Quercetin and aconitine synergistically induces the human cervical carcinoma HeLa cell apoptosis via endoplasmic reticulum (ER) stress pathway

被引:39
作者
Li, Xiu-Mei [1 ,2 ]
Liu, Jing [1 ,2 ]
Pan, Fang-Fang [3 ]
Shi, Dong-Dong [1 ,2 ]
Wen, Zhi-Guo [1 ,2 ]
Yang, Pei-Long [1 ,2 ]
机构
[1] Chinese Acad Agr Sci, Feed Res Inst, Minist Agr, Key Lab Feed Biotechnol, Beijing, Peoples R China
[2] Chinese Acad Agr Sci, Feed Res Inst, Natl Engn Res Ctr Biol Feed, Beijing, Peoples R China
[3] Tianjin Univ Sci & Technol, Coll Biotechnol, Tianjin Key Lab Ind Microbiol, Key Lab Ind Fermentat Microbiol,Minist Educ, Tianjin, Peoples R China
关键词
UNFOLDED PROTEIN RESPONSE; P-GLYCOPROTEIN; IRE1; PATHWAY; TOXICITY; PROLIFERATION; GENE;
D O I
10.1371/journal.pone.0191062
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Up till now, studies have not been conducted on how the combination of Quercetin (Q), Aconitine (A) and apoptosis induction affects human cervical carcinoma HeLa cells. The result of our findings shows that the combination of Q and A (QA) is capable of synergistically inhibiting the proliferation of HeLa cells in a number of concentrations. QA synergistically inhibits the proliferation of MDR1 gene in the HeLa cells. It is concluded based on our result that QA induces apoptosis and ER stress just as QA-induced ER stress pathway may mediate apoptosis by upregulating mRNA expression levels of eIF2 alpha, ATF4, IRE1, XBP1, ATF6, PERK and CHOP in the HeLa cells. The up-regulating of mRNA expression level of GRP78 and activation of UPR are a molecular basis of QA-induced ER stress.
引用
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页数:12
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