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多不饱和脂肪酸在两种人类癌细胞系中对细胞增殖和内源性大麻素系统的差异调节作用。

Polyunsaturated Fatty Acids Differentially Modulate Cell Proliferation and Endocannabinoid System in Two Human Cancer Lines.

机构信息

Biología Celular, Histología y Embriología, Facultad de Ciencias Médicas, Universidad Nacional Córdoba, Argentina; Cátedra de Histología y Embriología, Universidad Nacional de La Rioja, La Rioja, Argentina; INICSA, CONICET-UNC, Córdoba, Argentina.

Biología Celular, Histología y Embriología, Facultad de Ciencias Médicas, Universidad Nacional Córdoba, Argentina.

出版信息

Arch Med Res. 2017 Jan;48(1):46-54. doi: 10.1016/j.arcmed.2017.01.009.

Abstract

BACKGROUND AND AIMS

Evidence suggests that quantity and quality of dietary polyunsaturated fatty acids (PUFAs) play a role in the development of cancer. However, the mechanisms involved in this interaction(s) are not clear. Endocannabinoids are lipid metabolites known to have growth modulatory actions. We studied the effect of supplementation with PUFAs ω-6 and ω-3 (essential fatty acids, EFAs), saturated and monounsaturated fatty acids (non-EFAs) on the growth of tumor cells and modifications in their endocannabinoid content.

METHODS

Cell cultures of human glioblastoma (T98G) and breast cancer (MCF7) were supplemented with 50 or 100 mmol EFAs and non-EFAs for 72 h. Cell proliferation was then determined by MTT, anandamide (AEA) levels by HPLC, total fatty acids profiles by GLC, CB1 receptor expression by WB and FAAH activity by spectrophotometric method.

RESULTS

Fatty acids profile reflected the incorporation of the lipids supplemented in each assay. Arachidonic acid (EFA ω-6) supplementation increased AEA levels and inhibited the growth of T98G, whereas palmitic acid (non-EFA) enhanced their proliferation. In breast cancer (MCF7) cells, eicosapentaenoic acid (EFA ω-3) reduced and oleic acid (non-EFA) enhanced their proliferation. CB1 expression was higher in T98G and no differences were observed in FAAH activity.

CONCLUSIONS

The growth of tumor cells can be differentially modulated by fatty acids and, at least in part, can be attributed to their ability to act on the components of the endocannabinoid system.

摘要

背景与目的

有证据表明,膳食多不饱和脂肪酸(PUFAs)的数量和质量在癌症的发展中起作用。然而,涉及这种相互作用的机制尚不清楚。内源性大麻素是已知具有生长调节作用的脂质代谢物。我们研究了补充 ω-6 和 ω-3(必需脂肪酸,EFAs)、饱和和单不饱和脂肪酸(非 EFAs)对肿瘤细胞生长的影响及其内源性大麻素含量的变化。

方法

用人脑胶质瘤(T98G)和乳腺癌(MCF7)细胞培养物补充 50 或 100mmol EFAs 和非 EFAs 72h。然后通过 MTT 测定细胞增殖,通过 HPLC 测定花生四烯酸(AEA)水平,通过 GLC 测定总脂肪酸谱,通过 WB 测定 CB1 受体表达,通过分光光度法测定 FAAH 活性。

结果

脂肪酸谱反映了每种测定中补充的脂质的掺入。花生四烯酸(EFA ω-6)的补充增加了 AEA 水平并抑制了 T98G 的生长,而棕榈酸(非 EFA)增强了它们的增殖。在乳腺癌(MCF7)细胞中,二十碳五烯酸(EFA ω-3)减少,油酸(非 EFA)增加其增殖。T98G 中 CB1 表达较高,FAAH 活性无差异。

结论

脂肪酸可以不同程度地调节肿瘤细胞的生长,至少部分归因于它们作用于内源性大麻素系统成分的能力。

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