Cell Biology International最新文献_第4页

Piwei Peiyuan Pill Ameliorates Chronic Atrophic Gastritis and Intestinal Metaplasia at Least in Part by Inhibiting the Pellino1/IRAK1/NF-κB Signaling Axis 脾胃培元丸通过抑制Pellino1/IRAK1/NF-κB信号轴部分改善慢性萎缩性胃炎和肠化生。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-08-12 DOI: 10.1002/cbin.70195

Cheng Zhang, Fei Lu, Ting Ye, Yueping Jin, Yunpeng Qin, Kairui Wu, Kai Liu, Xuncui Wang, Hang Song, Xuejun Li

{"title":"Piwei Peiyuan Pill Ameliorates Chronic Atrophic Gastritis and Intestinal Metaplasia at Least in Part by Inhibiting the Pellino1/IRAK1/NF-κB Signaling Axis","authors":"Cheng Zhang, Fei Lu, Ting Ye, Yueping Jin, Yunpeng Qin, Kairui Wu, Kai Liu, Xuncui Wang, Hang Song, Xuejun Li","doi":"10.1002/cbin.70195","DOIUrl":"10.1002/cbin.70195","url":null,"abstract":"<div>\u0000 \u0000 <p>Chronic atrophic gastritis (CAG) with intestinal metaplasia (IM) is a key precancerous lesion that may progress to intestinal-type gastric adenocarcinoma. Piwei Peiyuan Pill (PPP) has shown significant clinical efficacy in ameliorating CAG with IM, but its active components and underlying mechanisms remain unclear. High-performance liquid chromatography (HPLC) and ultra-high performance liquid chromatography coupled with high-resolution mass spectrometry (UHPLC-HRMS) were used to identify the components of PPP and the active ingredients in PPP-containing serum. The therapeutic efficacy and potential mechanisms of PPP were further investigated via transcriptomic sequencing and experimental validation. UHPLC-HRMS analysis of PPP-containing serum identified several bioactive components, including esculin, lithospermic acid, and atractylenolide III. In CAG rats, PPP significantly ameliorated gastric mucosal damage and reduced serum IL-6 and TNF-α levels. Transcriptomic results showed that IRAK1 was highly expressed in CAG patients with IM and associated with activation of the NF-κB pathway. PPP intervention dose-dependently suppressed hyperactivation of the Pellino1/IRAK1/NF-κB axis and decreased the expression of intestinal metaplasia markers CDX1 and MUC2. Additionally, PPP improved immune function by increasing the proportion of CD4<sup>+</sup> T cells and decreasing the proportion of CD8<sup>+</sup> T cells in CAG model rats. Taken together, these findings suggest that PPP mitigates CAG and attenuates IM at least in part by suppressing the Pellino1/IRAK1/NF-κB signaling pathway, indicating that it may serve as a promising therapeutic strategy for reducing inflammation-associated gastric carcinogenesis.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 8","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148711401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Berberine Inhibited Tumor Growth Through Suppressing the WDR54/β-catenin Signal Pathway in Colorectal Cancer 小檗碱通过抑制结直肠癌WDR54/β-catenin信号通路抑制肿瘤生长。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-08-11 DOI: 10.1002/cbin.70196

Qin Chen, Qi Chen, Fenqiong Tang

{"title":"Berberine Inhibited Tumor Growth Through Suppressing the WDR54/β-catenin Signal Pathway in Colorectal Cancer","authors":"Qin Chen, Qi Chen, Fenqiong Tang","doi":"10.1002/cbin.70196","DOIUrl":"10.1002/cbin.70196","url":null,"abstract":"<p>Berberine (BBR), a natural alkaloid, exhibits potent anti-tumor activity in colorectal cancer (CRC), but its mechanisms are not fully elucidated. Analysis of GEO datasets (GSE216908 and GSE184414) identified WDR54 as a key target of BBR treatment. In vitro, BBR treatment of CRC cell lines (HT-29 and SW480) markedly inhibited cell proliferation, DNA synthesis, and colony formation. Notably, BBR triggered G1-phase cell cycle arrest and promoted apoptosis, as validated by flow cytometry and molecular marker analysis. WDR54 overexpression partially rescued these anti-tumor effects, confirming its functional importance. Mechanistically, cellular thermal shift assays (CETSA) and mRNA stability assays revealed that BBR suppresses WDR54 expression via indirect transcriptional inhibition rather than direct protein binding or altered mRNA stability. Dual-luciferase reporter assays further confirmed that BBR dose-dependently inhibits WDR54 promoter activity. In vivo, an AOM/DSS-induced CRC mouse model showed that BBR reduced tumor number and size, alleviated pathological progression, and suppressed the WDR54/β-catenin axis. These findings suggest that BBR exerts significant anti-tumor effects in CRC by downregulating WDR54 and inhibiting Wnt/β-catenin signaling, highlighting WDR54 as a potential therapeutic target and BBR as a promising treatment for CRC.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 8","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70196","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Perillaldehyde Attenuates Diabetic Nephropathy through Modulation of the Nrf2/Keap1 and NF-κB Signalling Pathways 紫苏醛通过调节Nrf2/Keap1和NF-κB信号通路减轻糖尿病肾病。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-08-06 DOI: 10.1002/cbin.70193

Harini Ramachandran, Akash Kumar Mourya, Ashutosh Kumar

{"title":"Perillaldehyde Attenuates Diabetic Nephropathy through Modulation of the Nrf2/Keap1 and NF-κB Signalling Pathways","authors":"Harini Ramachandran, Akash Kumar Mourya, Ashutosh Kumar","doi":"10.1002/cbin.70193","DOIUrl":"10.1002/cbin.70193","url":null,"abstract":"<div>\u0000 \u0000 <p>Diabetic nephropathy (DN) is a one of the common microvascular complication of diabetes that involves oxidative stress, inflammation, activation and overexpression of Nuclear factor kappa B (NF-κB), and chronic renal dysfunction. In this study, we evaluated the renoprotective role of perillaldehyde (PA) in protecting kidneys from diabetic nephropathy using in vitro and in vivo models of Streptozotocin-induced diabetic nephropathy. PA pre-treatment of NRK-52E cells under high-glucose conditions resulted in a significant reduction of reactive oxygen species formation, up-regulation of nuclear factor erythroid 2-related factor 2 (Nrf2), suppression of Kelch-like ECH-associated protein 1 (Keap1), and elevation of antioxidant enzyme biomarkers, such as heme oxygenase 1, superoxide dismutase 1, and NAD(P)H dehydrogenase quinone 1. PA also inhibited the overexpression of NF-κB, inducible nitric oxide synthase, and poly (ADP-ribose) polymerase in high-glucose exposed NRK-52E cells. Administration of PA (35 and 70 mg/kg) to streptozotocin-induced diabetic rats showed beneficial effects on renal function parameters such as creatinine and blood urea nitrogen. PA treatment attenuated glomerular and tubular structural damage, as evidenced by H&E and PAS staining. At molecular level, PA was found to maintain the redox balance in the kidneys by stimulating the Nrf2/Keap1/HO-1 signalling pathway and inhibiting the NF-κB-dependent inflammatory response. Moreover, PA lowered lipid peroxidation and enhanced antioxidant status via reduction in MDA and elevation in GSH. The above results indicated that PA showed considerable reno-protective actions through coordinated regulation of both oxidative stress and inflammation pathways in experimental models of diabetic nephropathy</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 8","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677334","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Immortalization of Adipose-Derived Stromal Cells From Japanese Black Cattle 日本黑牛脂肪来源基质细胞的永生化研究。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-08-06 DOI: 10.1002/cbin.70194

Rei Sasaki, Hanami Matsukura, Ryo Meguro, Lanlan Bai, Ken Sawai, Eriko Sugano, Hiroshi Tomita, Tohru Kiyono, Tomokazu Fukuda

{"title":"Immortalization of Adipose-Derived Stromal Cells From Japanese Black Cattle","authors":"Rei Sasaki, Hanami Matsukura, Ryo Meguro, Lanlan Bai, Ken Sawai, Eriko Sugano, Hiroshi Tomita, Tohru Kiyono, Tomokazu Fukuda","doi":"10.1002/cbin.70194","DOIUrl":"10.1002/cbin.70194","url":null,"abstract":"<p>Adipose tissue plays a critical role in determining the characteristic palatability of Japanese Black cattle beef, including its distinctive aroma, tenderness, and flavor. These quality traits are closely associated with adipogenic differentiation and lipid metabolism; however, the underlying molecular mechanisms remain poorly understood. Adipose-derived stromal cells (ASCs) residing within adipose tissue possess the capacity to differentiate into adipocytes and other mesenchymal lineages and are, therefore, considered valuable experimental resources for adipose tissue research. Nevertheless, primary cells are subject to several limitations, including a restricted proliferative lifespan caused by culture-induced stress and reduced experimental reproducibility due to inter-individual variability, which hamper their use in long-term <i>in vitro</i> analyses. In this study, we immortalized ASCs derived from Japanese Black cattle using the K4DT method, which involves the introduction of the R24C mutant form of cyclin-dependent kinase 4 (CDK4<sup>R24C</sup>), Cyclin D1, and telomerase reverse transcriptase. The established bovine ASCs (bASCs) [bASCs-K4DT] exhibited a stable proliferative capacity during long-term culture while retaining their ability to undergo adipogenic differentiation. These immortalized bASCs may serve as a useful <i>in vitro</i> model for elucidating the molecular mechanisms underlying adipocyte differentiation and formation of breed-specific aroma and flavor characteristics.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 8","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13445999/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677281","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Molecular Mechanism of TRIM16 Regulating Osteogenic Differentiation of Periodontal Ligament Stem Cells Under Inflammatory Microenvironment 炎症微环境下TRIM16调控牙周韧带干细胞成骨分化的分子机制

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-08-06 DOI: 10.1002/cbin.70192

Xudong Ma

{"title":"Molecular Mechanism of TRIM16 Regulating Osteogenic Differentiation of Periodontal Ligament Stem Cells Under Inflammatory Microenvironment","authors":"Xudong Ma","doi":"10.1002/cbin.70192","DOIUrl":"10.1002/cbin.70192","url":null,"abstract":"<div>\u0000 \u0000 <p>This study explores the mechanism of TRIM16 on osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) in an inflammatory microenvironment. hPDLSCs were cultured and identified by flow cytometry and osteogenesis/adipogenesis induction. hPDLSCs were maintained with <i>P. gingivalis</i> LPS and induced by osteogenic differentiation. TRIM16, HOXA10, and KLF5 expression was tested via RT-qPCR and Western blot. After overexpression of TRIM16, TNF-α, IL-6, and IL-1β levels were examined via ELISA. Osteogenic differentiation of hPDLSCs was validated by Alizarin red staining, ALP staining, and Western blot. The binding of TRIM16 to HOXA10 was detected by Co-IP, and the ubiquitinated HOXA10-containing complexes were measured. Dual luciferase assay and ChIP analyzed the enrichment of HOXA10 on the KLF5 promoter. LPS treatment reduces TRIM16 and KLF5 expression, while elevating HOXA10 protein level. Overexpression of TRIM16 alleviates inflammation in LPS-induced hPDLSCs and enhances osteogenic differentiation. Mechanistically, TRIM16 inhibits HOXA10 protein level via ubiquitination, thereby abating the enrichment of HOXA10 on the KLF5 promoter and promoting the expression of KLF5. In conclusion, TRIM16 facilitates osteogenic differentiation of hPDLSCs in an inflammatory microenvironment via HOXA10/KLF5 axis.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 8","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148677223","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Kinesins in Bladder Cancer: Integrating Molecular Mechanisms and Treatment Approaches 运动蛋白在膀胱癌中的作用：整合分子机制和治疗方法

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-07-30 DOI: 10.1002/cbin.70191

Usamah Sayed, Noor Mazin Basheer, Malathi. H, Priya Priyadarshini Nayak, Aman Shankhyan, Rasulbek Eshmetov, Sabokhat Sadikova, Zokir Ataullaev

{"title":"Kinesins in Bladder Cancer: Integrating Molecular Mechanisms and Treatment Approaches","authors":"Usamah Sayed, Noor Mazin Basheer, Malathi. H, Priya Priyadarshini Nayak, Aman Shankhyan, Rasulbek Eshmetov, Sabokhat Sadikova, Zokir Ataullaev","doi":"10.1002/cbin.70191","DOIUrl":"https://doi.org/10.1002/cbin.70191","url":null,"abstract":"<div>\u0000 \u0000 <p>Bladder cancer is a long-standing clinical issue, with frequent recurrence and continuously disappointing results in patients, so that therapeutic development is primarily reliant on delineating the original molecular defects. Increasing interest has turned to the Kinesin Superfamily Proteins (KIFs), basic molecular motors that move along microtubule rails, and are now emerging as important key oncogenic derivers in bladder cancer pathogenesis. This review synthesizes available evidence indicating that several KIFs, specifically KIF4A, KIF14, KIF20A, and KIFC1, function as key oncogenic regulators and represent important prognostic biomarkers and therapeutic targets in bladder cancer. When KIF expression or activity is disrupted, it provides mechanical and signaling support for all the cancer hallmarks, facilitating cellular proliferation, invasion, metastasis, and resistance to highly effective cell death. Its oncogenic activity is generally facilitated by the activation of principal signaling pathways. A remarkable proportion of certain KIF isoforms are commonly overexpressed in cancer, and the scale of such overexpression increases with the severity of adverse clinical predictors, such as increasing disease stage, and patient survival worsens. This nuanced molecular image renders KIFs so highly promising targets for therapeutic intervention and prognostic stratification, and initial exploration of kinesin inhibitors is encouraging to abate chemoresistance, aside from optimizing the efficacy of current immunotherapies. Uncovering modalities that exploit the aggressive bladder cancer cell dependence on KIF motor activity is a highly promising path to clinical application.</p>\u0000 </div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 8","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148616913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RETRACTION: Fibronectin Promotes Migration and Invasion of Ovarian Cancer Cells through Up-Regulation of FAK–PI3K/Akt Pathway 结论：纤连蛋白通过上调FAK-PI3K /Akt通路促进卵巢癌细胞的迁移和侵袭

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-07-29 DOI: 10.1002/cbin.70190

{"title":"RETRACTION: Fibronectin Promotes Migration and Invasion of Ovarian Cancer Cells through Up-Regulation of FAK–PI3K/Akt Pathway","authors":"","doi":"10.1002/cbin.70190","DOIUrl":"https://doi.org/10.1002/cbin.70190","url":null,"abstract":"<p><b>RETRACTION:</b> Nasser Ghaly Yousif, “Fibronectin Promotes Migration and Invasion of Ovarian Cancer Cells through Up-Regulation of FAK–PI3K/Akt Pathway,” <i>Cell Biology International</i> 38, no. 1 (2014): 85–91, https://doi.org/10.1002/cbin.10184.</p><p>The above article, published online on 21 September 2013 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Xuebiao Yao; the International Federation for Cell Biology; and John Wiley & Sons Ltd. The retraction has been agreed upon following concerns raised by a third party. An investigation confirmed several duplications of western blot bands within figures 2A, 2B, and 3A. Further duplications of western blot bands were found between figures 2A and 4A. In addition, large portions of the introduction were taken from an earlier article published by a different author group, without attribution. Although the author initially responded to the concerns and agreed to provide the original data, they failed to provide any supporting information or to respond to subsequent reminders. They also did not provide a plausible explanation for the reused text in the introduction. The editors consider the results and conclusions of this article to be compromised. The author did not respond to our notice of retraction.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 8","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70190","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148616562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Probing Centromere Plasticity and Chromatin Remodeling Using Single-Molecule Techniques 利用单分子技术探测着丝粒可塑性和染色质重塑。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-07-27 DOI: 10.1002/cbin.70189

Ran Liu, Jiayi Zhao, Hongfei Ma, Wenping Hu, Zhen Dou, Xing Liu

{"title":"Probing Centromere Plasticity and Chromatin Remodeling Using Single-Molecule Techniques","authors":"Ran Liu, Jiayi Zhao, Hongfei Ma, Wenping Hu, Zhen Dou, Xing Liu","doi":"10.1002/cbin.70189","DOIUrl":"10.1002/cbin.70189","url":null,"abstract":"<div>\u0000 \u0000 <p>The centromere functions as an essential interactive hub for mediating the equal distribution of sister chromatids during eukaryotic cell division and is subject to cell cycle-specific plasticity regulation. To ensure the replication, transcription, and repair of genetic information, chromatin remodeling is an indispensable molecular biology event. Both centromere plasticity and chromatin remodeling involve numerous protein components (e.g., Constitutive Centromere-Associated Network (CCAN), SWItch/Sucrose Non-Fermentable (SWI/SNF)) and exhibit highly dynamic spatiotemporal regulation, posing significant challenges for traditional ensemble approaches in elucidating their detailed mechanisms. In recent years, single-molecule techniques have revolutionized the study of chromatin remodeling and kinetochore assembly. By capturing real-time, high-resolution dynamics of molecular interactions, these methods uncover mechanistic insights inaccessible to conventional approaches. This review summarizes key advances and emerging paradigms enabled by single-molecule analysis tools, highlighting how they are reshaping our understanding of the mechanism of mitotic fidelity and epigenetic regulation, and providing a roadmap for future research in these fields.</p></div>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 8","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148590469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cytokeratin Detection in Lymphoid Tumor Cell Lines: Implications for Flow Cytometry and Molecular Analyses 淋巴肿瘤细胞系细胞角蛋白检测：流式细胞术和分子分析的意义

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-07-16 DOI: 10.1002/cbin.70187

Natsuko Mizutani, Shiori Takeuchi, Akemi Koyanagi, Takeshi Hirano, Yumi Kumagai, Manoho Okabe, Kanade Asou, Komai Kido, Haruka Kayano, Yuki Shimazu, Momoko Ichikawa, Rio Kato, Yasuhiko Ito, Shuji Matsuoka

{"title":"Cytokeratin Detection in Lymphoid Tumor Cell Lines: Implications for Flow Cytometry and Molecular Analyses","authors":"Natsuko Mizutani, Shiori Takeuchi, Akemi Koyanagi, Takeshi Hirano, Yumi Kumagai, Manoho Okabe, Kanade Asou, Komai Kido, Haruka Kayano, Yuki Shimazu, Momoko Ichikawa, Rio Kato, Yasuhiko Ito, Shuji Matsuoka","doi":"10.1002/cbin.70187","DOIUrl":"https://doi.org/10.1002/cbin.70187","url":null,"abstract":"<p>Cytokeratins are widely used as epithelial markers in diagnostic pathology and flow cytometry, and malignant lymphomas are generally considered cytokeratin-negative except for undifferentiated large cell lymphomas. During antibody screening experiments using flow cytometry, intracellular cytokeratin signals were unexpectedly detected in cultured lymphoma cell lines after cell permeabilization. Although cytokeratin is a component of the cytoskeleton, this finding raised concerns regarding the interpretation of cytokeratin positivity in lymphoid cells. To elucidate the nature of cytokeratin detection in lymphomas, cultured T-cell, B-cell, and natural killer cell lymphoma lines were analyzed using immunohistochemistry, flow cytometry, and quantitative RT-PCR (qRT-PCR), with epithelial carcinoma cell lines and keratin-free cells as references. Because malignant lymphomas disseminate systemically, we examined whether this behavior was associated with epithelial–mesenchymal transition–like features. Cytokeratins were not detected on the cell surface of lymphoid or epithelial cells but were detected intracellularly in multiple lymphoma cell lines. qRT-PCR confirmed the expression of multiple keratin transcripts in lymphoid cells, without correlation with epithelial–mesenchymal transition–related markers, including <i>CDH1</i>. These findings indicate that intracellular cytokeratin detection can occur in lymphoma cell lines without evidence of epithelial differentiation or association with EMT-related markers and should be considered when interpreting cytokeratin positivity.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70187","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148467479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

The Landscape of BRCA1-Associated Post-Translational Modifications brca1相关的翻译后修饰的前景。

IF 3.5 3区生物学

Cell Biology International Pub Date : 2026-07-11 DOI: 10.1002/cbin.70186

Nethma Hewa Waduge, Junhua Xiao, Gregory M. Davis

{"title":"The Landscape of BRCA1-Associated Post-Translational Modifications","authors":"Nethma Hewa Waduge, Junhua Xiao, Gregory M. Davis","doi":"10.1002/cbin.70186","DOIUrl":"10.1002/cbin.70186","url":null,"abstract":"<p>The BRCA1-BARD1 complex is a vital protein that promotes homologous recombination, acting through its E3 ubiquitin ligase activity. Although ubiquitination remains its only confirmed enzymatic function, emerging evidence suggests that the complex influences a broad range of post-translational modifications (PTMs), including methylation, phosphorylation, acetylation, and PARylation, involving other proteins. This review examines findings from various eukaryotic biological models to elucidate how BRCA1 regulates key PTMs. We explore how BRCA1 shapes chromatin architecture by modulating key PTMs such as ubiquitination, methylation, and acetylation. While BRCA1-driven changes in methylation appear to have widespread effects throughout the cell, its influence on ubiquitination and acetylation tends to be more region- or site-specific. Furthermore, this review discusses BRCA1's role in modifying specific target proteins, such as PLK-1, Aurora A, and p53, and explores its involvement in non-ubiquitin PTMs. Beyond its well-established role in DNA repair, BRCA1 also contributes to other cellular processes involving non-ubiquitin PTMs, such as in meiotic sex chromosome inactivation, which is also detailed in this review. Collectively, this review expands the functional landscape of BRCA1 beyond DNA repair, providing new insights into its regulatory impact across various post-translational pathways.</p>","PeriodicalId":9806,"journal":{"name":"Cell Biology International","volume":"50 7","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/cbin.70186","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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