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:The Role of Arginine Metabolism in Oral Tongue Squamous Cell Carcinoma.
The Role of Arginine Metabolism in Oral Tongue Squamous Cell Carcinoma.
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口腔舌鳞状细胞癌(TSCC)即使早期诊断和治疗,仍有较高发病负担且预后较差。早期研究表明,TSCC中ARG1信号失调。本研究考察该癌症亚部位中ARG1代谢的复杂性,以评估这一潜在生物学脆弱点的治疗价值。多项功能研究显示,与对照相比,口腔癌细胞中ARG1过表达可抑制细胞增殖和侵袭。此外,RNA测序显示ARG1过表达会扰动大量差异表达基因及相关网络,包括缺氧诱导因子(HIFα)信号、NK 细胞信号通路和干扰素信号。本研究为理解TSCC中精氨酸代谢紊乱的作用机制奠定了基础,并可能推动进一步治疗方法开发。
Early diagnosis and treatment do not prevent the high morbidity and poor prognosis of oral tongue squamous cell carcinoma (TSCC). Earlier studies have shown that ARG1 signaling is deregulated in TSCC.
Here, we investigated the complexity of ARG1 metabolism in this cancer subsite to appreciate the therapeutic potential of this potential biological vulnerability. Various functional studies show that ARG1 overexpression in oral cancer cells inhibits cell proliferation and invasion compared with controls.
Further, RNA-sequencing revealed numerous differentially expressed genes (DEGs) and associated networks were dysregulated by ARG1 overexpression, including hypoxia-inducible factor (HIFα) signaling, the natural killer cell signaling pathway and interferon signaling.
Our work provides a foundation for understanding the mechanism of action of disrupted arginine metabolism in oral tongue squamous cell carcinoma. This may impact the community for developing further therapeutic approaches.
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