Journal of Cellular and Molecular Medicine最新文献

{"title":"Corrigendum to \"The Role of PAX7 in Breast Cancer Prognosis and Its Mechanistic Involvement in the Wnt/β-Catenin Pathway\".","authors":"","doi":"10.1111/jcmm.71176","DOIUrl":"10.1111/jcmm.71176","url":null,"abstract":"","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71176"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13162342/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147874284","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AP-1-Targeting Decoy Oligonucleotides: Mechanisms and Therapeutic Potential as Modulators of Inflammatory Pathways.","authors":"Maryam Mahjoubin-Tehran, Samaneh Rezaei, Vasily N Sukhorukov, Amin Jalili, Prashant Kesharwani, Amirhossein Sahebkar","doi":"10.1111/jcmm.71178","DOIUrl":"10.1111/jcmm.71178","url":null,"abstract":"<p><p>Numerous cellular functions, such as apoptosis, proliferation, differentiation, survival, transformation and cell migration, are regulated by a crucial transcription factor called activator protein 1 (AP-1). Growing evidence indicates that AP-1 is involved in severe conditions like fibrosis, cancer, and organ damage, as well as inflammatory diseases, including rheumatoid arthritis, psoriasis, and asthma. In recent years, AP-1 has become a significant focus in drug research. The activation of AP-1 by TNF is crucial for essential components of the inflammatory reaction, including the expression of tissue remodelling proteases such as collagenase, as well as pro-inflammatory cell adhesion molecules like E-selectin. This transcription factor is formed by the assembly of jun-jun homodimers, jun-fos heterodimers, and jun-ATF (Activating Transcription Factor) heterodimers. As a member of the basic leucine zipper (bZIP) class, AP-1 regulates target genes by binding to their promoters in a sequence-specific way. New research suggests that reducing AP-1 function could improve various disease outcomes and treatments. Transfection of decoy oligonucleotides (ODNs) offers an innovative approach to gene therapy by targeting specific gene regulatory elements. Transcription factor decoys mimic the sites where transcription factors bind, competing with promoter regions within the cell nucleus. These molecules can regulate interactions between DNA sequences and transcription factors, which play a role in altering gene activation during both normal and disease-related cellular processes. This review aims to summarize the effects of AP-1-targeted decoys on various conditions. The studies demonstrated the great promising role of AP-1 decoys as therapeutics for various diseases, especially cardiovascular diseases and cancers. Moreover, it was shown that modifications of AP-1 (circular and hairpin as well as phosphorothioate backbones structures) decoys made them more stable and effective.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71178"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13167699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147929961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YTHDF3 Mediates the Occurrence and Development of Breast Cancer by Regulating Glycolysis Through the mTOR-HIF1α-LHDA Axis.","authors":"ZiQian Liu, TengFei Jiang, Peng Li, Ke Dong, XiMei Wang, ChenChen Geng, XiaoDong Zhang, Dan Zuo, GuangHui Zhao","doi":"10.1111/jcmm.71105","DOIUrl":"10.1111/jcmm.71105","url":null,"abstract":"<p><p>Breast cancer, a malignant tumour that frightens women, ruthlessly claims the lives of tens of thousands of women around the world every year. However, the mechanism by which YTHDF3 regulates the occurrence and development of breast cancer is still imperfect. In this study, we used bioinformatics to analyse the expression of YTHDF3 in breast cancer and verified it in clinical specimens. In addition, YTHDF3 knockdown breast cancer cell lines were used to determine the biological role of YTHDF3 in breast cancer through functional experiments such as CCK-8 assay, transwell assay, clonal proliferation and cell cycle assay. Lactate analysis, seahorse assay, RT-qPCR and Western blot were used to explore the downstream mechanism of YTHDF3, and rescue experiments were performed with small molecule activators to repeatedly confirm the downstream targets. Finally, YTHDF3 knockout breast cancer cell lines were used to establish cell line-derived xenograft (CDX) mouse models to further confirm the biological function of YTHDF3 in breast cancer and the possible regulatory mechanism. Our results showed that YTHDF3 was highly expressed in breast cancer cells and clinical tissues, and YTHDF3 enhanced the proliferation and migration ability of breast cancer. Mechanistically, YTHDF3 enhances the expression of HIF1α and LDHA and glycolysis by inducing the phosphorylation of mTOR, and finally promotes the occurrence and development of breast cancer. In addition, YTHDF3 can be used as a helpful biomarker in various cancers, including breast cancer. We aimed to elucidate the role of YTHDF3 in breast cancer development and provide evidence for improving the diagnosis and treatment of breast cancer. In this study, we elucidated that YTHDF3 regulates the glycolysis level, proliferation and migration of breast cancer through the mTOR-HIF1α-LDHA axis. Interference of the YTHDF3 expression is a potential target for breast cancer treatment, which provides strong evidence for improving diagnosis and treatment methods.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71105"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13111412/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated Bulk and Single-Cell RNA-Seq Analysis Reveals Transcriptional Activation of PTGS2 by FOS in Progression From T2DM to T2DM-Associated NAFLD.","authors":"Rong Lin, Leqin Xu, Yi Zhou, Yanjing Fan, Huan Xie, Wanzhang Li, Tianchi Hu, Chao Liu","doi":"10.1111/jcmm.71182","DOIUrl":"10.1111/jcmm.71182","url":null,"abstract":"<p><p>Type 2 diabetes mellitus (T2DM) and nonalcoholic fatty liver disease (NAFLD) frequently coexist, exacerbating disease burden. However, the molecular mechanisms underlying the progression from T2DM to T2DM-associated NAFLD remain unclear. This study investigated the regulatory function of FOS-mediated PTGS2 activation in this transition. We integrated bulk RNA-seq data from GEO, single-cell transcriptomic data and transcriptomes from patients with T2DM-associated NAFLD. Differentially expressed genes were identified using the limma package, and T2DM-related gene modules were defined by weighted gene co-expression network analysis. LASSO regression and random forest identified 14 candidate genes, with PTGS2 and FOS prioritised. Single-cell analysis showed increased FOS and PTGS2 expression in monocytes, CD8⁺ T cells and Kupffer cells. Transcription factor prediction and dual-luciferase assays confirmed that FOS directly binds the PTGS2 promoter and drives its transcription. In vitro, FOS silencing decreased PTGS2 expression, cytokine secretion and apoptosis under high-glucose and free fatty acid conditions, whereas PTGS2 overexpression exacerbated inflammation and apoptosis independently of FOS expression. These findings demonstrate that FOS transcriptionally activates PTGS2, contributing to hepatic inflammation and apoptosis during the progression from T2DM to NAFLD. PTGS2 may serve as a promising biomarker and therapeutic target for T2DM-associated NAFLD.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71182"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13158135/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868519","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mutation in MSH5 Causes Primary Ovarian Insufficiency and Successful Therapeutic Intervention by In Vitro Fertilisation.","authors":"Bin Mao, Lili Zhang, Xiaodong Zhao, Xiaojuan Xu, Hongfang Liu, Dexiao Song, Peiqiang Li, Santasree Banerjee, Xiaoling Ma, Yongxiu Yang","doi":"10.1111/jcmm.70745","DOIUrl":"10.1111/jcmm.70745","url":null,"abstract":"<p><p>Primary ovarian insufficiency (POI) is a genetically heterogeneous disorder characterised by cessation of menstruation before the age of 40 years with elevated levels of follicle-stimulating hormone. Germline variants in the MSH5 gene cause POI. In this study, we investigated a Han Chinese family with POI. The proband and her two younger sisters are clinically diagnosed with POI. The proband's parents are phenotypically normal. Whole exome sequencing identified a novel homozygous splice-donor site (c.271+1G>A) variant in the first nucleotide of intron 3 of the MSH5 gene in this proband. Sanger sequencing confirmed that both the younger sisters of the proband also harbour the same homozygous variant, while the proband's parents are carrying this variant in a heterozygous state. This variant causes aberrant splicing of MSH5 mRNA followed by the formation of an alternative MSH5 transcript with complete loss of exon 3. Relative expression of mutant MSH5 mRNA is significantly reduced compared to that of the wild-type transcript. Mutant MSH5 impaired DNA homologous recombination repair as well as significantly lowering the clonogenic survival rate of cell clone formation compared with the wild type. In addition, we also found a significantly higher apoptotic rate and lower cell proliferation rate in the mutant than that of the wild type. We performed egg donation-based in vitro fertilisation for this proband, and two healthy baby girls have been successfully delivered. Our present study reports the first splice-site variant in the MSH5 gene in patients with POI. We also report for the first time the successful therapeutic intervention by in vitro fertilisation for patients with MSH5-associated POI.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e70745"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13156242/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147856487","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Secretome Derived From Serum-Free Media of SHED-MSCs Can Modulate THP-1-Derived Macrophage Cells.","authors":"Azadeh Mohammad-Hasani, Saeed Mohammadi, Mohsen Saeidi, Ali Fallah, Ayyoob Khosravi","doi":"10.1111/jcmm.71063","DOIUrl":"10.1111/jcmm.71063","url":null,"abstract":"<p><p>Although culturing cells in serum-free or low-serum media may lead to reduced cell proliferation, it is crucial to minimise the presence of foreign proteins and other impurities that could compromise the validity of experimental findings on immunomodulation. The study aimed to investigate the immunomodulatory effects of the secretome derived from the serum-free media (SFM) of stem cells obtained from human exfoliated deciduous teeth on THP-1-derived macrophage polarisation and the assessment of inflammatory and oxidative stress mediators. THP-1 cells were polarised into M0 and M1 macrophages, and their differentiation was confirmed using flow cytometry to analyse specific markers of M0 (CD14 and CD68) and M1 (CD80 and CD86). The secretome was collected from SHED-MSCs cultured for 48 h in serum-free DMEM/F12 media. After treating THP-1-derived M0/M1 macrophages with SFM-secretome from SHED-MSCs, cells and supernatants were evaluated for immunosuppressive (anti-inflammatory and antioxidant) and immunostimulatory (pro-inflammatory and pro-oxidant) indicators. Secretome treatment decreased the population of M1 macrophages, along with the expression of pro-inflammatory and pro-oxidative markers, including CD80, CD86, TNF-α, IL-12, NO, MDA and IL-6R. The immunomodulatory effect of the secretome produced by SFM, which may help reduce inflammation, is demonstrated by an increase in M2 macrophages and anti-inflammatory and antioxidant markers, including CD206, TGFβ-2, IL-10, TAC, CAT, SOD and ARG1. The secretome produced by SFM-derived SHED-MSCs may reduce the risk of introducing foreign proteins and other potentially hazardous chemicals and enhance the efficacy of cellular secretions for applications such as immunotherapy or regenerative medicine by modulating the immune system.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71063"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13143868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating Flow Cytometry in the Diagnostic Work of HIV-Associated Hodgkin's Lymphomas.","authors":"Maria Santa, Diana Cenariu, Adrian-Bogdan Tigu, Marc Damian, Patricia Rantshabeng, Tendani Gaolathe, Andrew K Ndlovu, Khalid Abdelrahman, Madalina Nistor, David Kegyes, Diana Gulei, Cristian Jinca, Anamaria Bancos, Ioana Rus, Horia Bumbea, Victor Tomacinschii, Sanda Buruiana, Rand Bilal, Cristina Selicean, Mihnea Zdrenghea, Bogdan Fetica, Cristina Stefan, Jonathan Fromm, Ciprian Tomuleasa","doi":"10.1111/jcmm.71143","DOIUrl":"10.1111/jcmm.71143","url":null,"abstract":"<p><p>Hodgkin lymphoma (HL) is prevalent worldwide and typically presents symptoms like sudden pain, swelling, and weight loss. Classical HL (cHL) is largely treatable with modern risk-adapted and response-based therapy. cHL represents one of the most common malignancies occurring during the course of evolution in patients living with HIV. The present manuscript aimed to present the diagnostic work-up with an emphasis on flow cytometry in patients with HIV-associated lymphoma, of important clinical benefit both in the HIV-endemic setting as well as in state-of-the-art pathology departments. Three clinical cases of HIV patients, including HIV-associated cHL, are presented in the chapter dedicated to HIV-induced lymphomas diagnosed by FC, as Supporting Information, to support the particularities of the abundance of clonal B-cell populations among different types of HIV-related lymphomas. This adds to the proof-of-concept that the specific antibody panel design may help practitioners in discriminating among similar subtypes of HIV-associated lymphomas. Recent data emphasise the importance of FC detection of cHL rapidly and effectively, adding diagnostic value to these small biopsies. FC is an important tool for clinical decision-making in the management of HL patients, providing a noninvasive and accurate biomarker evaluation. For these considerations, we can conclude that FC is a very useful research tool, and the clinical cases presented in this paper indicate their importance in the rapid diagnosis of cHL as well.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71143"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13143871/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory Activity of Conferone on FAK Activity and Glutamine Metabolism in Human Colorectal Cancer.","authors":"Hien Thi My Ong, Eda Ates, Jaeyong Jung, Jeong Soo Sung, Jae-Chul Pyun, Min-Jung Kang","doi":"10.1111/jcmm.71165","DOIUrl":"10.1111/jcmm.71165","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is a major global cause of death, with metastases and chemotherapy resistance contributing to poor outcomes. To identify natural compounds with anticancer potential against CRC and elucidate their action mechanisms, the cytotoxicity of 37 natural compounds was evaluated against the HCT116, leading to the identification of conferone as the lead candidate. Its anti-migratory and anti-invasive effects were evaluated in HCT116, Colo205, and SW480 cells. The interactions between conferone and focal adhesion kinase (FAK) were assessed through protein expression analysis and molecular docking. Glutaminolysis regulation was determined by LC-MS/MS, and related enzyme levels were detected by western blotting. Conferone inhibited migration and invasion in all three CRC cell lines, though it showed limited anti-proliferative activity. At 10 μM, conferone reduced FAK and p-FAK (Tyr397) protein levels, reversing the epithelial-mesenchymal transition. Docking analysis confirmed direct FAK binding and predicted inhibition of its phosphorylation, with greater affinity than the FAK inhibitor 1,2,4,5-benzene tetramine tetrahydrochloride. Conferone also downregulated glutaminase and glutamate-ammonia ligase, increasing glutamine and decreasing glutamic acid. Additionally, it suppressed c-raf phosphorylation and reduced c-Myc expression, blocking glutaminolysis-driven metabolism. These findings highlight conferone as a potential therapeutic agent that targets FAK, alters metabolic reprogramming, and impedes CRC progression.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71165"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13128536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LINC00240 Knockdown Suppresses the Proliferation, Migration, and Invasion of Ovarian Cancer Cells Through the miR-30c-5p/P4HA2 Axis.","authors":"Yunjie Tian, Jianlei Wu, HaiBo Zhang","doi":"10.1111/jcmm.71171","DOIUrl":"10.1111/jcmm.71171","url":null,"abstract":"<p><p>Ovarian cancer is a particularly lethal malignancy often diagnosed at advanced stages, highlighting the urgent need for novel therapeutic strategies. This study investigates the expression and functional role of LINC00240, miR-30c-5p, and P4HA2 in ovarian cancer pathogenesis. Using datasets GSE66957 and the GEPIA database, we assessed LINC00240 expression levels and employed quantitative real-time polymerase chain reaction (qRT-PCR) to evaluate the expression of LINC00240, miR-30c-5p, and P4HA2 in ovarian cancer samples. Bioinformatics analysis via TargetScan software predicted interactions between these molecules, which were validated through dual-luciferase reporter assays. Functional assays, including colony formation and Transwell assays, assessed the impact of LINC00240 and miR-30c-5p on cell proliferation, migration, and invasion. Our results indicate that LINC00240 and P4HA2 are significantly overexpressed, while miR-30c-5p is downregulated in ovarian cancer. Furthermore, LINC00240 modulates ovarian cancer malignancy by regulating P4HA2 expression through binding with miR-30c-5p. These findings elucidate the role of the LINC00240/miR-30c-5p/P4HA2 axis in ovarian cancer and suggest new avenues for targeted therapeutic interventions.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71171"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13158136/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868517","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-Cell Transcriptome-Wide Mendelian Randomization and Colocalization Uncover Potential Immunocytes-Related Therapeutic Targets for Obesity.","authors":"Xingjian Zhang, Yong Tian, Xiaoying Ren, Juan Tian, Jia Liu, Guang Wang","doi":"10.1111/jcmm.71185","DOIUrl":"10.1111/jcmm.71185","url":null,"abstract":"<p><p>Weight-loss treatment is crucial for individuals with obesity to prevent various complications. The role of Immune cells in obesity has been recently recognized, whereas its translation into therapy requires identifying key target genes. We performed Mendelian randomization (MR) analysis to assess causal relationships between expression quantitative trait loci (eQTL) of 14 immune cells and obesity-related traits (obesity, body mass index and body fat percentage), and validated the results in colocalization analysis. For the putative causal genes identified by the MR and colocalization analyses, we conducted pathway enrichment, differential expressed gene (DEG) analysis and search of druggable evidence, and utilized a Tier system to prioritize drug targets for obesity. MR and colocalization evidence was observed for 1630 genes associated with one or more obesity-related traits, mainly expressed in CD4⁺ naive/central memory T cells and enriched in antigen processing and presentation pathways. Forty-one genes showed causal relationship with all three outcomes, among which 19 genes have not been reported for obesity previously. DEG analysis using single-cell RNA sequencing data of blood or adipose tissue indicated that the differential expression of UBE2Z in monocytes, ZCCHC7 in T cells, and FNBP4 in B cells between lean and obese individuals were consistent with the MR results. By searching drug-gene interaction databases, we found targeted drugs for PYGB and PRUNE1, and PYGB was the top gene ranked in the Tier system. This study provides evidence for the involvement of immune cells in obesity, and the potential cell-specific, immune-related targets for obesity treatment.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"30 9","pages":"e71185"},"PeriodicalIF":4.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13162345/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147874309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}