JOURNAL OF CELLULAR AND MOLECULAR MEDICINE最新文献_第9页

Emodin Alleviates Acute Pancreatitis-Associated Acute Lung Injury by Inhibiting Serum Exosomal miRNA-21-3p-Induced M1 Alveolar Macrophage Polarisation 大黄素通过抑制血清外泌体mirna -21-3p诱导的M1肺泡巨噬细胞极化减轻急性胰腺炎相关急性肺损伤

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-08-22 DOI: 10.1111/jcmm.70758

Bowen Lan, Xuanchi Dong, Qi Yang, Haiyun Wen, Yibo Zhang, Fan Li, Yinan Cao, Zhe Chen, Hailong Chen

{"title":"Emodin Alleviates Acute Pancreatitis-Associated Acute Lung Injury by Inhibiting Serum Exosomal miRNA-21-3p-Induced M1 Alveolar Macrophage Polarisation","authors":"Bowen Lan, Xuanchi Dong, Qi Yang, Haiyun Wen, Yibo Zhang, Fan Li, Yinan Cao, Zhe Chen, Hailong Chen","doi":"10.1111/jcmm.70758","DOIUrl":"https://doi.org/10.1111/jcmm.70758","url":null,"abstract":"Severe acute pancreatitis (SAP) is a common abdominal emergency in clinical practice. Approximately 20%–40% of patients with SAP will be associated with acute lung injury (SAP-ALI), which is a major cause of death. Emodin (EMO) is a naturally occurring anthraquinone derivative with various pharmacological properties. EMO has a therapeutic effect on SAP-ALI; however, the underlying mechanism remains unclear. Exosomes mediate intercellular communication in disease progression. Therefore, this study aimed to explore the role of serum exosomes in SAP-ALI and the potential mechanisms by which EMO regulates the composition of exosomes for treatment. miR-21-3p was highly expressed in serum exosomes of the SAP group and exacerbated M1 polarisation of alveolar macrophages (AMs). EMO treatment reduced serum exosomal miR-21-3p and relatively attenuated M1 polarisation. Transfection with an miR-21-3p inhibitor attenuated LPS-induced M1 polarisation of AMs in vitro; however, its effects were partially reversed when the downstream target gene PTEN was knocked down simultaneously. This study suggests that EMO reduced the enrichment of miR-21-3p in serum-derived exosomes of rats with SAP, inhibiting the M1 polarisation of AMs caused by the transfer of miR-21-3p through the exosome pathway. This mechanism is related to miR-21-3p targeting of the PTEN/PI3K/AKT signalling pathway.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 16","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70758","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144891604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cinobufotalin Ameliorates the Development of Pulmonary Fibrosis by Suppressing the TGF-β/Smad Pathway via Regulating PI15 Cinobufotalin通过调节PI15抑制TGF-β/Smad通路改善肺纤维化的发展

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-08-22 DOI: 10.1111/jcmm.70788

Dong Xia, Xingyan Liu, Qiuting Yang, Jie Li, Li Li, Yong You, Jing Wang, Weiyi Fang, Huiling Yang

{"title":"Cinobufotalin Ameliorates the Development of Pulmonary Fibrosis by Suppressing the TGF-β/Smad Pathway via Regulating PI15","authors":"Dong Xia, Xingyan Liu, Qiuting Yang, Jie Li, Li Li, Yong You, Jing Wang, Weiyi Fang, Huiling Yang","doi":"10.1111/jcmm.70788","DOIUrl":"https://doi.org/10.1111/jcmm.70788","url":null,"abstract":"Pulmonary fibrosis (PF) is a common hallmark of several types of interstitial lung diseases (ILDs), for which effective therapeutic drugs are lacking. The small-molecule chemical compound cinobufotalin (CB) has demonstrated significant anti-cancer effects in lung cancer. In this study, we first found that CB attenuated bleomycin (BLM)-induced PF and inhibited transforming growth factor-beta 1 (TGF-β1)-induced myofibroblast activation and epithelial-mesenchymal transition (EMT). Subsequently, comparative RNA sequencing (RNA-Seq) was conducted to analyse the lung gene expression profiles in mice. Interestingly, peptidase inhibitor 15 (PI15) was identified as a significantly differentially expressed gene (DEG) and may be a potential target in PF progression. Mechanistic studies showed that CB exerts anti-PF effects by inhibiting PI15 and thereby regulating the TGF-β/Smad signalling pathway. Our data demonstrated that CB represents a promising anti-PF drug and may be a candidate therapeutic for PF patients.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 16","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70788","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144891606","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Investigating Liquid–Liquid Phase Separation in Lung Adenocarcinoma to Improve Prognostic Accuracy and Treatment Efficacy 探讨液-液相分离在肺腺癌诊断中的应用，提高预后准确性和治疗效果

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-08-22 DOI: 10.1111/jcmm.70807

Zipei Song, Yuting Li, Pengpeng Zhang, Ke Wei, Miaolin Zhu, Yuheng Wang, Zhihua Li, Liang Chen, Jianan Zheng

{"title":"Investigating Liquid–Liquid Phase Separation in Lung Adenocarcinoma to Improve Prognostic Accuracy and Treatment Efficacy","authors":"Zipei Song, Yuting Li, Pengpeng Zhang, Ke Wei, Miaolin Zhu, Yuheng Wang, Zhihua Li, Liang Chen, Jianan Zheng","doi":"10.1111/jcmm.70807","DOIUrl":"https://doi.org/10.1111/jcmm.70807","url":null,"abstract":"Liquid–Liquid Phase Separation (LLPS) refers to the separation of biomacromolecules into separate liquid phases within the cells, plays a critical role in lung cancer pathogenesis. Using machine learning, we developed an LLPS-associated signature (LLPSAS) based on 79 key genes. The LLPSAS demonstrated superior prognostic performance compared to 140 existing lung adenocarcinoma (LUAD) prognostic models. Patients stratified by LLPSAS risk scores revealed significantly lower overall survival in the high-risk group. Comparative analysis between the high-risk and low-risk groups showed distinct pathway enrichment, genomic alterations, tumour immune microenvironment (TIME) profiles, immunotherapy responses and drug sensitivities. The low-risk group exhibited an inflamed TIME, suggesting potentially better immunotherapy response. Furthermore, potential effective small molecule drugs were identified for high-risk patients. Finally, immunohistochemistry confirmed upregulation of LLPS-associated proteins (PLK1, HMMR, PRC1) in LUAD tissues, and immunofluorescence validated their LLPS occurrence. Conclusively, the LLPSAS provides a valuable tool for LUAD prognosis and treatment optimisation.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 16","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70807","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144891607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Decoy Receptor 2 as a Cell Cycle Arrest Biomarker for Predicting Renal Recovery Following Acute Kidney Injury 诱饵受体2作为预测急性肾损伤后肾恢复的细胞周期阻滞生物标志物

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-08-22 DOI: 10.1111/jcmm.70800

Xiangling Yi, Liming Wang, Xiao-yue Wang, Yu Fang, Jiarui Liu, Kehong Chen, Ya-ni He, Jia Chen

{"title":"Decoy Receptor 2 as a Cell Cycle Arrest Biomarker for Predicting Renal Recovery Following Acute Kidney Injury","authors":"Xiangling Yi, Liming Wang, Xiao-yue Wang, Yu Fang, Jiarui Liu, Kehong Chen, Ya-ni He, Jia Chen","doi":"10.1111/jcmm.70800","DOIUrl":"https://doi.org/10.1111/jcmm.70800","url":null,"abstract":"Renal recovery following acute kidney injury (AKI) is a key determinant of long-term prognosis, while non-recovery significantly increases the risk of chronic kidney disease and progression to end-stage renal disease. Although cell cycle arrest is implicated in renal non-recovery and fibrosis, its association with decoy receptor 2 (DcR2) remains unclear. In this study, we evaluated 139 patients with biopsy-confirmed AKI, defining renal non-recovery as a ≥ 50% increase in baseline serum creatinine (Cr) or the initiation of dialysis. Patients were divided into recovery (n = 79) and non-recovery (n = 60) groups. Urinary DcR2/creatinine (uDcR2/Cr) levels were significantly higher in non-recovery cases, with an area under the curve of 0.733 and a diagnostic cut-off of 378 ng/gCr. Elevated uDcR2/Cr predicted poor renal survival and was independently correlated with non-recovery. In mouse models of ischemia–reperfusion-induced AKI, increased urinary and tubular DcR2 levels were also associated with impaired recovery. Proteomics analysis revealed GSK3b enrichment in cell cycle pathways. Functional studies showed that DcR2 mediated cell cycle arrest through GSK3b/cyclin D1 signalling. In conclusion, DcR2 functions as a biomarker of cell cycle arrest and renal recovery, offering both diagnostic and mechanistic insights, and may serve as a potential therapeutic target in AKI.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 16","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70800","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144891603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tamarixetin Suppresses Colorectal Cancer Progression by Targeting DPP7-Mediated WNT3A/β-Catenin Signalling Pathway 他玛西汀通过靶向dpp7介导的WNT3A/β-Catenin信号通路抑制结直肠癌进展

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-08-22 DOI: 10.1111/jcmm.70787

Peng Ouyang, Jin Gong, Jinlin Nie, Sridhar Kandala, Yangdong Shi, Yao Tian, Zhijing Zhang, Sifu Fang, Fan Pan, Lin Qiu, Zhen Bao

{"title":"Tamarixetin Suppresses Colorectal Cancer Progression by Targeting DPP7-Mediated WNT3A/β-Catenin Signalling Pathway","authors":"Peng Ouyang, Jin Gong, Jinlin Nie, Sridhar Kandala, Yangdong Shi, Yao Tian, Zhijing Zhang, Sifu Fang, Fan Pan, Lin Qiu, Zhen Bao","doi":"10.1111/jcmm.70787","DOIUrl":"https://doi.org/10.1111/jcmm.70787","url":null,"abstract":"Colorectal cancer (CRC) patients have had limited benefits from conventional chemotherapy, highlighting the need for improved therapeutic strategies. Natural compounds have emerged as promising alternatives due to their potent anti-cancer properties and reduced side effects. Tamarixetin is an O-methylated flavonol derived from Azadirachta indica, but its potential and clinical utility to suppress CRC progression remain unknown. To figure out the underlying mechanism, the inhibitory effects of Tamarixetin on CRC were evaluated by in vitro assays; the validation of Tamarixetin-mediated tumour suppression was performed with CRC xenografts and patient-derived organoids. Our results demonstrated that Tamarixetin significantly reduced the proliferation of CRC cells (HT-29 and HCT-116) in a dose-dependent manner, with minimal effects on normal colonic epithelial cells (NCM460). Furthermore, Tamarixetin inhibited proliferation, migration, and invasion of CRC cells, leading to reduced xenograft tumour growth and sensitising CRC to Oxaliplatin. Mechanistically, The expression and protein levels of DPP7 in CRC cells were suppressed by Tamarixetin, which lead to the downregulation of WNT3A/β-catenin signalling pathway. This study highlights Tamarixetin as a promising natural compound for CRC treatment by interfering with DPP7-mediated WNT3A/β-catenin signalling pathway. These findings provide a novel therapeutic strategy to improve outcomes of CRC.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 16","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70787","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144891605","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sirt4 Deficiency Promotes Cardiomyocyte Proliferation and Cardiac Repair Sirt4缺乏促进心肌细胞增殖和心脏修复

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-08-21 DOI: 10.1111/jcmm.70741

Weijing Liu, Jie Feng, Yuan Zhang, Yanyan Hao, Jiajun Zhong, Xinchang Liu, Dongcheng Cai, Haorui Liu, Lina Bai, Miaoqing Hu, Hong Lian, Yu Nie, Houzao Chen, Yuyao Wang

{"title":"Sirt4 Deficiency Promotes Cardiomyocyte Proliferation and Cardiac Repair","authors":"Weijing Liu, Jie Feng, Yuan Zhang, Yanyan Hao, Jiajun Zhong, Xinchang Liu, Dongcheng Cai, Haorui Liu, Lina Bai, Miaoqing Hu, Hong Lian, Yu Nie, Houzao Chen, Yuyao Wang","doi":"10.1111/jcmm.70741","DOIUrl":"https://doi.org/10.1111/jcmm.70741","url":null,"abstract":"The mammalian heart exhibits transient but remarkable regenerative capacity during the early postnatal period, after which most cardiomyocytes exit the cell cycle. While the sirtuin family is well-established as regulators of cell cycle progression, its specific role in cardiomyocyte proliferation and cardiac regeneration remains unclear. In this study, we found that Sirt4 expression increased during postnatal heart development. Adenovirus-mediated Sirt4 overexpression in vitro inhibited cardiomyocyte proliferation by inducing oxidative DNA damage. Moreover, cardiomyocyte-specific Sirt4 overexpression in vivo suppressed cardiomyocyte proliferation and impaired neonatal heart regeneration. Using Sirt4-knockout mice, we found that Sirt4 deficiency promoted cardiomyocyte proliferation and extended the heart regeneration window. Furthermore, Sirt4 deficiency improved cardiac function and reduced myocardial fibrosis after ischaemia–reperfusion injury in adult mice. These findings establish Sirt4 as a critical regulator of cardiomyocyte proliferation and cardiac repair, suggesting that targeted Sirt4 inhibition may represent a promising therapeutic strategy for ischaemic heart diseases.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 16","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70741","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

N7-Methylguanine-Related Gene Signature Highlights EIF4E as a Novel Therapeutic Target in HER2-Negative Breast Cancer n7 -甲基鸟嘌呤相关基因标记强调EIF4E是her2阴性乳腺癌的新治疗靶点

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-08-21 DOI: 10.1111/jcmm.70808

Yangyang Cui, Yuhan Dai, Yiqin Xia, Wenxin Yu, Jiangdong Jin, Shui Wang, Hui Xie

{"title":"N7-Methylguanine-Related Gene Signature Highlights EIF4E as a Novel Therapeutic Target in HER2-Negative Breast Cancer","authors":"Yangyang Cui, Yuhan Dai, Yiqin Xia, Wenxin Yu, Jiangdong Jin, Shui Wang, Hui Xie","doi":"10.1111/jcmm.70808","DOIUrl":"https://doi.org/10.1111/jcmm.70808","url":null,"abstract":"Globally, breast cancer remains one of the most prevalent malignancies and a leading cause of cancer-related death in women, with over 2.3 million new cases reported annually. Despite treatment advances, one breast cancer type in particular, HER2-negative breast cancer, lacks precise therapeutic targets. Given the role of N7-methylguanosine (m7G) in gene regulation and its links to cancer progression, we investigated m7G regulatory gene expression and prognostic potential in HER2-negative breast cancer. We analysed publicly available breast cancer datasets (The Cancer Genome Atlas and the Gene Expression Omnibus (GEO)) to analyse the differential expression of 14 m7G-regulatory genes. Clustering analysis, based on m7G patterns, categorised HER2-negative patients into two subgroups. A prognostic model was established through LASSO and Cox regression; subsequently validated by survival analysis, and further supported by functional assays confirming gene function. Our model identified CCNB1 and EIF4E as high-risk genes, with EIF4E overexpression enhancing cell proliferation, migration and invasion. RNA-sequencing (RNA-seq) and pathway analyses showed that upregulated EIF4E activated Wnt signalling and extracellular matrix (ECM) components, processes required for tumour progression. High-risk patients showed reduced immune cell infiltration and poorer survival outcomes. We highlight m7G regulatory gene potential, particularly EIF4E, as prognostic markers and therapeutic targets for HER2-negative breast cancer. Targeting EIF4E-related pathways could provide new therapeutic strategies to improve breast cancer patient outcomes.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 16","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70808","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Comparative Analysis of miRNA Expression 106a-5p and 375-3p and Proteins ERK1/2, p38, β-Catenin and E-Cadherin in Prostate Cancer and Benign Prostatic Hyperplasia miRNA 106a-5p、375-3p及ERK1/2、p38、β-Catenin、E-Cadherin在前列腺癌和良性前列腺增生组织中的表达比较分析

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-08-21 DOI: 10.1111/jcmm.70695

Magdalena Smereczańska, Natalia Domian, Grzegorz Młynarczyk, Irena Kasacka

{"title":"Comparative Analysis of miRNA Expression 106a-5p and 375-3p and Proteins ERK1/2, p38, β-Catenin and E-Cadherin in Prostate Cancer and Benign Prostatic Hyperplasia","authors":"Magdalena Smereczańska, Natalia Domian, Grzegorz Młynarczyk, Irena Kasacka","doi":"10.1111/jcmm.70695","DOIUrl":"https://doi.org/10.1111/jcmm.70695","url":null,"abstract":"Prostate cancer is the most frequently diagnosed cancer in men and the second most common cause of death. PSA is performed in men to detect prostate cancer early, but PSA levels increase in both cancer and BPH. Therefore, there is an important need to understand prostate-specific molecular signatures. Considering the importance of the MAPK and Wnt/β-catenin pathways in the progression of many cancers and the fact that the miRNA expression profile is unique in each cancer type, evaluation of 106a-5p and 375-3p miRNAs may be an important factor in cancer detection. The research was carried out on tissue fragments taken from 30 patients with BPH and 30 with cancer. IHC and qRT-PCR were used to identify the expression of tested proteins, while the expression of miRNAs was examined using dPCR. The results of the present study showed significantly higher fluorescence intensity of miRNAs 106a-5p and 375-3p, and lower immunoreactivity and the expression of genes encoding ERK1/2, p38, β-catenin and E-cadherin in prostate cancer compared to BPH. It is possible that thanks to miRNA 106a-5p and 375-3p, the proteins we studied belonging to the MAPK and Wnt/β-catenin pathways play a protective suppressor role in prostate cancer cells.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 16","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70695","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Magnolol as a Radiotherapy Enhancer in Oral Squamous Cell Carcinoma: Targeting the EGFR/NF-κB Pathway and Immune Modulation 厚朴酚作为口腔鳞状细胞癌的放疗增强剂：靶向EGFR/NF-κB通路和免疫调节

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-08-19 DOI: 10.1111/jcmm.70699

Yu-Chang Liu, Chih-Ying Liao, Fei-Ting Hsu, Hsing-Ju Wu, Kuan-Tin Chen, Pei-Hsuan Lee, Wei-Ting Hsueh

{"title":"Magnolol as a Radiotherapy Enhancer in Oral Squamous Cell Carcinoma: Targeting the EGFR/NF-κB Pathway and Immune Modulation","authors":"Yu-Chang Liu, Chih-Ying Liao, Fei-Ting Hsu, Hsing-Ju Wu, Kuan-Tin Chen, Pei-Hsuan Lee, Wei-Ting Hsueh","doi":"10.1111/jcmm.70699","DOIUrl":"https://doi.org/10.1111/jcmm.70699","url":null,"abstract":"Oral cancer, particularly oral squamous cell carcinoma (OSCC), often exhibits resistance to standard treatments like surgery, chemotherapy, and radiation therapy (RT). Magnolol, a bioactive compound from the bark of Magnolia officinalis, is recognised for its anti-inflammatory, antioxidant, antimicrobial, and antitumor properties. This study aims to explore magnolol's potential to enhance the therapeutic efficacy of RT in oral cancer models. Using MOC1-bearing animals, we evaluated the combined effect of magnolol and RT. The results showed that magnolol significantly suppressed tumour growth, delayed progression, and reduced tumour weight compared to control groups. Immune profiling revealed that magnolol plus RT promoted positive immune regulation by increasing M1 macrophages, dendritic cells, and activated cytotoxic T cells, while suppressing negative regulators like myeloid-derived suppressor cells (MDSCs) and regulatory T cells (Tregs). Immunohistochemical analysis also demonstrated enhanced activation of apoptosis-related pathways including the cleavage of caspase-3, -8, and -9. Furthermore, the combination of magnolol and RT did not induce significant toxicity, as evidenced by stable body weight, normal tissue pathology, and normal liver and kidney function markers. Notably, the phosphorylation levels of EGFR and NF-κB were significantly reduced in the magnolol plus RT group, similar to the effects seen with erlotinib plus RT. In conclusion, these findings highlight magnolol's ability to enhance the efficacy of RT in oral cancer by targeting the EGFR/NF-κB axis, inducing apoptosis, and modulating immune responses, presenting a promising therapeutic strategy for OSCC.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 16","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70699","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144869630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetics and Vitamin D Interactions in Osteoporosis: A Path to Precision Medicine 骨质疏松症的遗传学和维生素D相互作用：通往精准医学的道路

IF 4.2

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE Pub Date : 2025-08-19 DOI: 10.1111/jcmm.70780

Sepideh Abdollahi, Forough Taheri, Amirhossein Sangi Nasab Lahijan, Saba Hatefi Shoga, Ali Didehban, Saeid Doaei

{"title":"Genetics and Vitamin D Interactions in Osteoporosis: A Path to Precision Medicine","authors":"Sepideh Abdollahi, Forough Taheri, Amirhossein Sangi Nasab Lahijan, Saba Hatefi Shoga, Ali Didehban, Saeid Doaei","doi":"10.1111/jcmm.70780","DOIUrl":"https://doi.org/10.1111/jcmm.70780","url":null,"abstract":"Osteoporosis is a systemic skeletal disease characterized by reduced bone mineral density (BMD) and increased fracture risk; it poses a significant global health challenge. The multifactorial pathogenesis of osteoporosis involves complex interactions between genetic factors and vitamin D metabolism, particularly involving key genes such as the vitamin D receptor (VDR), CYP27B1 and CYP24A1. Polymorphisms in these genes, including FokI, BsmI, TaqI and ApaI in the VDR gene, have been associated with variations in BMD, fracture susceptibility and differential responses to vitamin D supplementation, underscoring the importance of personalized medicine. Genome-wide association studies (GWAS) have identified over 500 loci, including WNT16, ESR1 and SOST, linked to osteoporosis-related traits, underlining the disease's polygenic nature and the impact of gene–environment interactions, including dietary vitamin D intake, sun exposure and gene variations. Despite these advancements, translating genetic insights into clinical practice remains challenging, especially due to the variability in genetic determinants and limited access to genotype assessment such as gene sequencing. This review advocates for precision medicine approaches to osteoporosis management. By addressing the gaps in the studies on osteoporosis aetiology, integrating genetic screening into routine diagnosis and care and promoting collaborative efforts in genomics, nutrition and public health, the global burden of osteoporosis can be significantly reduced. This approach offers a promising pathway to improve patient outcomes and advance personalized medicine strategies for osteoporosis as a debilitating condition.","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 16","pages":""},"PeriodicalIF":4.2,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70780","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144869629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0