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Sphingolipid metabolism in colorectal adenomas varies depending on histological architecture of polyps and grade of nuclear dysplasia

机译：大肠腺瘤中的鞘脂代谢取决于息肉的组织学结构和核异型增生的程度

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摘要

Incidence of colorectal cancer (CRC) is growing worldwide. Pathogenetic mechanisms responsible for its onset and progression need further clarification. Colorectal adenomatous polyps are precancerous lesions with malignant potential dependent on histological architecture and grade of nuclear dysplasia. One of the factors conditioning CRC development are abnormalities in sphingolipid metabolism. The aim of this study was to assess the levels of sphingolipids in human colorectal adenomas. The control group (C, n = 12) consisted of patients with no colonic polyps. The examined group consisted of patients with prior diagnosed colonic polyps, qualified to endoscopic polypectomy. This group was further divided due to histological architecture into tubular adenomas group (TA, n = 10), tubulovillous adenomas with low-grade dysplasia (LGD-TVA, n = 10), and tubulovillous adenomas group with high-grade dysplasia (HGD-TVA, n = 11). In tissue samples, sphingolipd metabolite contents were measured using high performance liquid chromatography (HPLC). In cases of polypoid lesions with low malignancy potential (tubular adenomas), concentration of ceramide, which is characterized by proapoptotic and anti-proliferative properties, increases compared with control group (p < 0.05), whereas content of sphingosine-1-phosphate with anti-apoptotic and stimulating cellular proliferation properties is reduced in comparison with control group (p < 0.05). On the contrary, in cases of more advanced form of adenomatous polyps (tubulovillous adenomas with high-grade dysplasia), the ceramide level decreases compared with control group (p < 0.05) while sphingosine-1-phosphate concentration is elevated (p < 0.05). We found that concentrations of pro-apoptotic ceramide are decreased and pro-proliferative S1P levels are increased in polypoid lesions with high malignancy potential, and it was the opposite in those with low malignancy potential.
机译：世界范围内大肠癌（CRC）的发病率正在增长。对其发病和进展负责的致病机制需要进一步阐明。大肠腺瘤性息肉是癌前病变，其恶性潜能取决于组织学结构和核异型增生的程度。限制CRC发生的因素之一是鞘脂代谢异常。这项研究的目的是评估人类大肠腺瘤中鞘脂的水平。对照组（C，n = 12）由无结肠息肉的患者组成。检查组包括事先诊断为结肠息肉且符合内镜息肉切除术要求的患者。根据组织学结构，该组又分为肾小管腺瘤组（TA，n = 10），低度增生的肾小管腺瘤（LGD-TVA，n = 10）和高度增生的肾小管腺瘤组（HGD- TVA，n = 11）。在组织样本中，使用高效液相色谱（HPLC）测量了鞘脂代谢产物的含量。在具有低恶性潜能的息肉样病变（肾小管腺瘤）的情况下，以促凋亡和抗增殖特性为特征的神经酰胺浓度与对照组相比有所增加（p <0.05），而鞘氨醇-1-磷酸神经鞘氨醇的含量却高于对照组。与对照组相比，细胞凋亡和刺激性细胞增殖特性降低（p <0.05）。相反，在晚期腺瘤性息肉（具有高度不典型增生的肾小管腺瘤）的情况下，神经酰胺水平较对照组降低（p <0.05），而鞘氨醇-1-磷酸的浓度升高（p <0.05） 。我们发现，在具有高恶性潜能的息肉样病变中，促凋亡神经酰胺的浓度降低，而促增殖S1P水平升高，而在恶性潜能低的病变中则相反。

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