摘要：目的 总结近年来关于肿瘤恶液质的分子机制研究。方法 应用PubMed、维普中文科技期刊全文数据库和中国期刊全文数据库，以“恶性肿瘤、恶液质、骨骼肌萎缩、分子机制、泛素蛋白酶体途径”作为关键词，检索近10年来此类文献。纳入标准：①恶性肿瘤；②恶液质；③泛素蛋白酶体途径；④骨骼肌萎缩。根据标准收入以下参考文献。结果 肿瘤恶液质的分子机制比较复杂，主要包括泛素-蛋白酶体途径、促恶液质细胞因子的调节途径、神经内分泌途径以及其他途径；泛素蛋白酶体途径的研究较明确，主要是通过E1、E2、E3及蛋白酶体参与；促恶液质细胞因子的调节途径主要通过NF-κB通路、P38β MAPK通路及肌抑素/激活素通路；神经内分泌途径主要是糖皮质激素的作用，在抑制蛋白质合成过程中，主要通过下调mTOR、损害起始阶段的信使核糖核酸的翻译，影响这些蛋白质合成并涉及到Akt通路。结论 各项调节机制之间有一定关联性，其中和E3酶关联较大。分子机制的具体调控和调控中与其他途径的关系是继续研究的切入点。

Abstract: Objective To summarize processes about molecular mechanisms for the tumor cachexia in recent years. Methods Applying the PubMed, the VIP and the CNKI, with "the malignant tumor, cachexia, skeletal muscle atrophy, the molecular mechanism, the ubiquitin proteasome pathway"as key words, for the retrieval of such literature in recent 10 years. Inclusion criteria: ①malignanttumor; ②cachexia; ③ubiquitin proteasome way; ④skeletal muscle atrophy, according to the standard income the references below. Results In the cachexia, the molecular mechanisms are more complex, mainly including the ubiquitin-proteasome pathway, the regulation pathway of pro-inflammatory cytokines, neuroendocrine pathway and other ways. The study of ubiquitin proteasome pathway research is clear, with proteasomes participation like E1, E2, E3; The regulation pathway of pro-inflammatory cytokines mainly includes the NF-κB pathway, P38β MAPK pathway and muscle inhibin/activin pathway; Neuroendocrine way is mainly glucocorticoids effect, with inhibiting protein synthesis by cutting mTOR, damaging the starting phase of the messenger RNA translation which influences on the protein synthesis and involves the Akt pathway. Conclusions There is correlation among the regulating mechanisms, including with the association of E3 enzymes the most. At the same time, study of the molecular mechanisms of the concrete in the regulation and control and the other way is on the way and the relationships among them may be the breakthrough points.