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:Fatty Acid Metabolism in Ovarian Cancer: Therapeutic Implications.
Fatty Acid Metabolism in Ovarian Cancer: Therapeutic Implications.
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卵巢癌是最恶性的妇科肿瘤。既往研究报道,脂质代谢失调导致的代谢改变促进卵巢癌的侵袭性。脂质代谢涉及脂肪酸的氧化,从而产生能量或合成新的脂质代谢产物。脂肪酸合成及相关信号的上调促进肿瘤细胞增殖和迁移,进而导致不良预后。肿瘤微环境(TME)中脂肪酸介导的脂质代谢通过调节免疫细胞(包括 T 细胞、B 细胞、巨噬细胞和NK 细胞)来调节肿瘤细胞免疫,这些免疫细胞在卵巢癌细胞的存活中发挥重要作用。本文综述了脂肪酸的类型和来源及其与卵巢癌 TME 的相互作用。此外,本综述聚焦于脂肪酸代谢在肿瘤免疫中的作用,并提出脂肪酸及相关脂质代谢通路是卵巢癌的潜在治疗靶点。
Ovarian cancer is the most malignant gynecological tumor. Previous studies have reported that metabolic alterations resulting from deregulated lipid metabolism promote ovarian cancer aggressiveness. Lipid metabolism involves the oxidation of fatty acids, which leads to energy generation or new lipid metabolite synthesis.
The upregulation of fatty acid synthesis and related signaling promote tumor cell proliferation and migration, and, consequently, lead to poor prognosis. Fatty acid-mediated lipid metabolism in the tumor microenvironment (TME) modulates tumor cell immunity by regulating immune cells, including T cells, B cells, macrophages, and natural killer cells, which play essential roles in ovarian cancer cell survival.
Here, the types and sources of fatty acids and their interactions with the TME of ovarian cancer have been reviewed.
Additionally, this review focuses on the role of fatty acid metabolism in tumor immunity and suggests that fatty acid and related lipid metabolic pathways are potential therapeutic targets for ovarian cancer.
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