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丙烯酰胺通过上调miR-21表达诱导HepG2细胞增殖。

Acrylamide induces HepG2 cell proliferation through upregulation of miR-21 expression.

作者信息

Xu Yuyu, Wang Pengqi, Xu Chaoqi, Shan Xiaoyun, Feng Qing

机构信息

Department of Nutrition and Food Safety, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, China.

Station of Sanitary Surveillance of Lianyungang, Lianyungang, Jiangsu 222002, China.

出版信息

J Biomed Res. 2019 Jun 4;33(3):181-191. doi: 10.7555/JBR.31.20170016.

DOI:10.7555/JBR.31.20170016
PMID:28963442
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6551424/
Abstract

Acrylamide, a potential carcinogen, exists in carbohydrate-rich foods cooked at a high temperature. It has been reported that acrylamide can cause DNA damage and cytotoxicity. The present study aimed to investigate the potential mechanism of human hepatocarcinoma HepG2 cell proliferation induced by acrylamide and to explore the antagonistic effects of a natural polyphenol curcumin against acrylamide via miR-21. The results indicated that acrylamide (≤100 μmol/L) significantly increased HepG2 cell proliferation and miR-21 expression. In addition, acrylamide reduced the PTEN expression in protein level, while induced the expressions of p-AKT, EGFR and cyclin D1. The PI3K/AKT inhibitor decreased p-AKT protein expression and inhibited the proliferation of HepG2 cells. In addition, curcumin effectively reduced acrylamide-induced HepG2 cell proliferation and induced apoptosis through the expression of miR-21. In conclusion, the results showed that acrylamide increased HepG2 cell proliferation via upregulating miR-21 expression, which may be a new target for the treatment and prevention of cancer.

摘要

丙烯酰胺是一种潜在致癌物,存在于高温烹制的富含碳水化合物的食物中。据报道,丙烯酰胺可导致DNA损伤和细胞毒性。本研究旨在探讨丙烯酰胺诱导人肝癌HepG2细胞增殖的潜在机制,并通过miR-21探索天然多酚姜黄素对丙烯酰胺的拮抗作用。结果表明,丙烯酰胺(≤100μmol/L)显著增加HepG2细胞增殖和miR-21表达。此外,丙烯酰胺降低了PTEN蛋白水平的表达,同时诱导了p-AKT、EGFR和细胞周期蛋白D1的表达。PI3K/AKT抑制剂降低了p-AKT蛋白表达并抑制了HepG2细胞的增殖。此外,姜黄素通过miR-21的表达有效降低了丙烯酰胺诱导的HepG2细胞增殖并诱导了细胞凋亡。总之,结果表明丙烯酰胺通过上调miR-21表达增加了HepG2细胞增殖,这可能是癌症治疗和预防的新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212e/6551424/f2ca06101986/jbr-33-3-181-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212e/6551424/22040caa3bf6/jbr-33-3-181-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212e/6551424/edfbc8b28207/jbr-33-3-181-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212e/6551424/b4a23b416f81/jbr-33-3-181-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212e/6551424/d16abe3135f4/jbr-33-3-181-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212e/6551424/f1de23f44ced/jbr-33-3-181-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212e/6551424/f2ca06101986/jbr-33-3-181-fig6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212e/6551424/22040caa3bf6/jbr-33-3-181-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212e/6551424/edfbc8b28207/jbr-33-3-181-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212e/6551424/b4a23b416f81/jbr-33-3-181-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212e/6551424/d16abe3135f4/jbr-33-3-181-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212e/6551424/f1de23f44ced/jbr-33-3-181-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212e/6551424/f2ca06101986/jbr-33-3-181-fig6.jpg

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