Natural killer (NK) cells are triggered by the innate immune response in the tumor microenvironment. The extensive set of stimulating and inhibiting receptors mediates the target recognition of NK cells, and controls the strength of the effector reaction countering specific targeted cells. Yet, lacking major MHC (histocompatibility complex) MICA/B class I chain-related proteins on the membrane of tumor cells results in the failure of NK cell recognition and ability to resist NK cell destruction. Searching databases and molecular docking suggested that in cervical cancer, pterostilbene (3,5-dimethoxy-40-hydroxystilbene; PTS) in extract could constrain PI3K/AKT signaling and improving the MICA/B expression. In flow cytometry, MTT assay, viability/cytotoxicity assay, and colony development assays, PTS reduced the development of cervical cancer cells and increased apoptosis. The quantitative real-time PCR (qRT-PCR) and a Western blot indicate that PTS controlled the cytolytic action of NK cells in tumor cells via increasing the MICA/B expression, thus modifying the anti-tumor immune response in cervical cancer.

中文翻译：

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紫檀芪通过PI3K/AKT信号通路上调MICA/B，增强自然杀伤细胞杀伤宫颈癌细胞的能力

自然杀伤 (NK) 细胞由肿瘤微环境中的先天免疫反应触发。广泛的刺激和抑制受体介导 NK 细胞的靶标识别，并控制针对特定靶细胞的效应反应的强度。然而，肿瘤细胞膜上缺乏主要的MHC（组织相容性复合体）MICA/B I类链相关蛋白，导致NK细胞无法识别和抵抗NK细胞破坏的能力。检索数据库和分子对接表明，在宫颈癌中，提取物中的紫檀芪（3,5-二甲氧基-40-羟基芪；PTS）可以抑制 PI3K/AKT 信号传导并改善 MICA/B 表达。在流式细胞术、MTT 测定、活力/细胞毒性测定和集落发育测定中，PTS 减少了宫颈癌细胞的发育并增加了细胞凋亡。实时定量PCR（qRT-PCR）和Western印迹表明PTS通过增加MICA/B表达来控制肿瘤细胞中NK细胞的溶细胞作用，从而改变宫颈癌的抗肿瘤免疫反应。