Hospital Universitari de Tarragona Joan XXIII, Institut d´Investigació Sanitària Pere Virgili Universitat Rovira i Virgili, Tarragona, Spain.
CIBER de Diabetes y Enfermedades Metabólicas Asociadas, Instituto de Salud Carlos III, Madrid, Spain.
Cell Death Dis. 2017 May 18;8(5):e2802. doi: 10.1038/cddis.2017.209.
Adipose tissue (AT) has a central role in obesity-related metabolic imbalance through the dysregulated production of cytokines and adipokines. In addition to its known risk for cardiovascular disease and diabetes, obesity is also a major risk for cancer. We investigated the impact of obesity for the expression of survivin, an antiapoptotic protein upregulated by adipokines and a diagnostic biomarker of tumor onset and recurrence. In a cross-sectional study of 111 subjects classified by body mass index, circulating levels of survivin and gene expression in subcutaneous AT were significantly higher in obese patients and positively correlated with leptin. Within AT, survivin was primarily detected in human adipocyte-derived stem cells (hASCs), the adipocyte precursors that determine AT expansion. Remarkably, survivin expression was significantly higher in hASCs isolated from obese patients that from lean controls and was increased by proinflammatory M1 macrophage soluble factors including IL-1β. Analysis of survivin expression in hASCs revealed a complex regulation including epigenetic modifications and protein stability. Surprisingly, obese hASCs showed survivin promoter hypermethylation that correlated with a significant decrease in its mRNA levels. Nonetheless, a lower level of mir-203, which inhibits survivin protein translation, and higher protein stability, was found in obese hASCs compared with their lean counterparts. We discovered that survivin levels determine the susceptibility of hASCs to apoptotic stimuli (including leptin and hypoxia). Accordingly, hASCs from an obese setting were protected from apoptosis. Collectively, these data shed new light on the molecular mechanisms governing AT expansion in obesity through promotion of hASCs that are resistant to apoptosis, and point to survivin as a potential new molecular player in the communication between AT and tumor cells. Thus, inhibition of apoptosis targeting survivin might represent an effective strategy for both obesity and cancer therapy.
脂肪组织(AT)通过失调的细胞因子和脂肪因子产生在肥胖相关的代谢失衡中起核心作用。除了已知的心血管疾病和糖尿病风险外,肥胖也是癌症的主要风险因素。我们研究了肥胖对存活素表达的影响,存活素是一种由脂肪因子上调的抗凋亡蛋白,也是肿瘤发生和复发的诊断生物标志物。在一项根据体重指数对 111 名受试者进行的横断面研究中,肥胖患者的循环存活素水平和皮下 AT 中的基因表达显著升高,并且与瘦素呈正相关。在 AT 内,存活素主要在人脂肪细胞源性干细胞(hASC)中检测到,hASC 是决定 AT 扩张的脂肪细胞前体。值得注意的是,从肥胖患者中分离的 hASC 中存活素的表达显著高于从瘦对照组中分离的 hASC,并且由促炎 M1 巨噬细胞可溶性因子(包括 IL-1β)增加。对 hASC 中存活素表达的分析显示出复杂的调控,包括表观遗传修饰和蛋白质稳定性。令人惊讶的是,肥胖的 hASC 表现出存活素启动子超甲基化,这与其 mRNA 水平的显著降低相关。尽管如此,与瘦对照组相比,肥胖的 hASC 中发现了抑制存活素蛋白翻译的 mir-203 水平较低,以及蛋白质稳定性较高。我们发现,存活素水平决定了 hASC 对凋亡刺激(包括瘦素和缺氧)的敏感性。因此,肥胖环境中的 hASC 可以免受凋亡的影响。总之,这些数据揭示了通过促进对凋亡有抗性的 hASC 来控制肥胖时 AT 扩张的分子机制,并指出存活素可能是 AT 和肿瘤细胞之间通讯的新分子靶点。因此,针对存活素的凋亡抑制可能代表肥胖和癌症治疗的有效策略。