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149 records · Page 9Linked to original sources
PubMed2025

Elevated expression of transferrin receptor-1 in pancreatic cancer: clinical implications and prognostic significance.

PURPOSE: Many advanced-stage pancreatic cancers are fatal, highlighting the need for solid prognostic indicators. This study evaluates transferrin receptor-1 (TfR1) expression in pancreatic cancer tissues and cell lines for clinical and therapeutic potential. METHOD: The GuangRe database, which integrates mRNA data from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) project, was used to assess TFRC gene expression in pancreatic cancer and normal tissues. ROC curves and Kaplan-Meier and Log-rank tests were used to evaluate TFRC gene expression's diagnostic and survival efficacy. In vitro Western blotting and immunofluorescence experiments on pancreatic cancer cell lines assessed TfR1 expression. IHC staining was done on tissue samples from 90 patients to determine TfR1's clinical importance. RESULTS: The study found that TFRC mRNA levels were significantly higher in pancreatic cancer tissues compared to nearby normal tissues (P&#x2009;<&#x2009;0.05), with an AUC of 0.936. We found higher TfR1 protein levels in pancreatic cancer cell lines (P&#x2009;<&#x2009;0.01) using western blot and immunofluorescence studies. Immunohistochemistry showed that pancreatic cancer tissues expressed 30.1% TfR1 compared to paracancer (11.1%) (P&#x2009;=&#x2009;0.003). In COX regression analysis, increased TfR1 expression was related with lower overall survival (OS) and progression-free survival (PFS), making it an independent prognostic factor. CONCLUSION: Higher TfR1 expression is associated with poor pancreatic cancer outcomes, suggesting its potential as a prognostic biomarker and therapeutic target.

Humans↗
PubMed2025

Transcriptomic analysis at 48&#xa0;h postmortem: a proof of concept for the identification of biomarkers to estimate time since death.

BACKGROUND: The postmortem interval (PMI) refers to the time elapsed between an individual's death and the examination of the body. Tissues undergo a sequence of anatomical changes following death, which are routinely used to estimate the PMI. METHODS: To determine if these anatomical changes are associated with identifiable genomic adaptations that could characterize the PMI more accurately, we analyzed the rat skeletal muscle transcriptome at 0 and 48&#xa0;h postmortem using Clariom&#x2122; S arrays. This study investigates whether specific transcriptomic changes correlate with PMI progression, offering a potential molecular tool to complement established anatomical methods. RESULTS: A total of 3,873 differentially expressed mRNAs were identified, of which 2,787 downregulated and 1,086 upregulated transcripts. The most significantly downregulated mRNA was Tnni1 (FC = -30.95, p&#x2009;=&#x2009;1&#x2009;&#xd7;&#x2009;10-3), while the most upregulated were mt-ATP6, mt-ATP8, and mt-CO3 (FC&#x2009;>&#x2009;7.78, p&#x2009;<&#x2009;1.36&#x2009;&#xd7;&#x2009;10-12). Gene ontology (GO) enrichment analyses revealed that mRNAs upregulated at 48&#xa0;h in the PMI were primarily associated with vascular and endothelial processes, including nitric oxide transport and angiogenesis. Conversely, downregulated mRNAs were linked to mitochondrial activity and cellular metabolism, reflecting both a transient vascular response and metabolic pathway shutdown in the rat skeletal muscle. CONCLUSION: Our results demonstrate significant transcriptomic changes at 48&#xa0;h postmortem, highlighting specific genes and biological pathways that may serve as candidate biomarkers for PMI estimation.

Animals↗
PubMed2026

MicroRNAs and predicted targets in the switch from monolayered to spheroids of cholangiocarcinoma cells.

BACKGROUND: Extrahepatic cholangiocarcinoma (eCCA) is characterized by marked molecular heterogeneity and limited therapeutic options. MicroRNAs (miRNAs) are key post-transcriptional regulators of cancer-related pathways, but their contribution to tumor adaptation in physiologically relevant models remains poorly understood. Three-dimensional (3D) tumor spheroids better mimic in vivo conditions than conventional two-dimensional (2D) cultures. METHODS: We compared miRNA expression profiles in two eCCA cell lines (Sk-ChA-1 and Mz-ChA-1) grown as monolayers (2D) or multicellular tumor spheroids (3D). MiRNA profiling was performed using NanoString technology. Predicted targets were analyzed by over-representation analysis, and selected miRNAs and genes were validated by RT-qPCR and ELISA-based assays. RESULTS: 3D growth induced extensive miRNA remodeling, with distinct (54 deregulated in Sk-ChA-1 and 29 in Mz-ChA-1 cells) and partially overlapping signatures (miR-1283, miR-577, and miR-2113). Among the shared miRNAs, predicted targets included DUSP10 and RBFOX1, while in spheroids, cell-specific multiple miRNAs converged on shared targets (TNRC6B, SMARCAD1, ATG14, HMGA2, and CLOCK) displaying inverse expression patterns. The transcriptional program impacted MAPK signaling, enhanced EMT, and activated stress-adaptive networks but attenuated proliferation in 3D Sk-ChA-1 cells, while Mz-ChA-1 cells retained a more epithelial and proliferative profile. In this context, we point out the involvement of miR-19b-3p using anti-miR transfection experiments. CONCLUSION: Our findings reveal a miRNA-driven regulatory landscape associated with 3D growth in eCCA, linking tumor architecture to signaling rewiring and cellular plasticity, and highlight potentially druggable candidate targets and pathways to investigate as candidates using inhibitors or gene therapy-based interventions.

Humans↗
PubMed2025

Identification of intragenic variants in pediatric patients with intellectual disability in Peru.

BACKGROUND: Intellectual disability in Latin America can reach a frequency of 12% of the population, these may include nutritional deficiencies, exposure to toxic or infectious agents, and the lack of universal neonatal screening programs. In 90% of patients with intellectual disability, the etiology can be attributed to variants in the genome. OBJECTIVE: to determine intragenic variants in patients with intellectual disability between 5 and 18 years old at Instituto Nacional de Salud del Ni&#xf1;o. METHODS: It is a descriptive cross-sectional study with convenience sampling. A total of 124 children diagnosed with intellectual disability were selected based on psychological test results and availability for whole exome sequencing. In addition, a chromosomal analysis of 6.55&#xa0;M was performed on ten patients with a negative result in sequencing. Relative and absolute frequencies and measures of central tendency and dispersion were determined according to their nature. In addition, multiple linear regression and Poisson regression were used to determine the association between some clinical characteristics and the probability of occurrence in patients with positive results. RESULTS: The median age of the patients was 6.3 (IQR&#x2009;=&#x2009;5.95), males accounted for 57.3%, and 91.9% of the cases had mild intellectual disability. Exome sequencing determined the etiology in 30.6% of patients with intellectual disability, of which 52.6% were autosomal dominant inheritance. The most frequent genes found were MECP2, STXBP1 and LAMA2. A broad genotype-phenotype correlation was identified, highlighting the genetic heterogeneity of intellectual disability in this population. The presence of dermatologic lesions, dystonia, peripheral neurological disorders, and fourth finger flexion limitation were observed more frequently in patients with intellectual disability with "positive results". CONCLUSIONS: This study shows that one-third of patients with intellectual disability exhibit intragenic variants, highlighting the importance of genetic analysis for accurate diagnosis. The identification of genes such as MECP2, STXBP1, and LAMA2 underscores the genetic heterogeneity of intellectual disability in the studied population. These findings emphasize the need for genetic testing in clinical management and the implementation of early detection programs in Peru.

Humans↗
PubMed2025

Identification of a PRDM1-regulated T cell network to regulate atherosclerotic plaque inflammation.

BACKGROUND: Inflammation is a key driver of atherosclerosis, yet the mechanisms sustaining inflammation in human plaques remain poorly understood. This study uses a network-based approach to identify immune gene programs involved in the transition from low- to high-risk (rupture-prone) human atherosclerotic plaques. METHODS: Expression data from human carotid artery plaques, both stable (low-risk, n&#x2009;=&#x2009;16) and unstable (high-risk, n&#x2009;=&#x2009;27), were analyzed using Weighted Gene Co-expression Network Analysis (WGCNA). Bayesian network inference, operated on the eigengene values from the WGCNA, further extended the WGCNA analysis, and similarity to the signature of T cell subsets was validated in single-cell RNA sequencing data of human plaques, and a&#xa0;loss-of-function study in a mouse model of atherosclerosis. In silico drug repurposing was performed to identify potential therapeutic targets. RESULTS: Our analysis revealed a distinct gene module with a prominent T cell signature, particularly in unstable plaques. Key regulatory factors, RUNX3, IRF7 and in particular PRDM1, were significantly downregulated in plaque T cells from symptomatic versus asymptomatic patients, indicating a protective role. Additionally, as PRDM1 is downstream of IRF7, we opted for PRDM1 as a key target. T cell-specific Prdm1 deficiency in Western-type diet fed Ldlr knockout mice&#xa0;featured accelerated plaque progression. Finally, as PRDM1 targeting&#xa0;drugs are not yet available, we performed in silico drug repurposing, identifying EGFR inhibitors as promising therapeutic candidates. CONCLUSIONS: This study highlights a PRDM1-regulated T cell network that distinguishes high-risk from low-risk plaques and demonstrates the regulatory role of T cell PRDM1 in controlling atherosclerosis, positioning this pathway as a promising therapeutic target.

Plaque, Atherosclerotic↗