RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Differential roles of highly expressed PFKFB4 in colon adenocarcinoma patients.
Differential roles of highly expressed PFKFB4 in colon adenocarcinoma patients.
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结肠腺癌(COAD)是一种常见的恶性肿瘤,而蛋白PFKFB4在糖酵解和磷酸戊糖途径中的作用至关重要。研究人员通过免疫组化研究79份组织样本中PFKFB4的表达,探讨了其在COAD中的临床意义。
我们发现,PFKFB4在COAD患者中的表达显著升高,尤其是在乙状结肠中。有趣的是,PFKFB4高表达与COAD患者总生存期(OS)改善和无进展生存期(PPS)恶化均相关。
进一步分析显示,与PFKFB4相关的基因与多种代谢途径有关,包括氨基酸生物合成、糖酵解、糖异生、葡萄糖代谢和炎症反应。PFKFB4表达还与COAD患者中不同免疫细胞类型的浸润相关,如CD8+ T细胞、CD4+ T细胞、调节性T细胞(Tregs)、巨噬细胞、中性粒细胞、树突状细胞、活性肥大细胞和静息NK细胞。
总体而言,PFKFB4表达与COAD预后之间的关系复杂多样,可能在疾病的不同阶段发挥不同作用。此外,其机制可能涉及与肿瘤微环境中多种代谢途径和免疫浸润的相互作用。这些发现为PFKFB4作为COAD生物标志物或治疗靶点的潜在作用提供了有价值的见解。
Colon adenocarcinoma (COAD) is a common malignant tumor, and the role of the protein PFKFB4 in glycolysis and pentose phosphate pathways is crucial. Researchers investigated the clinical significance of PFKFB4 in COAD by studying its expression in 79 tissue samples using immunohistochemistry.
We found that PFKFB4 expression was significantly higher in COAD patients, particularly in the sigmoid colon. Interestingly, high PFKFB4 expression was associated with both improved overall survival (OS) and worse progression-free survival (PPS) in COAD patients.
Further analysis revealed that genes associated with PFKFB4 were linked to various metabolic pathways, including amino acid biosynthesis, glycolysis, gluconeogenesis, glucose metabolism, and inflammatory response. PFKFB4 expression also showed correlations with the infiltration of different immune cell types in COAD patients, such as CD8+ T cells, CD4+ T cells, regulatory T cells (Tregs), macrophages, neutrophils, dendritic cells, active mast cells, and resting NK cells.
Overall, the relationship between PFKFB4 expression and the prognosis of COAD is complex and diverse, possibly playing different roles at different stages of the disease.
Moreover, its mechanism might involve interactions with various metabolic pathways and immune infiltration in the tumor microenvironment.
These findings provide valuable insights into the potential role of PFKFB4 as a biomarker or therapeutic target in COAD.
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