Ha Xiaodan, Wang Jingzhou, Chen Keru, Deng Yuchun, Zhang Xueting, Feng Jiale, Li Xue, Zhu Jiaojiao, Ma Yinghua, Qiu Tongtong, Wang Cuizhe, Xie Jianxin, Zhang Jun
Shihezi University School of Medicine, Bei-Er-Lu, Shihezi, Xinjiang 832000, People's Republic of China.
Cancer Manag Res. 2020 Feb 24;12:1355-1369. doi: 10.2147/CMAR.S236301. eCollection 2020.
As one of the most common forms of cancer that threatens men's health, prostate cancer (PCa) is under a trend of increasing morbidity and mortality in most countries. More and more studies have pointed out that obesity is closely linked to the occurrence and development of PCa, although there are still many undiscovered molecular mechanisms between the two.
In the present study, we compare serum lipid levels in patients with PCa and normal individuals. PCa cells (PC3 and 22RV1) were cultured in vitro, the TC/TG/HDL/GLU assay kit was used to detect the glucose and lipid metabolism level of PCa cells, the flow cytometry technique was used to detect the proliferation ability of PCa cells, and the Transwell was used to detect the invasion and migration ability of PCa cells. Western blot/quantitative real-time PCR was used to detect peroxisome proliferator-activated receptor γ (PPARγ) and vimentin/vascular endothelial growth factor-A (VEGF-A) expression levels, and immunohistochemistry was used to observe tumor-associated gene expression levels in nude mice. All data were analysed using the Independent samples -test or rank sum test.
We found higher levels of FFA in the serum of patients with PCa. In vitro experiments have demonstrated that high levels of FFA can promote the proliferation, migration and invasion of two PCa cells (PC3 and 22RV1) and affect the energy metabolism of PCa cells. The upregulated PPARγ plays a key role in this process, and vimentin may be involved in this signaling pathway.
We infer that high levels of FFA may promote PCa development by upregulating PPARγ expression.
前列腺癌（PCa）作为威胁男性健康的最常见癌症形式之一，在大多数国家其发病率和死亡率呈上升趋势。越来越多的研究指出，肥胖与PCa的发生和发展密切相关，尽管两者之间仍存在许多未被发现的分子机制。
在本研究中，我们比较了PCa患者和正常个体的血清脂质水平。体外培养PCa细胞（PC3和22RV1），使用TC/TG/HDL/GLU检测试剂盒检测PCa细胞的糖脂代谢水平，采用流式细胞术检测PCa细胞的增殖能力，使用Transwell检测PCa细胞的侵袭和迁移能力。采用蛋白质免疫印迹法/定量实时聚合酶链反应检测过氧化物酶体增殖物激活受体γ（PPARγ）和波形蛋白/血管内皮生长因子-A（VEGF-A）的表达水平，并通过免疫组织化学观察裸鼠肿瘤相关基因的表达水平。所有数据均采用独立样本t检验或秩和检验进行分析。
我们发现PCa患者血清中游离脂肪酸（FFA）水平较高。体外实验表明，高水平的FFA可促进两种PCa细胞（PC3和22RV1）的增殖、迁移和侵袭，并影响PCa细胞的能量代谢。上调的PPARγ在这一过程中起关键作用，波形蛋白可能参与这一信号通路。
我们推断高水平的FFA可能通过上调PPARγ表达促进PCa的发展。
