ArticleClinical epigenetics2025
Investigating the mechanisms by which low NAT1 expression in tumor cells contributes to chemo-resistance in colorectal cancer.
Article in Clinical epigenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Colitis-Associated Colorectal Cancer-STAT3 Inhibition as a Preventive Strategy.International journal of molecular sciences · 2026Article
- Mechanisms and advances of drug resistance in colorectal cancer: A systematic overview of multi-layered regulatory networks.Translational oncology · 2026Review
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Authors and funding
11 authors.
Funding
Abstract
backgroundIn the therapeutic landscape of colorectal cancer (CRC), chemo-resistance poses a significant and prevalent obstacle that complicates treatment efficacy and patient outcomes. Over time, cancer cells can develop mechanisms to resist the toxic effects of chemo-therapy drugs, leading to reduced sensitivity or complete insensitivity to these agents. The enzyme Arylamine N-acetyltransferase 1 (NAT1) has emerged as a promising target in strategies aimed at overcoming this challenge. NAT1 is involved in the metabolism of various xenobiotics, including some chemotherapeutic agents. Understanding the complex interactions between NAT1 and chemotherapeutic agents, as well as the molecular mechanisms underlying chemo-resistance, is crucial for the development of novel therapeutic approaches.
objectiveThis study aimed to assess the role of NAT1 in mediating chemo-resistance in CRC, with the goal of identifying novel strategies to overcome this clinical challenge.
methodsWe conducted a comprehensive analysis using various bioinformatics tools and in vitro experiments to evaluate the effect of NAT1 expression on chemo-resistance in CRC. Furthermore, we employed a multi-omics approach, including metabolomics and next-generation sequencing, to uncover the mechanisms by which NAT1 influences chemo-resistance. Additionally, we utilized single-cell RNA sequencing (scRNA-seq), the Cellchat assay, and western blot to explore the intercellular communication between tumor and endothelial cells in the context of anti-PD-1 therapy and NAT1's impact.
resultsOur study reveals that decreased NAT1 expression in CRC tumor tissues, relative to adjacent normal tissues, is significantly associated with a poorer patient prognosis. Experimental data indicate that silencing NAT1 in CaCO2 and HCT116 cell lines results in heightened resistance to five chemotherapeutic agents: vinblastine, docetaxel, gemcitabine, vincristine, and daporinad. Additionally, NAT1 silencing increases the proportion of LGR5
conclusionOur study underscores the multifaceted role of NAT1 in modulating chemo-sensitivity, cellular metabolism, and angiogenesis in CRC. These findings position NAT1 as a compelling candidate for a biomarker and a potential therapeutic target, offering new avenues for CRC management.
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