pan, Yi Zhao, Yu Zhang, Yuhe Zhou, Fengxuan Zhang, Yitian Chen, Xiaoyuan Chu

引用次数: 0

Effect of CDX2 on proliferation, invasion, migration, and apoptosis of duodenal cancer cells. CDX2对十二指肠癌细胞增殖、侵袭、迁移及凋亡的影响。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-04-07 Epub Date: 2025-04-24 DOI: 10.4081/ejh.2025.4203

Jun Pan, Yi Zhao, Yu Zhang, Yuhe Zhou, Fengxuan Zhang, Yitian Chen, Xiaoyuan Chu

{"title":"Effect of CDX2 on proliferation, invasion, migration, and apoptosis of duodenal cancer cells.","authors":"Jun Pan, Yi Zhao, Yu Zhang, Yuhe Zhou, Fengxuan Zhang, Yitian Chen, Xiaoyuan Chu","doi":"10.4081/ejh.2025.4203","DOIUrl":"10.4081/ejh.2025.4203","url":null,"abstract":"This study investigates the expression and biological role of caudal homologous transcription factor 2 (CDX2) in duodenal carcinoma. Paraffin-embedded samples from 40 duodenal carcinoma cases were analyzed using immunohistochemistry on a tissue microarray to assess CDX2 expression and its prognostic significance. CDX2 overexpression plasmids and CDX2-siRNA were transfected into colon and duodenal cancer cells. Transfection efficiency was confirmed by RT-PCR and Western blotting. Cell proliferation was assessed using CCK8 assay, migration via scratch assay, and cell cycle and apoptosis by flow cytometry. CDX2 staining was primarily nuclear, with a positive rate of 65% in duodenal carcinoma tissues, significantly lower than in adjacent non-tumor tissues (p<0.05). CDX2-positive patients had better prognoses than negative patients (p<0.05). Reduced CDX2 expression significantly enhanced the proliferation of CaCO2 and HuTu-80 cells (p<0.001), whereas CDX2 overexpression suppressed proliferation (p<0.001). CDX2 knockdown increased migration, while its overexpression reduced migration (p<0.05). CDX2 overexpression led to a significant increase in G0/G1 phase cells and a decrease in S phase cells (p<0.05), whereas knockdown reduced G0/G1 phase cells and increased S and G2/M phase cells (p<0.05). Apoptosis was significantly increased following CDX2 overexpression (p<0.001) and decreased after CDX2 knockdown (p<0.001). CDX2 expression is downregulated or lost in duodenal carcinoma, acting as a tumor suppressor. CDX2 may serve as a crucial biomarker for predicting the onset, progression, and treatment of duodenal carcinoma.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 2","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12067183/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144040018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exploring the efficacy of AMACR, ERG, and AR immunostains in prostatic adenocarcinoma and their association with novel grade groups. 探讨AMACR、ERG和AR免疫染色在前列腺腺癌中的疗效及其与新型分级组的关系。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-02-11 DOI: 10.4081/ejh.2025.4172

Mohamed O Andarawi, Hassan Otifi, Hesham Hassan, Adil A Yousif, Saadalnour A Mustafa, Shawgi A Elsiddig, Asad Ma Babker, Elryah I Ali, Omer Osman Elhag

{"title":"Exploring the efficacy of AMACR, ERG, and AR immunostains in prostatic adenocarcinoma and their association with novel grade groups.","authors":"Mohamed O Andarawi, Hassan Otifi, Hesham Hassan, Adil A Yousif, Saadalnour A Mustafa, Shawgi A Elsiddig, Asad Ma Babker, Elryah I Ali, Omer Osman Elhag","doi":"10.4081/ejh.2025.4172","DOIUrl":"10.4081/ejh.2025.4172","url":null,"abstract":"The study examines the utility of AMACR, ERG, and AR immunostains in diagnosing prostatic adenocarcinoma (PCa) and assessing prognosis in comparison to the Gleason score and new WHO grading groups. Seventeen PCa biopsies and five benign prostatic hyperplasia (BPH) biopsies were analyzed. Immunoreactivity, scored from 1 to 3 based on percentage of positive cells and intensity of expression, was assessed, revealing 76.47% positivity for AMACR, 35.29% for ERG, and 94.12% for AR in PCa cases, with variable scores and intensity among markers and grade groups. AMACR sensitivity and ERG specificity were noted. Higher-grade PCa exhibited increased positivity for both markers, indicating prognostic significance. In BPH cases, AMACR showed positivity in 2 cases, ERG in 1, and AR in all cases, albeit with lower expression. Differential expression was observed among immunomarkers and grade groups of malignancy. AMACR and ERG stains serve as sensitive and specific markers for PCa diagnosis and prognosis. Their increasing positivity with higher-grade groups underscores prognostic value. These findings highlight the importance of immunostains in refining PCa diagnosis and prognostication.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11864098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143392401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Expression of S100β during mouse cochlear development. 小鼠耳蜗发育过程中S100β的表达。

IF 2.1 4区生物学

European Journal of Histochemistry Pub Date : 2025-01-21 Epub Date: 2025-03-10 DOI: 10.4081/ejh.2025.4189

Wenjing Liu, Yongchun Zhang, Cheng Liang, Lizhong Su

{"title":"Expression of S100β during mouse cochlear development.","authors":"Wenjing Liu, Yongchun Zhang, Cheng Liang, Lizhong Su","doi":"10.4081/ejh.2025.4189","DOIUrl":"10.4081/ejh.2025.4189","url":null,"abstract":"In the present study, the expression of S100β was examined in the mouse cochlea from embryonic day 17 (E17) to postnatal day 32 (P32) using immunofluorescence, aiming to explore its possible role in auditory system. At E17, S100β expression was not detected, except in the external cochlear wall. Starting at E18.5, S100β staining appeared in the organ of Corti and the stria vascularis. In the E18.5 and P1 organ of Corti, S100β was confined to the developing pillar cells. By P6, cytoplasmic staining of S100β was evident in the inner and outer pillar cells, forming the tunnel of Corti. Additionally, S100β expression extended medially into the three rows of Deiter's cells, with labeling of their phalangeal processes. At P8, S100β continued to be expressed in the heads, bodies, and feet of the two pillar cells, as well as in the soma and phalangeal processes of the three rows of Deiter's cells. In the lateral wall of the P8 cochlea, S100β was expressed not only in the stria vascularis but also in the spiral ligament. Between P10 and P12, S100β expression was maintained in the Deiter's cells and pillar cells of the organ of Corti, as well as in the lateral wall, and spiral limbus. From P14 onwards, S100β expression ceased in the stria vascularis, though it persisted in the spiral ligament and spiral limbus into adulthood. Within the P14 and P21 organ of Corti, S100β remained in the Deiter's and pillar cells. S100β immunostaining was not observed in the phalangeal processes of Deiter's cells but was specifically present in the Deiter's cell cups at P21. In the adult cochlea (P28 and P32), S100β expression declined in both Deiter's and pillar cells. The dynamic spatiotemporal changes in S100β expression during cochlear ontogeny suggest its role in cochlear development and hearing function.","PeriodicalId":50487,"journal":{"name":"European Journal of Histochemistry","volume":"69 1","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11956554/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143607051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0