Department of Immunology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan.
WPI Nano Life Science Institute (NanoLSI), Kanazawa University, Kanazawa, Ishikawa, Japan.
Int J Cancer. 2021 Apr 15;148(8):1982-1992. doi: 10.1002/ijc.33418. Epub 2020 Dec 28.
Cancer-associated cachexia (CAC) is a common syndrome in cancer patients and is characterized by loss of body weight accompanied by the atrophy of fat and skeletal muscle. Metabolic changes are a critical factor in CAC; however, the mechanisms through which tumors inhibit adipogenesis and promote lipolysis are poorly understood. To clarify these mechanisms, we investigated adipogenesis-limiting factors released by tumors in a cell culture system. We identified proliferin-1 (PLF-1), a member of the growth hormone/prolactin gene family, as a key factor secreted from certain tumors that inhibited preadipocyte maturation and promoted the lipolysis of mature adipocytes. Importantly, mice transplanted with PLF-1-depleted tumor cells were protected from fat loss due to CAC. These data show that tumor-secreted PLF-1 plays an essential role in impaired adipogenesis and accelerated lipolysis and is a potential therapeutic target against CAC.
癌症相关性恶病质(CAC)是癌症患者中常见的综合征,其特征是体重减轻,同时伴随着脂肪和骨骼肌萎缩。代谢变化是 CAC 的一个关键因素;然而,肿瘤抑制脂肪生成和促进脂肪分解的机制还不太清楚。为了阐明这些机制,我们在细胞培养系统中研究了肿瘤释放的脂肪生成限制因子。我们鉴定出增殖素-1(PLF-1)是生长激素/催乳素基因家族的一个成员,是某些肿瘤分泌的关键因子,它抑制前体脂肪细胞的成熟,并促进成熟脂肪细胞的脂肪分解。重要的是,移植了 PLF-1 耗尽的肿瘤细胞的小鼠由于 CAC 而免受脂肪损失的影响。这些数据表明,肿瘤分泌的 PLF-1 在受损的脂肪生成和加速的脂肪分解中发挥着重要作用,是治疗 CAC 的一个潜在靶点。