Department of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND, 58202, USA.
Department of Biomedical Sciences, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND, 58202, USA.
Biochimie. 2018 Oct;153:171-180. doi: 10.1016/j.biochi.2018.07.006. Epub 2018 Jul 24.
Colorectal cancer (CRC) is the third most diagnosed cancer in the western world, affecting 1 out of approximately 22 people in their lifetime. Several epidemiological studies suggest a positive association between high plasma cholesterol levels and colorectal cancer. However, the molecular mechanisms by which cholesterol may alter the risk of colorectal cancer (CRC) are ill-defined as the cholesterol lowering drugs statins do not appear to decrease a patient's risk of developing colorectal cancer. Cholesterol is metabolized to active derivatives including cholesterol oxidization products (COP), known as oxysterols, which have been shown to alter cellular proliferation. These metabolites and not cholesterol per se, may therefore affect the risk of developing colorectal cancer. The cholesterol metabolite or the oxysterol 27-hydroxycholesterol (27-OHC) is the most abundant oxysterol in the plasma and has been shown to be involved in the pathogenesis of several cancers including breast and prostate cancer. However, the role of 27-OHC in colorectal cancer has not been investigated. We treated Caco2 and SW620, two well characterized colon cancer cells with low, physiological and high concentrations of 27-OHC, and found that 27-OHC reduces cellular proliferation in these cells. We also found that the effects of 27-OHC on cell proliferation are not due to cellular cytotoxicity or apoptotic cellular death. Additionally, 27-OHC-induced reduction in cell proliferation is independent of actions on its target nuclear receptors, liver-X-receptors (LXR) and estrogen receptors (ER) activation. Instead, our study demonstrates that 27-OHC significantly decreases AKT activation, a major protein kinase involved in the pathogenesis of cancer as it regulates cell cycle progression, protein synthesis, and cellular survival. Our data shows that treatment with 27-OHC substantially decreases the activation of AKT by reducing levels of its active form, p-AKT, in Caco2 cells but not SW620 cells. All-together, our results show for the first time that the cholesterol metabolite 27-OHC reduces cell proliferation in colorectal cancer cells.
结直肠癌(CRC)是西方世界第三大常见癌症,一生中每 22 个人中就有 1 人受到影响。几项流行病学研究表明,血浆胆固醇水平高与结直肠癌呈正相关。然而,胆固醇改变结直肠癌(CRC)风险的分子机制尚不清楚,因为降低胆固醇的药物他汀类药物似乎不会降低患者患结直肠癌的风险。胆固醇代谢为活性衍生物,包括胆固醇氧化产物(COP),称为氧化固醇,已被证明会改变细胞增殖。因此,这些代谢物而不是胆固醇本身可能会影响患结直肠癌的风险。胆固醇代谢物或氧化固醇 27-羟胆固醇(27-OHC)是血浆中含量最丰富的氧化固醇,已被证明参与了几种癌症的发病机制,包括乳腺癌和前列腺癌。然而,27-OHC 在结直肠癌中的作用尚未得到研究。我们用低、生理和高浓度的 27-OHC 处理了 Caco2 和 SW620 两种具有特征的结肠癌细胞,并发现 27-OHC 降低了这些细胞的细胞增殖。我们还发现,27-OHC 对细胞增殖的影响不是由于细胞毒性或细胞凋亡性死亡。此外,27-OHC 诱导的细胞增殖减少与作用于其靶核受体肝 X 受体(LXR)和雌激素受体(ER)的激活无关。相反,我们的研究表明,27-OHC 显著降低 AKT 的激活,AKT 是一种参与癌症发病机制的主要蛋白激酶,因为它调节细胞周期进程、蛋白质合成和细胞存活。我们的数据表明,用 27-OHC 处理可显著降低 Caco2 细胞中 AKT 的激活,减少其活性形式 p-AKT 的水平,但不能降低 SW620 细胞中 p-AKT 的水平。总的来说,我们的研究结果首次表明,胆固醇代谢物 27-OHC 可降低结直肠癌细胞的增殖。