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Fas signaling in adipocytes promotes low-grade inflammation and lung metastasis of colorectal cancer through interaction with Bmx
Cancer Letters ( IF 9.7 ) Pub Date : 2021-09-16 , DOI: 10.1016/j.canlet.2021.09.024
Fei Yang 1 , Meng Duan 1 , Faxiang Zheng 1 , Lei Yu 2 , Yuan Wang 1 , Guowei Wang 1 , Jie Lin 1 , Shuang Han 3 , Da Gan 1 , Zhuoxian Meng 4 , Shankuan Zhu 1
Affiliation  

Obesity is a global public health issue. Obesity-related chronic low-grade inflammation (meta-inflammation) can lead to aberrant adipokine release and promote cardiometabolic diseases and obesity-related tumors. However, the mechanisms involved in the initiation of inflammatory responses in obesity and obesity-related tumors as well as metastasis are not fully understood. In this study, we found that the increased tumor necrosis factor-alpha (TNF-α) in adipocytes promoted the lung metastasis of MC38 colon cancer cells via Fas signaling. The release of TNF-α and interleukin (IL)-6 by Fas signaling in adipocytes was caused by the activation of the nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways mediated by the interaction of Fas with Bmx, a non-receptor tyrosine kinase. Moreover, the Fas/Bmx complex is involved in the inflammation of adipocytes via Fas at the Tyr189 site and SH2 domain of Bmx. This is the first study to report the interaction between Fas and Bmx in adipocyte inflammation, which may provide clues for the development of potential new treatment strategies for obesity-related diseases.



中文翻译:

脂肪细胞中的 Fas 信号通过与 Bmx 相互作用促进结直肠癌的低度炎症和肺转移

肥胖是一个全球性的公共卫生问题。肥胖相关的慢性低度炎症(meta-inflammation)可导致脂肪因子异常释放并促进心脏代谢疾病和肥胖相关肿瘤。然而,在肥胖和肥胖相关肿瘤中引发炎症反应以及转移的机制尚不完全清楚。在这项研究中,我们发现脂肪细胞中增加的肿瘤坏死因子-α (TNF-α) 通过 Fas 信号传导促进了 MC38 结肠癌细胞的肺转移。Fas 信号传导在脂肪细胞中释放 TNF-α 和白细胞介素 (IL)-6 是由核因子-κ B (NF-κB) 和丝裂原活化蛋白激酶 (MAPK) 通路的激活引起的,这些通路由Fas 与 Bmx,一种非受体酪氨酸激酶。而且,Fas/Bmx 复合物通过 Bmx 的 Tyr189 位点和 SH2 结构域的 Fas 参与脂肪细胞的炎症。这是第一个报告脂肪细胞炎症中 Fas 和 Bmx 之间相互作用的研究,这可能为肥胖相关疾病的潜在新治疗策略的开发提供线索。

更新日期:2021-09-20
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