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:Unraveling the role of exercise in cancer suppression: insights from a mathematical model.
Unraveling the role of exercise in cancer suppression: insights from a mathematical model.
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近期实验研究显示,体育锻炼可能抑制肿瘤进展。据报道,这种抑制作用由锻炼诱导的细胞因子 IL-6 释放激活自然杀伤(NK)细胞介导。为阐明运动诱导的 NK 细胞激活如何抑制癌症,我们建立了一个粗粒度数学模型,以常微分方程描述 IL-6、NK 细胞和肿瘤细胞间的相互作用,并用该模型研究运动时长和强度对肿瘤抑制的影响。结果显示,提高运动强度或延长运动时间会带来更强且更持久的肿瘤抑制作用。此外,多次分段运动模式可通过调整运动强度和频率,为改进癌症治疗策略带来希望。因此,该数学模型有助于深入理解运动在肿瘤抑制中的作用,并可指导未来实验研究,最终有望设计更有效的运动干预方案。
Recent experimental studies have shown that physical exercise has the potential to suppress tumor progression. Such suppression has been reported to be mediated by the exercise-induced activation of natural killer (NK) cells through the release of IL-6, a cytokine.
Aimed at shedding light on how exercise-induced NK cell activation helps in the suppression of cancer, we developed a coarse-grained mathematical model based on a system of ordinary differential equations describing the interaction between IL-6, NK-cells, and tumor cells. The model is then used to study how exercise duration and exercise intensity affect tumor suppression.
Our results show that increasing exercise intensity or increasing exercise duration leads to greater and sustained tumor suppression.
Furthermore, multi-bout exercise patterns hold promise for improving cancer treatment strategies by adjusting exercise intensity and frequency.
Thus, the proposed mathematical model provides insights into the role of exercise in tumor suppression and can be instrumental in guiding future experimental studies, potentially leading to more effective exercise interventions.
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