James P. Wilmot Cancer Institute, Rochester, NY, USA; Division of Hematology/Oncology, Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA.
Department of Public Health Sciences, University of Rochester Medical Center, Rochester, NY, USA.
Exp Gerontol. 2024 Mar;187:112364. doi: 10.1016/j.exger.2024.112364. Epub 2024 Jan 25.
Tumor necrosis factor (TNF)α is a major regulator of inflammation. However, the epigenetic regulation of TNFα in the context of an exercise intervention among older adults with cancer is understudied. In this exploratory analysis, we used data from a single-arm mobile health (mHealth) exercise intervention among older adults with myeloid malignancies to 1) assess changes in TNFα promoter methylation, TNFα mRNA expression, serum TNFα and other related-cytokine levels after intervention; and 2) assess correlations between blood markers and exercise levels. Twenty patients were included. From baseline to post-intervention, there was no statistical changes in TNFα promoter methylation status at seven CpG sites, TNFα mRNA expression, and serum TNFα levels. Effect sizes, however, were moderate to large for several CpG sites (-120, -147, -162, and -164; Cohen's d = 0.44-0.75). Median serum TNFα sR1 levels increased (83.63, IQR 130.58, p = 0.06; Cohen's d = 0.18) but not the other cytokines. Increases in average daily steps were correlated with increases in TNFα promoter methylation at CpG sites -147 (r = 0.48; p = 0.06) and -164 (r = 0.51; p = 0.04). Resistance training minutes were negatively correlated with TNFα promoter methylation at CpG site -120 (r = -0.62; p = 0.02). All effect sizes were moderate to large. In conclusion, after a mHealth exercise intervention, we demonstrated changes with moderate to large effect sizes in several CpG sites in the TNFα promoter region. Exercise levels were correlated with increases in TNFα promoter methylation. Larger exercise trials are needed to better evaluate TNFα regulation to inform interventions to augment TNFα regulation in order to improve outcomes in older adults with cancer.
肿瘤坏死因子 (TNF)α 是炎症的主要调节剂。然而,在癌症老年患者的运动干预中,TNFα 的表观遗传调控研究较少。在这项探索性分析中,我们使用了一项针对骨髓恶性肿瘤老年患者的移动健康 (mHealth) 运动干预的单臂数据,以:1) 评估干预后 TNFα 启动子甲基化、TNFα mRNA 表达、血清 TNFα 和其他相关细胞因子水平的变化;2) 评估血液标志物与运动水平之间的相关性。共纳入 20 例患者。从基线到干预后,七个 CpG 位点的 TNFα 启动子甲基化状态、TNFα mRNA 表达和血清 TNFα 水平没有统计学变化。然而,几个 CpG 位点 (-120、-147、-162 和 -164;Cohen's d=0.44-0.75) 的效应大小为中等至较大。血清 TNFα sR1 水平中位数增加(83.63,IQR 130.58,p=0.06;Cohen's d=0.18),但其他细胞因子没有增加。平均每日步数的增加与 CpG 位点-147(r=0.48;p=0.06)和-164(r=0.51;p=0.04)的 TNFα 启动子甲基化增加相关。抗阻训练分钟与 CpG 位点-120 的 TNFα 启动子甲基化呈负相关(r=-0.62;p=0.02)。所有效应大小均为中等至较大。总之,在 mHealth 运动干预后,我们在 TNFα 启动子区域的几个 CpG 位点观察到具有中等至较大效应大小的变化。运动水平与 TNFα 启动子甲基化的增加相关。需要更大规模的运动试验来更好地评估 TNFα 调节,以告知干预措施来增强 TNFα 调节,从而改善癌症老年患者的结局。