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14,15-环氧二十碳三烯酸诱导人癌细胞增殖和抗细胞凋亡。

14,15-Epoxyeicosatrienoic acid induces the proliferation and anti- apoptosis of human carcinoma cell.

机构信息

Institute of Cardiovascular Diseases of Chengdu, The Third Peoples Hospital of Chengdu, Chengdu.

出版信息

Daru. 2011;19(6):462-8.

PMID:23008693
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3436084/
Abstract

BACKGROUND AND THE PURPOSE OF THE STUDY

Epoxyeicosatrienoic acids (EETs), which are cytochrome P450 epoxygenase metabolites of arachidonic acid, have anti-inflammatory effects, modulate smooth muscle proliferation, and inhibit smooth muscle migration. This study was designed to determine whether exogenous EETs have any effect on the cell proliferation and apoptosis of carcinoma cell as well as the possible signaling pathways of EETs in this regulation.

METHODS

The effects of EETs on the proliferation and anti-apoptosis of human carcinoma cells were measured by MTT assay and flowcytometric analysis, and the regulation of PPARγ, epithelial growth factor receptor (EGFR), extracellular signal-regulated kinase (ERK), phosphatidylinositol 3 (PI3)-Kinase/AKT pathways was investigated by reverse transcriptase polymerase chain reaction (RT-PCR) and western blot analysis.

RESULTS

Results of this study suggested that 14, 15-EET may activate the expression of PPARγ in Tca-8113 cells. 14,15-EET may stimulate cell proliferation, and increase the percentage of cells during S-G2-M phase in Tca-8113 cells significantly. The levels of EGFR, ERK, and PI3 kinase/AKT proteins were significantly induced by treatment of 14, 15-EET and 14,15-EET/AUDA, but no significant changes were observed by addition of GW9662.

CONCLUSION

These findings suggest that exogenous 14,15-EET has potent inhibitory effect on proliferation, and could induce apoptosis in Tca-8113 cell, and these changes are related to the expression of PPARγ, the activation of EGFR, ERK, and PI3 kinase/AKT proteins.

摘要

背景与研究目的

环氧二十碳三烯酸（EETs）是花生四烯酸细胞色素 P450 环氧化物酶的代谢产物，具有抗炎作用，调节平滑肌增殖，并抑制平滑肌迁移。本研究旨在确定外源性 EETs 是否对癌细胞的增殖和凋亡有影响，以及 EETs 在这种调节中的可能信号通路。

方法

通过 MTT 测定法和流式细胞术分析测定 EETs 对人癌细胞增殖和抗凋亡的影响，并通过逆转录聚合酶链反应（RT-PCR）和蛋白质印迹分析研究 PPARγ、表皮生长因子受体（EGFR）、细胞外信号调节激酶（ERK）、磷脂酰肌醇 3（PI3）-激酶/AKT 通路的调节。

结果

本研究结果表明，14,15-EET 可能在 Tca-8113 细胞中激活 PPARγ 的表达。14,15-EET 可能刺激细胞增殖，并显著增加 Tca-8113 细胞中 S-G2-M 期的细胞百分比。14,15-EET 和 14,15-EET/AUDA 处理可显著诱导 EGFR、ERK 和 PI3 激酶/AKT 蛋白水平升高，但添加 GW9662 后无明显变化。

结论

这些发现表明，外源性 14,15-EET 对 Tca-8113 细胞的增殖有强烈的抑制作用，并能诱导其凋亡，这些变化与 PPARγ 的表达、EGFR、ERK 和 PI3 激酶/AKT 蛋白的激活有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9145/3436084/308b6f6b9194/DARU-19-462-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9145/3436084/76e32422afeb/DARU-19-462-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9145/3436084/06928148f374/DARU-19-462-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9145/3436084/ecbd7df82d51/DARU-19-462-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9145/3436084/8cb58e9798c1/DARU-19-462-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9145/3436084/940705ca5944/DARU-19-462-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9145/3436084/308b6f6b9194/DARU-19-462-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9145/3436084/76e32422afeb/DARU-19-462-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9145/3436084/06928148f374/DARU-19-462-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9145/3436084/ecbd7df82d51/DARU-19-462-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9145/3436084/8cb58e9798c1/DARU-19-462-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9145/3436084/940705ca5944/DARU-19-462-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9145/3436084/308b6f6b9194/DARU-19-462-g006.jpg

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