1,721,010 research outputs found
Antiproliferative Effects of Carvacrol on Neuroblastoma Cells
No full textObjective: Neuroblastoma is a pediatric solid tumor that originates from the neural crest. The survival rate of these malignancies is below 50 %. The most common treatments for the disease have several adverse effects which make them invasive for patients and limits the applicability as well as continuity of the treatment. Therefore, researchers seek new agents to reduce adverse effects in order to improve the treatment. In this wise, plant-derived phytochemicals are promising drug candidates, such as carvacrol which has anti-cancer features in some cancers
Multifaceted transcriptional reprogramming supports oxaliplatin chemoresistance in colorectal cancer cells
No full textOxaliplatin resistance remains a critical barrier to effective colorectal cancer treatment. The molecular mechanisms underlying this resistance are not fully understood, highlighting the need to define the transcriptional alterations that contribute to therapeutic failure. Accordingly, a comparative transcriptome analysis was performed on oxaliplatin-resistant colorectal cancer cells (HCT-116-ROx) and their parental counterparts (HCT-116) using RNA sequencing in this study. Differentially expressed gene (DEG) analysis was conducted using a quasi-likelihood negative binomial model. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment were carried out using the topGO and clusterProfiler packages, respectively. To confirm the robustness of the transcriptomic data, the genes with the most significant expression changes, based on false discovery rate-adjusted P value less than 0.05 and a |logFC| > 2 thresholds, were selected for validation by quantitative real-time PCR (qRT-PCR). A total of 313 DEGs were identified, including ALDH3A1 and TACSTD2 (upregulated) and IFITM1 (downregulated); these three genes were chosen for validation by qRT-PCR. Gene Ontology enrichment revealed significant changes in cell motility, redox regulation, and extracellular matrix remodeling. KEGG analysis indicated upregulation of ferroptosis, glutathione metabolism, and lysosome-related pathways, and downregulation of p53 signaling, oxidative phosphorylation, and cancer-specific pathways. Oxaliplatin-resistant colorectal cancer cells undergo multifaceted transcriptional reprogramming that promotes redox homeostasis, metabolic adaptation, and structural plasticity while suppressing apoptotic and mitochondrial functions. These changes support chemoresistance and may represent potential therapeutic targets to restore drug sensitivity
Immunological landscape of colorectal cancer: tumor microenvironment, cellular players and immunotherapeutic opportunities
No full textColorectal cancer (CRC) remains one of the most lethal malignancies worldwide, with outcomes shaped not only by genetic alterations but also by the complexity of the tumor microenvironment (TME). The TME encompasses stromal and endothelial cells, extracellular matrix components, gut microbiota, and a diverse array of immune cells that dynamically interact to influence tumor initiation, progression, and therapeutic response. This review delineates the immunological landscape of CRC, highlighting the dual functions of innate immune cells-including tumor-associated macrophages, natural killer cells, dendritic cells, neutrophils, and mast cells-and adaptive immune players such as cytotoxic T lymphocytes, helper T-cell subsets, and B/plasma cells. These cellular interactions contribute to the heterogeneity between immunologically "hot" microsatellite instability-high (MSI-H) tumors, which are highly responsive to immunotherapy, and "cold" microsatellite-stable (MSS) tumors, which remain resistant. Key mechanisms of immune evasion, such as cancer immunoediting, checkpoint signaling, and exosome-mediated communication, are examined alongside prognostic tools like the Immunoscore that serve as biomarkers of immune infiltration. Emerging immunotherapeutic strategies, including checkpoint blockade, macrophage reprogramming, natural killer cell agonists, and microbiome modulation, are discussed with emphasis on both their promise and limitations in CRC management. By integrating current insights into immune-tumor interactions, the review underscores opportunities for developing personalized, TME-targeted interventions to improve CRC outcomes
Relationship of c-Kit Gene and Microsatellit Instability in the Pathogenesis of Wilms Tumors
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