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薏苡仁油通过调节PI3K/AKT信号通路对HT-29结肠癌细胞的抗癌特性

Anti-Cancer Properties of Coix Seed Oil against HT-29 Colon Cells through Regulation of the PI3K/AKT Signaling Pathway.

作者信息

Ni Chunlei, Li Bailiang, Ding Yangyue, Wu Yue, Wang Qiuye, Wang Jiarong, Cheng Jianjun

机构信息

College of Food Science, Northeast Agricultural University, Harbin 150030, China.

出版信息

Foods. 2021 Nov 17;10(11):2833. doi: 10.3390/foods10112833.

DOI:10.3390/foods10112833
PMID:34829119
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8621869/
Abstract

This study aims to observe the effects of coix seed oil (CSO) on HT-29 cells and investigate its possible regulation mechanism of the PI3K/Akt signaling pathway. Fatty acid analysis showed that coix seed oil mainly contains oleic acid (50.54%), linoleic acid (33.76%), palmitic acid (11.74%), and stearic acid (2.45%). Fourier transform infrared results found that the fatty acid functional groups present in the oil matched well with the vegetable oil band. The results from CCK-8 assays showed that CSO dose-dependently and time-dependently inhibited the viability of HT-29 cells in vitro. CSO inhibited cell viability, with IC values of 5.30 mg/mL for HT-29 obtained after 24 h treatment. Morphological changes were observed by apoptotic body/cell nucleus DNA (Hoechst 33258) staining using inverted and fluorescence microscopy. Moreover, flow cytometry analysis was used to evaluate the cell cycle and cell apoptosis. It showed that CSO induced cell apoptosis and cycle arrest in the G phase. Quantitative real-time PCR and Western blotting revealed that CSO induced cell apoptosis by downregulating the PI3K/AKT signaling pathway. Additionally, CSO can cause apoptosis in cancer cells by activating caspase-3, up-regulating Bax, and down-regulating Bcl-2. In conclusion, the results revealed that CSO induced G arrest and apoptosis of HT-29 cells by regulating the PI3K/AKT signaling pathway.

摘要

本研究旨在观察薏苡仁油（CSO）对HT-29细胞的影响，并探讨其对PI3K/Akt信号通路可能的调控机制。脂肪酸分析表明，薏苡仁油主要含有油酸（50.54%）、亚油酸（33.76%）、棕榈酸（11.74%）和硬脂酸（2.45%）。傅里叶变换红外光谱结果发现，该油中存在的脂肪酸官能团与植物油谱带匹配良好。CCK-8检测结果表明，CSO在体外对HT-29细胞的活力具有剂量依赖性和时间依赖性抑制作用。CSO抑制细胞活力，24小时处理后HT-29细胞的半数抑制浓度（IC）值为5.30mg/mL。使用倒置显微镜和荧光显微镜通过凋亡小体/细胞核DNA（Hoechst 33258）染色观察形态学变化。此外，采用流式细胞术分析评估细胞周期和细胞凋亡。结果显示，CSO诱导细胞凋亡并使细胞周期停滞在G期。定量实时PCR和蛋白质印迹分析表明，CSO通过下调PI3K/AKT信号通路诱导细胞凋亡。此外，CSO可通过激活半胱天冬酶-3、上调Bax和下调Bcl-2导致癌细胞凋亡。总之，结果表明CSO通过调节PI3K/AKT信号通路诱导HT-29细胞的G期停滞和凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c642/8621869/0593628d55b6/foods-10-02833-g008.jpg
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