Biochemical Genetics最新文献

{"title":"SFRP4 Knockdown Attenuates Dsg2-Deficient Arrhythmogenic Cardiomyopathy by Down-Regulating TGF-β and Smad3.","authors":"Wei Li, Meixiang Wang, Zhongbao Ruan, Yin Ren, Li Zhu, Bo Zhang","doi":"10.1007/s10528-025-11052-z","DOIUrl":"10.1007/s10528-025-11052-z","url":null,"abstract":"<p><p>Although secreted frizzled-related protein 4 (SFRP4) has been linked to the development of cardiovascular diseases; it is yet unknown how exactly it functions in arrhythmogenic cardiomyopathy (ACM) remains unclear. Data from the Gene Expression Omnibus (GEO) were used to identify genes that were differentially expressed and linked to ACM. A mouse model known as desmoglein 2 (Dsg2) knockout (Dsg2^-/-) was employed to investigate ACM. Myocardial fibrosis was evaluated by histological analysis, while heart function was evaluated by echocardiography. Angiotensin II (Ang II) was used to stimulate cardiac fibroblasts (CFs) and cause a fibrotic phenotype. The ability of CFs to migrate was evaluate using a wound healing assay. Gene Set Enrichment Analysis (GSEA) was used to do an enrichment study of the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway. The levels of SFRP4, transforming growth factor beta receptor 2 (TGFBR2), TGF-β2, and Smad family member 3 (Smad3) were assessed using quantitative real-time PCR and Western blot. Our findings show that SFRP4 is highly expressed in Dsg2^-/- mice. SFRP4 knockdown markedly reduced myocardial fibrosis, ventricular compliance, and cardiac dilation in Dsg2^-/- mice. The level of SFRP4 was higher in CFs treated with Ang II, andSFRP4 inhibition markedly decreased the migration of Ang II-induced CFs. Moreover, SFRP4 activates the TGF-β signaling pathway, with SFRP4 knockdown resulting in a significant decrease in the expression levels of TGF-β2, TGFBR2, and Smad3 in Dsg2^-/- mice. In summary, SFRP4 knockdown reduced cardiac fibrosis in ACM by inhibiting the TGF-β signaling pathway.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":"1002-1017"},"PeriodicalIF":1.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522411","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of HLA-DRA, HLA-DQA1 and IL-6 Gene Variations to Glatiramer Acetate Resistance in Multiple Sclerosis Patients.","authors":"Aysegul Sahbaz, Busranur Oguz Selcuk, Fusun Mayda Domac, Serkan Demir, Mesrure Koseoglu, Ebru Hatun Uludasdemir, Gulsah Koc, Bayram Yılmaz, Deniz Kirac","doi":"10.1007/s10528-025-11077-4","DOIUrl":"10.1007/s10528-025-11077-4","url":null,"abstract":"<p><p>Multiple sclerosis (MS) is among the most common autoimmune disorders and is characterized by inflammation and degeneration affecting the central nervous system. Glatiramer acetate (GA) is an immunomodulatory drug utilized for treating relapsing-remitting MS. However, a considerable number of patients do not exhibit an appropriate response to this drug. This condition is known as GA resistance. This study aimed to investigate the relationship between nucleotide variations in the HLA-DRA, HLA-DQA1 and IL-6 genes and GA resistance. Additionally, the relationship of environmental factors with MS was investigated. One hundred thirty-nine MS patients were enrolled in this study. Patients were divided into two groups: non-responders (n = 58) and responders (n = 81). After DNA was isolated from peripheral blood, the rs3135388 and rs3135391 variations in HLA-DRA, the rs9272346 variation in HLA-DQA1, and the rs1800795 and rs1900796 variations in IL-6 were analyzed by Real-Time Polymerase Chain Reaction (RT-PCR). At the end of the study, it was found that the number of females was approximately 3 times greater in responders and 4 times greater in non-responders than in males. When nucleotide variations and allele distributions were compared between the groups, no significant relationships were found. Similarly, no significant relationship was found between risk factors and nucleotide variations. However, in non-responders, the expanded disability status scale and lesion load were found to be significantly high. In conclusion, by increasing the number of patients, more meaningful results can be achieved in future studies. Elucidating the pharmacogenetic characteristics (the drug-gene relationship) of MS patients using GA could lead to the development of personalized treatment strategies.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":"1161-1173"},"PeriodicalIF":1.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143612983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: CircMMP11 is a Potential Recurrence Biomarker and Facilitates Progression of Esophageal Squamous Cell Carcinoma.","authors":"Jingnan Yuan, Ying Cui, JiWen Zhang, Yan Cai, Xun Xu","doi":"10.1007/s10528-025-11153-9","DOIUrl":"10.1007/s10528-025-11153-9","url":null,"abstract":"","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":"1232"},"PeriodicalIF":1.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144223921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"On the Specific Status of Rhinogobius zhoui (Gobiiformes, Gobiidae) with mtDNA Characterization.","authors":"Shuang-Xi Jia, Zi-Xuan Wu, Chang-Hu Lu, Cheng-He Sun","doi":"10.1007/s10528-025-11073-8","DOIUrl":"10.1007/s10528-025-11073-8","url":null,"abstract":"<p><p>Rhinogobius zhoui is found only in streams on Lianhua Mountain, Guangdong Province, China. Juveniles of Rhinogobius zhoui bred in an artificial environment do not undergo a planktonic period and have a landlocked life history. At present, there is not much published literature regarding this species. To study the structural characteristics and phylogenetic information of the mtDNA of Rhinogobius zhoui, the mtDNA of R. zhoui was obtained by next-generation sequencing. The mtDNA was assembled, annotated, and analyzed using a bioinformatics method, followed by alignment of mtDNA and analysis of sequence differences. R. zhoui was analyzed phylogenetically using data on 48 species of Gobiiformes and 2 species of Cypriniformes downloaded from NCBI ( https://www.ncbi.nlm.nih.gov/ ), and phylogenetic trees were generated using maximum likelihood and Bayesian inference. The results of our analysis showed that (1) the length of the mtDNA of R. zhoui was 16,491 bp, according to next-generation sequencing and its mitochondrial structure included 13 protein-coding genes, 22 tRNA genes, two rRNA genes, and one non-coding region and (2) from the phylogenetic tree thus generated, it can be seen that R. zhoui and Rhinogobius duospilus are closely related. This study will re-examine the Phylogenetic tree of the major lineages in Gobiiformes.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":"1233-1251"},"PeriodicalIF":1.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143633178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Truncated Variants in FAM20A and WDR72 Genes Underlie Autosomal Recessive Amelogenesis Imperfecta in Four Pakistani Families.","authors":"Sadaqat Ullah, Sher Alam Khan, Samin Jan, Salah Ud Din, Nazif Muhammad, Zia Ur Rehman, Abid Jan, Muhammad Tariq, Noor Muhammad, Abdul Ghani, Naveed Wasif, Saadullah Khan","doi":"10.1007/s10528-025-11087-2","DOIUrl":"10.1007/s10528-025-11087-2","url":null,"abstract":"<p><p>Amelogenesis Imperfecta (AI) is a set of hereditary diseases affecting enamel development, leading to various types of enamel defects, potentially impacting oral health unassociated with other generalized defects. AI manifests in syndromic and non-syndromic forms and can be inherited through autosomal recessive, autosomal dominant, or X-linked inheritance patterns. Genetic studies have identified sequence variants in a number of genes (≥ 70) linked to both syndromic and non-syndromic AI, highlighting the genetic diversity underlying the condition. The current study involved clinical evaluation and exome sequencing, aimed at identifying the causative variants in four unrelated consanguineous Pakistani families presenting AI phenotypes. The exome sequencing results revealed a novel homozygous frameshift variant FAM20A: NM_017565.4, c.188dupA; p.(Asp63Glufs*17) in families A, B, and C while a nonsense homozygous variant WDR72: NM_182758.4, c.2686C > T; p. (Arg896*) in family D. The segregation of both variants was confirmed by Sanger sequencing. Bioinformatics analysis predicted the pathogenicity of these genetic variants. These alterations suggest functional consequences, potentially impairing the FAM20A and WDR72 proteins and causing dental anomalies. This investigation significantly broadens our understanding of FAM20A and WDR72's involvement in AI. Furthermore, this study highlights the genetic heterogeneity of AI (involving FAM20A and WDR72 in this study) within the Pakistani population.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":"1311-1323"},"PeriodicalIF":1.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12882964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143661829","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}

{"title":"Experimental Validation of miR-4443, miR-572, and miR-150-5p in Serum and Tissue of Breast Cancer Patients as a Potential Diagnostic Biomarker: A Study Based on Bioinformatics Prediction.","authors":"Amirhossein Mardi, Ali Ghovahi, Fereshteh Abbasvandi, Davar Amani","doi":"10.1007/s10528-025-11057-8","DOIUrl":"10.1007/s10528-025-11057-8","url":null,"abstract":"<p><p>Breast cancer is the most common invasive cancer diagnosed in females and is also the main cause of cancer-related deaths leading to more than 500,000 deaths annually. The present study aims to identify a promising panel of microRNAs (miRNAs) using bioinformatics analysis, and to clinically validate their utility for diagnosing breast cancer patients with high accuracy in a clinical setting. First, in the in silico phase of our study, using bioinformatics analysis and the data available in the GEO database, miRNAs that were increased in the interstitial fluid of the tumor tissues (differentially expressed miRNAs), were screened and their related target genes were selected. Multimir package of R software was utilized to determine the target genes of the differentially expressed miRNAs (DEMs). The biological functions of discovered genes were analyzed using Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. In order to determine the molecular mechanisms behind important signaling pathways and cellular functions, the protein-protein interaction network was built using STRING and Cytoscape software. After that, in the laboratory phase, the expression level of three candidate miRNAs on the serum samples of 26 breast cancer patients and 26 control, as well as 14 tumor tissue samples and 14 adjacent normal tissue samples, has been investigated by Real-time PCR method. Then sensitivity and specificity of candidate miRNAs were evaluated through the ROC curve analysis. After in silico analysis, we revealed that three miRNAs including miR-4443, miR-572, and miR-150-5p were highly increased in the interstitial fluid of breast cancer patients compared to breast cancer tissues. Moreover, our results revealed that the expression level of miR-4443, miR-572, and miR-150-5p were significantly decreased in the serum of breast cancer patients compare to normal controls. Also, the expression level of miR-4443 and miR-150-5p was significantly decreased in the tumor tissue compared to the adjacent non-tumor tissue. Also, ROC curve analysis showed that these three miRNAs have high sensitivity and specificity for the diagnosis of breast cancer patients. Data analysis was conducted with GraphPad Prism software. Our findings suggest the potential utility of measuring tumor-derived miRNAs in serum as an important approach for the blood-based detection of breast cancer patients. It appears that miR-4443, miR-572, and miR-150-5p may serve as promising diagnostic biomarkers with high sensitivity and specificity. However, it's important to note that further research will be needed to definitively establish the use of these miRNAs as potential biomarkers in clinical practice.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":"1117-1144"},"PeriodicalIF":1.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Coagulation-Related Genes in Glioblastoma: A Comprehensive Analysis of the Tumor Microenvironment, Prognosis, and Treatment.","authors":"Jingyi Yang, Lei Shen, Yuankun Cai, Ji Wu, Keyu Chen, Dongyuan Xu, Yu Lei, Songshan Chai, Nanxiang Xiong","doi":"10.1007/s10528-025-11086-3","DOIUrl":"10.1007/s10528-025-11086-3","url":null,"abstract":"&lt;p&gt;&lt;p&gt;The influence of coagulation on glioma biology has not been comprehensively elucidated. This study explores the role of coagulation-related genes (CRGs) in glioblastoma (GBM) from the perspectives of the tumor microenvironment (TME), differences in coagulation function among GBM patients, treatment, and prognosis. Somatic mutation analysis was performed on single nucleotide polymorphism (SNP) and copy number variation data from GBM patients in the TCGA cohort. Publicly available single-cell RNA sequencing data were used to analyze the role of coagulation in the GBM TME and its underlying biological mechanisms. Unsupervised clustering of GBM patients from the CGGA693 cohort was conducted, and coagulation function for each patient was assessed using ssGSEA scoring. Prognosis was assessed with Kaplan-Meier survival analysis, and immune infiltration was analyzed through ESTIMATE. A risk signature based on five CRGs (CFI, GNG12, MMP2, LEFTY2, and SERPINC1) was constructed and validated using LASSO regression and random survival forest analyses to predict responses to immunotherapy and identify potential sensitive drugs. Finally, the roles of LEFTY2 and SERPINC1 in GBM progression was verified by immunohistochemistry, cell counting kit-8 (CCK8) assay and wound healing assay, and the anti-GBM effect of the drug PLX4720 was verified by CCK8 assay, wound healing assay, and colony formation assay. Somatic mutation analysis revealed SNP events of CRG mutations in 117 out of 461 GBM cases (25.38%). Single-cell analysis of the GBM TME revealed significant activation of the coagulation pathway in endothelial cells, with intercellular communication mediated via the SPP1-integrin pathway (p &lt; 0.01). Clustering analysis and ssGSEA identified two coagulation-related subtypes in GBM: coagulation-activated and coagulation-inhibited subtypes. Patients in the coagulation-activated subtype exhibited shorter overall survival and poorer prognosis compared to those in the coagulation-inhibited subtype (p = 0.0085). Immune infiltration analysis showed lower tumor purity and higher levels of immune-suppressive cells in the coagulation-activated subtype (p &lt; 0.001). The CRG-based risk signature accurately predicted prognosis (p &lt; 0.0001) and responses to immunotherapy in the IMvigor210 cohort (p = 0.0062). Based on the risk model, PLX4720 was identified as a potential sensitive drug (p &lt; 0.001), and drug validation experiments demonstrated that PLX4720 inhibited the proliferation and migration of glioma cells (p &lt; 0.0001). In vitro experiments demonstrated that LEFTY2 and SERPINC1 were significantly overexpressed in GBM compared to normal brain tissue, and knockdown of LEFTY2 and SERPINC1 inhibited glioma cell proliferation and migration (p &lt; 0.05). The CRG-based risk signature model effectively predicts the prognosis of GBM patients and aids in assessing the efficacy of ICI therapy and chemotherapy. Furthermore, the genes LEFTY2, SERPINC1 and the drug PLX4720 offer po","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":"1369-1400"},"PeriodicalIF":1.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143668557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of DIO2 as a Molecular Therapeutic Target for Depression in Chronic Rhinosinusitis: A Comprehensive Bioinformatics and Experimental Study.","authors":"Hao Lv, Peiqiang Liu, Yunfei Wang, Jingyu Huang, Yulie Xie, Mengting Guan, Jianchao Cong, Yang Jiang, Yu Xu","doi":"10.1007/s10528-025-11085-4","DOIUrl":"10.1007/s10528-025-11085-4","url":null,"abstract":"<p><p>Chronic rhinosinusitis (CRS) and depression are both common conditions with significant socioeconomic impact. The high co-occurrence of depression in CRS patients suggests a common pathophysiology, but the mechanisms are unclear. This study aimed to identify potential molecular links between the two conditions. We retrieved gene expression datasets for CRS and depression from the GEO database. Using differentially expressed genes (DEGs) analysis and weighted gene co-expression network analysis (WGCNA), we identified co-expression genes associated with CRS and depression. Enrichment analyses including GO, KEGG, and GSEA were performed to explore biological pathways. Machine learning algorithms including random forest and LASSO regression were engaged to screen for shared hub genes predictive of CRS and depression. Single-cell RNA sequencing (scRNA-seq) data were analyzed to delineate the expression profiles of the shared hub genes across different cell types. Animal experiments were employed to validate the role of core genes in CRS-related depression. We identified five shared hub genes: CHRDL1, DIO2, HSD17B6, PDE3A, and PLA2G5, with the TGF-β signaling, cytokine-cytokine interaction receptors, and cell adhesion as key biological pathways. DIO2, as identified by machine learning, is a promising diagnostic biomarker for CRS and depression. The scRNA-seq analysis showed that DIO2 is primarily expressed in neurons and astrocytes. Animal experiments showed that overexpression of DIO2 improved the depressive-like behaviors in CRS mice. This study sheds new light on the molecular basis of the comorbidity between CRS and depression. DIO2 is a potential diagnostic and therapeutic target for CRS patients with comorbid depression.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":"1252-1273"},"PeriodicalIF":1.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143639354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative Phosphoproteomic and Metabolomic Analysis of Disruption of Metabolic Homeostasis in Breast Cancer: A Pilot Study.","authors":"Yicong Niu, Xinliang Zhu, Dachang Ma, Qing Pan, Xun Li","doi":"10.1007/s10528-025-11070-x","DOIUrl":"10.1007/s10528-025-11070-x","url":null,"abstract":"<p><p>Breast cancer is a heterogeneous tumor with 4 major molecular subtypes. Hormone receptor (HR)-positive and HER2-negative breast cancer accounts for 70% of invasive breast cancers. In our study, we collected 15 original Luminal B breast cancer tissue (LBBC) and paired non-cancerous adjacent tissue (NATs) from patients and performed LC-MS/MS-based label-free quantitative phosphoproteomic analysis. The untargeted metabolomics analysis was also used to determine the differences in metabolic patterns between LBBC and NATs. In addition, an integrative analysis of phosphoproteomics and metabolomics data was performed to investigate regulatory metabolic pathways. The main regulatory proteins were verified by western blot. Phosphoproteomics analysis identified 1385 differentially phosphorylated sites in 785 proteins. The protein kinase A (PKA) and protein kinase C (PKC) families and p70 ribosomal S6 kinase (RPS6K) were strongly activated in LBBC, whereas the cycle-dependent kinases (CDKs) were markedly inhibited. Cancer-specific activation of PI3K-mTORC and Hippo signaling pathways were also highlighted. Metabolomic analysis showed that 223 metabolites were significantly differentially accumulated, including fatty acids (3-hydroxycapric acid; dodecanoic acid; linoleic acid; stearic acid), glycerophospholipids, glycerophosphatidylcholines, and sphingolipids, which were mainly involved in fatty acid oxidation metabolism, sphingolipid metabolism, purine metabolism, and amino acid metabolism pathway. After integrative analysis, we found that the sphingolipid metabolic pathway played the major regulatory role. We also validated 3 phosphorylated proteins (p-YAP, p-SGK1, and p-SGPP2) in the PI3K-mTORC, Hippo signaling pathway, and sphingolipid metabolic pathway, respectively. The present study provides the first integrative phosphoproteome and metabolome profiles of LBBC, mainly involving dysregulation of sphingolipid homeostasis mediated by PI3K-mTORC and Hippo signaling pathways. This study described two phosphorylation pathways and sphingolipid metabolism regulation module for a better understanding of LBBC carcinogenesis and therapy.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":"1094-1116"},"PeriodicalIF":1.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: TFAP2C Activates CST1 Transcription to Facilitate Breast Cancer Progression and Suppress Ferroptosis.","authors":"Lin Yuan, Di Zhou, Weiwen Li, Jianhua Guan, Junda Li, Bo Xu","doi":"10.1007/s10528-025-11267-0","DOIUrl":"10.1007/s10528-025-11267-0","url":null,"abstract":"","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":"1524"},"PeriodicalIF":1.6,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145480505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}