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肿瘤分泌的增殖素-1调节恶病质中的脂肪生成和脂肪分解。

Tumor-secreted proliferin-1 regulates adipogenesis and lipolysis in cachexia.

机构信息

Department of Immunology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Ishikawa, Japan.

WPI Nano Life Science Institute (NanoLSI), Kanazawa University, Kanazawa, Ishikawa, Japan.

出版信息

Int J Cancer. 2021 Apr 15;148(8):1982-1992. doi: 10.1002/ijc.33418. Epub 2020 Dec 28.

Abstract

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.

摘要

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。

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