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ω-3多不饱和脂肪酸通过阻断PI3K/AKT/Bcl-2信号通路减轻N-甲基-N-亚硝基脲诱导的大鼠结直肠癌

Omega-3PUFA Attenuates MNU-Induced Colorectal Cancer in Rats by Blocking PI3K/AKT/Bcl-2 Signaling.

作者信息

Huang Zhe, Liu Chun-An, Cai Peng-Zhu, Xu Fei-Peng, Zhu Wen-Jing, Wang Wei-Wei, Jiang Hai-Ping

机构信息

The First Affiliated Hospital, Jinan University, Guangzhou 510000, People's Republic of China.

Department of Gastrointestinal Surgery, The Affiliated Hospital of Guangdong Medical University, Zhanjiang 524001, People's Republic of China.

出版信息

Onco Targets Ther. 2020 Mar 5;13:1953-1965. doi: 10.2147/OTT.S241298. eCollection 2020.

DOI:10.2147/OTT.S241298
PMID:32184629
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7062403/
Abstract

BACKGROUND

Omega 3 polyunsaturated fatty acid (Omega-3PUFA) is one of the essential nutrients for human body involved in intracellular metabolic regulation and cell signaling. Previous studies have shown that Omega-3PUFA is involved in the pathogenesis of digestive system tumors, including colorectal cancer (CRC), however, the effects of Omega-3PUFA on CRC has not been fully elucidated. In the current study, we evaluated whether Omega-3PUFA can alleviate N-methyl-N-nitrosourea(MNU) induced CRC in a rat model and illustrated the potential mechanism.

METHODS

The effects of Omga-3PUFA on MNU-induced colorectal cancer in rats were analyzed by in vivo experiments. The viability, apoptosis, colony formation and invasion of CRC cells treated with Omga-3PUFA were detected by CCK8, flow cytometry, clone formation assay and transwell invasion assay. The expression of apoptosis-related proteins in CRC cells treated with Omga-3PUFA was detected by Western blotting. Finally, after adding PI3K activator, the viability, apoptosis and protein expression of CRC cells treated with Omga-3PUFA were detected by CCK8, flow cytometry and Western blotting.

RESULTS

Our results showed that Omega-3PUFA attenuated MNU-induced CRC in rats and inhibited AKT/Bcl-2 signaling in rats. In addition, Omega-3PUFA inhibited CRC cell proliferation and induces CRC cell apoptosis. Moreover, Omega-3PUFA inhibited CRC cell colony formation and invasion, and inhibited PI3K/AKT/Bcl-2 signaling in CRC cells. Furthermore, The effects of Omega-3PUFA on cell proliferation and apoptosis were inhibited by blocking PI3K/AKT signaling.

CONCLUSION

Omega-3PUFA can attenuate MNU-induced colorectal cancer in rats by blocking PI3K/AKT/Bcl-2 signaling, which suggests that Omega-3PUFA may be a potent agent for CRC treatment.

摘要

背景

ω-3多不饱和脂肪酸（Omega-3PUFA）是人体必需营养素之一，参与细胞内代谢调节和细胞信号传导。既往研究表明，Omega-3PUFA参与消化系统肿瘤包括结直肠癌（CRC）的发病机制，然而，Omega-3PUFA对CRC的影响尚未完全阐明。在本研究中，我们评估了Omega-3PUFA是否能减轻N-甲基-N-亚硝基脲（MNU）诱导的大鼠CRC，并阐明其潜在机制。

方法

通过体内实验分析Omega-3PUFA对MNU诱导的大鼠结直肠癌的影响。采用CCK8、流式细胞术、克隆形成试验和Transwell侵袭试验检测经Omega-3PUFA处理的CRC细胞的活力、凋亡、集落形成和侵袭。通过蛋白质印迹法检测经Omega-3PUFA处理的CRC细胞中凋亡相关蛋白的表达。最后，加入PI3K激活剂后，采用CCK8、流式细胞术和蛋白质印迹法检测经Omega-3PUFA处理的CRC细胞的活力、凋亡和蛋白质表达。

结果

我们的结果表明，Omega-3PUFA减轻了MNU诱导的大鼠CRC，并抑制了大鼠的AKT/Bcl-2信号传导。此外，Omega-3PUFA抑制CRC细胞增殖并诱导CRC细胞凋亡。而且，Omega-3PUFA抑制CRC细胞集落形成和侵袭，并抑制CRC细胞中的PI3K/AKT/Bcl-2信号传导。此外，阻断PI3K/AKT信号传导可抑制Omega-3PUFA对细胞增殖和凋亡的影响。

结论

Omega-3PUFA可通过阻断PI3K/AKT/Bcl-2信号传导减轻MNU诱导的大鼠结直肠癌，这表明Omega-3PUFA可能是一种有效的CRC治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b7a/7062403/35277f3d870e/OTT-13-1953-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b7a/7062403/3c8ad2ab7edf/OTT-13-1953-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b7a/7062403/0c06b754872d/OTT-13-1953-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b7a/7062403/e0b080f209cb/OTT-13-1953-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b7a/7062403/860819f5c304/OTT-13-1953-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b7a/7062403/19dd6757211b/OTT-13-1953-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b7a/7062403/35277f3d870e/OTT-13-1953-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b7a/7062403/3c8ad2ab7edf/OTT-13-1953-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b7a/7062403/0c06b754872d/OTT-13-1953-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b7a/7062403/e0b080f209cb/OTT-13-1953-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b7a/7062403/860819f5c304/OTT-13-1953-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b7a/7062403/19dd6757211b/OTT-13-1953-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3b7a/7062403/35277f3d870e/OTT-13-1953-g0006.jpg

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