IUBMB Life最新文献

{"title":"Conventional and innovative approaches to black fungi control for stone heritage preservation","authors":"Domenico Celi,&nbsp;Massimiliano Marvasi,&nbsp;Brunella Perito","doi":"10.1002/iub.70010","DOIUrl":"10.1002/iub.70010","url":null,"abstract":"<p>Black Meristematic Fungi (BMF) are characterized by a thick melanized cell wall and an isodiametric cellular expansion. BMF represent one of the most damaging groups of microorganisms causing the deterioration of outdoor exposed stone monuments mainly due to the formation of dark spots and patches leading to the darkening of their surface, cracking, and bio-pitting. BMF are among the most stress-resistant organisms on Earth, known for their remarkable ability to withstand solar radiation, desiccation, and extreme temperature fluctuations, which has led to their widespread distribution across the globe. These features make BMF very difficult to remove and restrict, representing a challenge for restorers. Despite the number of scientific works about BMF isolation and ecology, little is known about their response to antimicrobial treatments. Conventional biocides remain the most used treatment for the control of biodeterioration on stone artworks. In recent years, interest in alternative and safer antimicrobial treatments has risen in conservation strategies. The number of scientific works in which their efficacy against BMF is evaluated is, however, still low. The aim of this review is to assess existing studies regarding the response of BMF to both conventional and innovative treatments. This will encompass an in-depth examination of methodologies for the application and evaluation of treatments. Furthermore, we aim to highlight future research directions that will contribute to a more informed selection of effective anti-BMF interventions for stone preservation. We underscore the significance of pioneering, environmentally low-impact solutions.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 3","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924882/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663589","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}

{"title":"Upstream transcription factor 1 suppresses laryngeal squamous cell carcinoma progression through transcriptional activation of junctional adhesion molecule 3","authors":"Yue Jia,&nbsp;Jiaojiao Liu,&nbsp;Yichen Lou,&nbsp;Xinfang Wang,&nbsp;Chunming Zhang,&nbsp;Yujia Guo,&nbsp;Hui Huangfu","doi":"10.1002/iub.70013","DOIUrl":"https://doi.org/10.1002/iub.70013","url":null,"abstract":"<p>Laryngeal squamous cell carcinoma (LSCC) exhibits aggressive growth, frequent recurrence, and a notable resistance to existing treatments. Building upon prior discoveries that identified junctional adhesion molecule 3 (JAM3) as a critical tumor suppressor in LSCC, this study delves into the transcriptional regulation by upstream stimulatory factor 1 (USF1) and its implications for LSCC pathogenesis. Employing dual-luciferase assays and chromatin immunoprecipitation–quantitative polymerase chain reaction (ChIP-qPCR), we confirmed USF1's direct binding to the E-box within the JAM3 promoter, thereby enhancing JAM3 expression in AMC-HN-8 and FD-LSC-1 cells. Complementary in vitro assays and in vivo experiments corroborated that USF1 overexpression markedly reduces tumor aggressiveness, linked to heightened JAM3 activity. Further analysis, including Western blot and immunohistochemistry of xenograft tumor tissues, revealed that increased JAM3, stimulated by USF1, activates the Hippo signaling pathway, underscoring its role in tumor suppression. These findings position USF1 and JAM3 as pivotal elements in the molecular framework of LSCC, suggesting their potential as targets for therapeutic intervention.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 3","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143595495","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}

{"title":"The cGAS-STING-related signature affects the prognosis of colorectal cancer through its regulation of multiple immune cells","authors":"Yunlong Li,&nbsp;Xunliang Jiang,&nbsp;Hui Cao,&nbsp;Xiao Wu,&nbsp;Huimin Zhang,&nbsp;Hongjiang Ma,&nbsp;Liangbo Wang,&nbsp;Boyu Kang,&nbsp;Mianjiao Xie,&nbsp;Shisen Li","doi":"10.1002/iub.70009","DOIUrl":"https://doi.org/10.1002/iub.70009","url":null,"abstract":"<p>The cGAS-STING signaling pathway has emerged as a critical player in the immune response against cancer, including colorectal adenocarcinoma (COAD). Understanding the impact of this pathway on COAD at multiple omics levels is crucial for advancing cancer immunotherapy and precision medicine. This study aimed to investigate the relationship between cGAS-STING-related genes and COAD, analyzing gene mutations, copy number variations, DNA methylation, and gene expression to uncover the pathway's influence on COAD prognosis. Utilizing multi-omics sequencing data from TCGA and GEO databases, key core genes in the cGAS-STING pathway were identified and further validated through PCR and Western blot analysis. Mutations and copy number variations in the CASP8 and RIPK1 genes, differential DNA methylation patterns, and mRNA expression levels of specific genes were assessed to determine their impact on COAD prognosis. Validation through tissue samples highlighted NLRC3, CASP1, AIM2, and CXCL10 as core genes in the cGAS-STING pathway. Our findings demonstrate that mutations and copy number variations in CASP8 and RIPK1, differential DNA methylation patterns, and altered gene expression levels significantly influence the prognosis of COAD. The identification of core genes in the cGAS-STING pathway, particularly NLRC3, CASP1, AIM2, and CXCL10, has led to the development of a prognostic model predicting poor tumor outcomes through immune cell infiltration. This study provides valuable insights into the mechanisms of the cGAS-STING pathway in COAD and offers potential directions for future research in cancer immunotherapy and precision medicine.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 3","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iub.70009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143533309","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}

{"title":"Histone demethylase LSD1 promotes castration-resistant prostate cancer by causing widespread gene expression derangements","authors":"Haiying Li,&nbsp;Xiujie Fan,&nbsp;Xiuxiu Fang,&nbsp;Yunshan Wang","doi":"10.1002/iub.70011","DOIUrl":"https://doi.org/10.1002/iub.70011","url":null,"abstract":"<p>Lysine-specific demethylase 1 (LSD1), a histone demethylase crucial for embryonic development and tissue differentiation, has an undefined role in prostate cancer (PCa), especially castration-resistant PCa. The present study represents a pioneering endeavor to comprehensively dissect the function of LSD1 within the PCa landscape. Our investigations revealed that attenuation of LSD1 expression exerts multiple inhibitory effects on PCa cells. Specifically, it curtails the proliferation and colony-forming ability of PC-3 cells, concomitantly promotes apoptosis, and impedes cell invasion. Notably, knockdown of LSD1 triggers significant perturbations in the expression profiles of pivotal proteins, such as prostate-specific antigen (PSA), forkhead box A1 (FOXA1), and NKX3.1, thereby shedding new light on the underlying molecular mechanisms governing PCa progression. Leveraging bioinformatics analysis and transcriptome sequencing, we unearthed that LSD1 knockdown precipitates widespread gene expression dysregulation, with 3166 genes exhibiting differential expression patterns, which in turn impact a broad spectrum of cellular processes. Importantly, we identified that LSD1 modulates the methylation modification of histone H3 lysine 4 monomethylation (H3K4me1) in the promoter region of matrix metallopeptidase 13 (MMP13), thereby orchestrating its expression. In both orthotopic and metastatic tumor models, as well as in vitro cell cultures, the LSD1 inhibitor GSK2879552 demonstrated potent efficacy in suppressing PCa progression. To sum up, this study not only uncovers the oncogenic role of LSD1 in PCa but also validates the therapeutic promise of GSK2879552, furnishing novel perspectives and prospective targets for the clinical management of PCa.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 3","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143533529","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}

{"title":"Purification and validation of asparaginyl-tRNA synthetase heterodimer with indistinguishable subunits","authors":"Ingrid Vallee,&nbsp;Ryan Shapiro,&nbsp;Xiang-Lei Yang","doi":"10.1002/iub.70000","DOIUrl":"https://doi.org/10.1002/iub.70000","url":null,"abstract":"<p>Oligomerization can influence the stability and activity of a protein. The majority of enzymes, including aminoacyl-tRNA synthetases, become catalytically active upon forming homodimers. Residues located at the dimerization interface are highly conserved and mutations arising within can cause severe disease phenotypes. Beyond homozygous mutations, other disease-causing mutations, such as compound heterozygous and mono-allelic mutations, can lead to the formation of heterodimers between two distinct subunits. Purifying a recombinant heterodimer is required for its thorough characterization in vitro, yet there is a lack of established biochemical methods for the preparation. Here we describe a heterodimer purification and validation method with the example of a disease-causing mono-allelic, nonsense mutation R534* in cytoplasmic asparaginyl-tRNA synthetase (NARS1 or AsnRS). Our method involves co-expression of two separately tagged constructs to allow for purification of the wild-type and the R534* mutant heterodimers. While the two subunits can hardly be distinguished by size, their separate detection is achieved by western blotting against the tags. Quantification analysis confirmed that the subunits within the heterodimer are present in nearly equal proportions. This simple protocol can be adapted to study other size-indistinguishable heterodimers.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143481525","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}

{"title":"Enhanced HER2 status detection in breast and gastric cancers using surrogate DNA methylation markers","authors":"Yajie Hu,&nbsp;Siyu Liu,&nbsp;Chunhui Cui,&nbsp;Xin Liu,&nbsp;Hui Li,&nbsp;Hong Liu,&nbsp;Shiyao Lu,&nbsp;Zhipeng Lu,&nbsp;Zhiwei Chen,&nbsp;Da Pang,&nbsp;Jian-Bing Fan,&nbsp;Dongmei Lin,&nbsp;Xianyu Zhang,&nbsp;Yu Sun","doi":"10.1002/iub.70004","DOIUrl":"https://doi.org/10.1002/iub.70004","url":null,"abstract":"<p>There is a limited understanding of specific DNA methylation patterns associated with HER2 overexpression in breast and gastric cancers. Here we aim to solve the problem using inferred DNA methylation markers. DNA methylation data from The Cancer Genome Atlas (TCGA) were analyzed for breast and gastric cancers regarding HER2 status. We further applied a targeted bisulfite sequencing approach to elaborate the DNA methylation profile of the <i>HER2</i> region, covering 7635 CpG sites. Based on these two sets of data, we selected specific DNA methylation markers inferring HER2 status for both breast and gastric cancers and validated their performance in assisting HER2-status determination on a retrospective cohort with 496 breast cancer and 372 gastric cancer. HER2-Meth could well distinguish HER2 IHC0/1+ from HER2 IHC3+ cases in both breast cancer (AUC = 0.983, <i>n</i> = 130) and gastric cancer (AUC = 0.974, <i>n</i> = 63), also could effectively discriminate HER2 IHC2+/FISH+ from HER2 IHC2+/FISH- cases in equivocal situations for both breast cancer (test set AUC = 0.879, <i>n</i> = 74; validation set AUC = 0.875, n = 75) and gastric cancer (test set AUC = 0.910, <i>n</i> = 70; validation set AUC = 0.941, n = 71), outperforming regular <i>HER2</i> copy number test (An AUC of 0.793 for breast cancer and an AUC of 0.759 for gastric cancer) on HER2 IHC2+ cases. Furthermore, HER2-Meth demonstrated its potential for stratifying HER2-positive patients, enabling predictions regarding overall survivals, and the potential benefits of HER2-targeted therapies in breast cancer. The strong agreement observed between the methylation qPCR test and the results of IHC and FISH indicates significant potential for this approach as a complementary tool in guiding HER2-targeted therapies for patients with breast and gastric cancers.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143475434","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}

{"title":"Hypoxia inducible factor 3-alpha promotes a malignant phenotype in colorectal cancer cells","authors":"Alejandro Lopez-Mejia,&nbsp;Angela Patricia Moreno-Londoño,&nbsp;Gabriela Fonseca Camarillo,&nbsp;Jesús Kazuo Yamamoto-Furusho,&nbsp;Juan Antonio Villanueva-Herrero,&nbsp;Jorge Luis de Leon-Rendón,&nbsp;Maria Cristina Castañeda Patlán,&nbsp;Martha Robles-Flores","doi":"10.1002/iub.70007","DOIUrl":"https://doi.org/10.1002/iub.70007","url":null,"abstract":"<p>Colorectal cancer (CRC) is the third most common cancer worldwide. Hypoxia is a hallmark of the tumor microenvironment, and cellular adaptation to it is primarily mediated by the family of Hypoxia-inducible factors (HIFs) HIF-1α, HIF-2α, and HIF-3α. However, in contrast to HIF-1α and HIF-2α, a specific role for HIF-3α in cancer biology has not yet been clearly established. This research was aimed to elucidate the role of HIF-3α in colon cancer. As reported previously for HIF-1α and HIF-2α, we found that HIF-3α is also overexpressed under normoxic conditions in all cancer cell lines examined and in patient-derived tumor tissue samples compared with non-malignant cells and normal tissue, but remarkably, pulse-chase experiments demonstrated that HIF-3α displays high stability in cells compared with HIF-1α and HIF-2α. <i>Progno Scan</i> data analysis showed that overexpression of HIF-3α correlated with a patient's lower survival rate and a poor prognosis in colon adenocarcinoma patients. Knockdown of HIF-3α expression was carried out to investigate the effects derived from its silencing on malignant phenotype. We found a significative decrease in the Hypoxia Response Element (HRE) reporter transcriptional activity mediated by HIF-3α and a reduction in cell viability under oxidative stress in colon cancer cells with HIF-3α knockdown compared with control HIF-3α expressing cells. In addition, HIF-3α silencing also produced an increase in apoptotic rate, decreased clonogenic capacity, altered autophagy flux, and modulated the canonical Wnt/β pathway in an isoform-dependent and cell context-dependent manner in colon cancer cells. Overall, these data show that transcriptional activity mediated by HI3-3α plays an essential role in promoting the malignant phenotype, cell survival, and resistance to cell death in CRC cells.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iub.70007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143455947","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}

{"title":"Adverse fetal and neonatal impact of war conflicts during pregnancy: A systematic review","authors":"Blanca Riquelme-Gallego,&nbsp;Lucía Ramos-Soberbio,&nbsp;Ester Leno-Duran,&nbsp;Sergio Martínez-Vázquez,&nbsp;Rafael A. Caparros-Gonzalez","doi":"10.1002/iub.70006","DOIUrl":"https://doi.org/10.1002/iub.70006","url":null,"abstract":"<p>The aim of the present study was to establish the fetal and neonatal impact of war conflicts during pregnancy. A systematic review was conducted according to The Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines and relevant publications available in the PubMed, Scopus and Web of Science, and PsycINFO databases. Primary and quantitative studies were eligible for inclusion. To be included, studies had to be redacted in Spanish or English and evaluate maternal exposure to a war or terrorist attack during pregnancy, with consideration being given of the consequences of this for fetal and/or neonatal development. Systematic, narrative and exploratory literature reviews were excluded, as were meta-analyses and studies in which the sample differed from the sample of interest, the focus was on other stressful factors that differed from a war conflict and the consequences examined did not comprise the impact of a war during pregnancy on the fetus or neonate. The methodological quality of included articles was assessed using the CASP (Critical Appraisal Skills Programme) tool. A total of 28 articles were included, with an included sample of <i>n</i> = 664,980 mother-infant dyads, exposed to war conflicts. The adverse impact of prenatal stress suffered by mothers during periods of war revealed that, (1) in the short-term, babies were at greater risk of having a low birth weight and impinged length and being born prematurely, whilst mothers were more likely to suffer a miscarriage. (2) In the long-term, babies exposed to war during the prenatal period had a higher risk of experiencing alterations to their neurodevelopment, mental disorders and pathophysiological diseases. The stress suffered by mothers during the prenatal period can bring about a number of negative consequences over both the short- and long-term in babies, especially, in terms of their physical and neurological development. It is important to conduct further research on the topic with the aim of detecting and treating the early stages of maternal psychological illnesses experienced during pregnancy due to war conflict and, in this way, achieve benefits for pregnant women and future generations.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143455982","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}

{"title":"Structure–function relationships between the human bitter taste receptor TAS2R38 and propylthiouracil: An in-silico investigation","authors":"Gowtham Subramanian,&nbsp;Vinithra Ponnusamy,&nbsp;Janaranjani Murugesan,&nbsp;Hemamalini Vedagiri,&nbsp;Prabha Panneerselvan,&nbsp;Keerthana Vasanthakumar,&nbsp;Vasanth Krishnan,&nbsp;Selvakumar Subramaniam","doi":"10.1002/iub.70008","DOIUrl":"https://doi.org/10.1002/iub.70008","url":null,"abstract":"<p>Taster categorisation uses bitter thiourea compounds like propylthiouracil (PROP) and phenylthiocarbamide (PTC), which are frequently associated with amino acid alterations at positions 49, 262 and 296 in human taste 2 receptor member 38 (hTAS2R38). Since the hTAS2R38 protein lacked a crystallographic structure, it was modelled using contact-guided iterative threading assembly refinement, its residues were mutated and refined, and the binding pocket area and volume were assessed using CASTp. Bitter thiourea molecules were docked using the ligand extra precision module and the receptor–ligand complex was manually positioned in a fully hydrated, equilibrated 1-palmitoyl-2-oleoylphosphatidylcholine bilayer using the CHARMM GUI membrane constructor, a 100 ns simulation was carried out using the Desmond program. Analysis revealed that the PROP binds to the allosteric hydrophobic pocket of hTAS2R38 and forms a hydrogen bond with ASN190. The native structure (hTAS2R38_PAV) has a higher glide energy (−24.164 kcal/mol) and docking score (−7.212 kcal/mol) than mutants, corroborating our taste preference study. In contrast, PTC lacks hydrogen bonds in the binding pocket but exhibits pi–pi stacking interactions with the native structure. Structures with mutations at the 49th or 296th position showed the largest root mean square deviations and fluctuations. A triple mutation increases surface area and volume, making the 262nd position critical to the binding pocket. These results highlight the functional roles of these three residues in hTAS2R38.</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143446801","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}

{"title":"Correction to “Caffeic acid phenethyl ester synergistically enhances docetaxel and paclitaxel cytotoxicity in prostate cancer cells”","authors":"","doi":"10.1002/iub.70005","DOIUrl":"https://doi.org/10.1002/iub.70005","url":null,"abstract":"<p>\u0000 <span>M. F. Tolba</span>, <span>A. Esmat</span>, <span>A. M. Al-Abd</span>, <span>S. S. Azab</span>, <span>A. E. Khalifa</span>, <span>H. A. Mosli</span>, <span>S. Z. Abdel-Rahman</span>, and <span>A. B. Abdel-Naim</span>, “ <span>Caffeic acid phenethyl Ester synergistically enhances docetaxel and paclitaxel cytotoxicity in prostate cancer cells</span>,” <i>IUBMB Life</i> <span>65</span>, no. <span>8</span> (<span>2013</span>): <span>716</span>–<span>729</span>, https://doi.org/10.1002/iub.1188.</p><p>Concerns were raised by a third party regarding duplication of image panels within the article (Figures 3 and 8). An investigation by the journal team confirmed these issues and discovered another instance of duplication between Figure 4A and B GAPDH panels.</p><p>The authors admitted to the image compilation errors in Figures 3 and 8. Regarding Figure 4, they stated that the samples and their controls were obtained from the same PCR/gel electrophoresis run. The authors cooperated with the investigation, however, the partial raw data provided were not sufficient to fully address the concerns; therefore, they repeated the experiments in question to provide further clarification.</p><p>The new data confirmed the same trends as observed before, therefore, the experimental results and the corresponding conclusions of the paper remain unaffected.</p><p>The corrected Figures 3, 4, and 8 and their corrected captions are as follows:</p>","PeriodicalId":14728,"journal":{"name":"IUBMB Life","volume":"77 2","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/iub.70005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143439104","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}