Mechanisms of high-fat induced prostate cancer progression through Monocyte Chemotactic Protein-1 secreted by adipose tissue

我们研究了不同饮食对前列腺癌细胞生长和相关循环因子的影响，包括血清胰岛素，生长因子和炎性细胞因子，使用体内和体外模型。前列腺癌LNCaP异种移植物的肿瘤生长在HFD组中显著高于HCD和对照饮食（CD）组。HFD组血清单核细胞趋化蛋白-1（MCP-1）水平显著高于HCD组和CD组。CC趋化因子受体2（CCR 2）的mRNA水平，这是一种MCP-1受体，活化Akt的表达在HFD组中最高。此外，来自HFD喂养的小鼠的血清增强了两种PCa细胞的增殖，并且CCR 2敲低抑制了HFD诱导的LNCaP细胞的增殖。总之，HFD比HCD或CD更强地增强前列腺癌细胞生长。MCP-1/CCR 2信号可能参与HFD诱导的前列腺癌进展。

We investigated the effects of different diets on prostate cancer cell growth and the relevant circulating factors including serum insulin, growth factors, and inflammatory cytokines using the in vivo and ex vivo model. The tumor growth of prostate cancer LNCaP xenograft was significantly higher in the HFD group than in the HCD and control diet (CD) groups. The mean level of the serum monocyte chemoattractant protein-1 (MCP-1) in the HFD group was significantly higher than that in the HCD and CD groups. The mRNA levels of CC chemokine receptor 2 (CCR2), which is an MCP-1 receptor, and the expression of activated Akt were the highest in the HFD group. Furthermore, serum from HFD-fed mice enhanced the proliferation of two PCa cells and CCR2 knockdown inhibited HFD-induced proliferation of LNCaP cells. In conclusion, an HFD enhanced prostate cancer cell growth more strongly than an HCD or CD. MCP-1/CCR2 signaling may be involved in an HFD-induced prostate cancer progression.