miR-21/PDCD4/AP-1对食管癌细胞增殖、侵袭及迁移的影响

摘要
图/表
参考文献(20)
相关文章 (15)

全文: PDF (1176 KB) HTML (1 KB)
输出: BibTeX | EndNote (RIS)

摘要目的研究miR-21/PDCD4/AP-1对食管癌细胞增殖、侵袭和迁移的影响。方法瞬时转染食管鳞癌细胞为实验对象，分组方法为单转染组：空白对照组、miR-21 mimic阴性对照（miR-21 mimic NC）组、miR-21 mimic组、miR-21 inhibitor NC组、miR-21 inhibitor组、siRNA NC组、PDCD4 siRNA组、c-Jun siRNA组；共转染组：miR-21 inhibitor NC+siRNA NC组、miR-21 inhibitor+siRNA NC组、miR-21 inhibitor+PDCD4 siRNA组。分别运用CCK-8、Transwell迁移和侵袭检测miR-21/PDCD4/AP-1反馈环路对食管癌EC9706细胞增殖、迁移和侵袭能力的影响。结果转染后2 d起，miR-21 mimic组EC9706细胞的增殖能力明显高于空白对照组、miR-21 mimic NC组、miR-21 inhibitor NC组和miR-21 inhibitor组（P ＜ 0.05）。miR-21 mimic组穿过小室的细胞计数多于空白对照组和miR-21 mimic NC组（P < 0.05）；miR-21 inhibitor组穿过小室的细胞计数少于miR-21 inhibitor NC组（P < 0.05）。miR-21 mimic组穿透Matrigel胶的侵袭细胞数多于空白对照组和miR-21 mimic NC组（P < 0.05）；miR-21 inhibitor组穿透Matrigel胶的侵袭细胞数少于miR-21 inhibitor NC组（P < 0.05）。转染后2 d起，PDCD4 siRNA组EC9706细胞的增殖能力高于空白对照组和siRNA NC组（P ＜ 0.05）。PDCD4 siRNA组穿过小室的细胞计数、穿透Matrigel胶的侵袭细胞数多于空白对照组和siRNA NC组（P ＜ 0.05）。miR-21 inhibitor+siRNA NC组EC9706细胞的增殖能力低于miR-21 inhibitor+PDCD4 siRNA组和miR-21 inhibitor NC+siRNA NC组（P ＜ 0.05）。miR-21 inhibitor+PDCD4 siRNA组穿过小室的细胞计数、穿透Matrigel胶的侵袭细胞数多于miR-21 inhibitor+siRNA NC组（P < 0.05）。c-Jun siRNA组EC9706细胞的增殖能力低于空白对照组和siRNA NC组（P ＜ 0.05）。c-Jun siRNA组穿过小室的细胞计数、穿透Matrigel胶的侵袭细胞数均少于siRNA NC组（P ＜ 0.05）。结论 miR-21/PDCD4/AP-1反馈环路可调控食管癌细胞的生长和侵袭，该环路为阻止的侵袭、转移提供新的治疗策略。

	服务

	把本文推荐给朋友
	加入我的书架
	加入引用管理器
	E-mail Alert
	RSS
	作者相关文章
	杨鲸蓉1
	2 吴健2 叶仕新2 连铎煌2 曾志勇1
	2▲

关键词 ： miR-21, PDCD4, AP-1, 食管癌

Abstract：Objective To study the effect of miR-21/PDCD4/AP-1 on the proliferation, invasion and migration of esophageal cancer cells. Methods Transient transfection of esophageal squamous cell carcinoma cells was used as experimental object. The single transfection group: blank control group, miR-21 mimics negative control (miR-21 mimic NC) group, miR-21 mimic group, miR-21 inhibitor NC group, miR-21 inhibitor group, siRNA NC group, PDCD4 siRNA group, c-Jun siRNA group. Cotransfection group: miR-21 inhibitor NC + siRNA NC group, miR-21 inhibitor + siRNA NC group, miR-21 inhibitor + siRNA NC group inhibitor + PDCD4 siRNA group. CCK-8, Transwell migration and invasion were used to detect the effect of miR-21/PDCD4/AP-1 feedback loop on the proliferation, migration and invasion of EC9706 cells. Results From the 2nd day after transfection, the proliferation ability of EC9706 cells in miR-21 mimic group was significantly higher than that in blank control group, miR-21 mimic NC group, miR-21 inhibitor NC group and miR-21 inhibitor group (P < 0.05). The number of cells passing through the chamber in miR-21 mimic group was more than that in blank control group and miR-21 mimic NC group (P < 0.05); the number of cells passing through the chamber in miR-21 inhibitor group was less than that in miR-21 inhibitor NC group (P < 0.05). The number of invasive cells penetrating Matrigel in miR-21 mimic group was more than that in blank control group and miR-21 mimic NC group (P < 0.05); the number of invasive cells penetrating Matrigel in miR-21 inhibitor group was less than that in miR-21 inhibitor NC group (P < 0.05). From the 2nd day after transfection, the proliferation ability of EC9706 cells in PDCD4 siRNA group was higher than that in blank control group and siRNA NC group (P < 0.05). The number of cells passing through the chamber and invading cells passing through Matrigel in PDCD4 siRNA group was higher than that in blank control group and siRNA NC group (P < 0.05). The proliferation ability of EC9706 cells in miR-21 inhibitor + siRNA NC group was lower than that in miR-21 inhibitor + PDCD4 siRNA group and miR-21 inhibitor NC + siRNA NC group (P < 0.05). The number of cells passing through the chamber and the number of cells penetrating Matrigel in miR-21 inhibitor + PDCD4 siRNA group was more than that in miR-21 inhibitor + siRNA NC group (P < 0.05). The proliferation ability of EC9706 cells in c-Jun siRNA group was lower than that in blank control group and siRNA NC group (P < 0.05). The number of cells passing through the chamber and the number of invasive cells passing through Matrigel in c-Jun siRNA group was less than that in siRNA NC group (P < 0.05). Conclusion miR-21/PDCD4/AP-1 feedback loop can regulate the growth and invasion of esophageal cancer cells, which provides a new therapeutic strategy for preventing invasion and metastasis.

Key words： miR-21 PDCD4 AP-1 Esophageal cancer

基金资助:福建省自然科学基金资助项目（2017J01320）；
福建省自然科学基金资助项目（2017J01223）。

通讯作者: ▲通讯作者

引用本文:

杨鲸蓉1，2 吴健2 叶仕新2 连铎煌2 曾志勇1，2▲. miR-21/PDCD4/AP-1对食管癌细胞增殖、侵袭及迁移的影响[J]. 中国医药导报, 2020, 17(20): 4-9.
YANG Jingrong1，2 WU Jian2 YE Shixin2 LIAN Duohuang2 ZENG Zhiyong1，2▲. Effect of miR-21/PDCD4/AP-1 on proliferation, invasion and migration of esophageal cancer cells. 中国医药导报, 2020, 17(20): 4-9.

链接本文:

http://www.yiyaodaobao.com.cn/CN/ 或 http://www.yiyaodaobao.com.cn/CN/Y2020/V17/I20/4

[1] Liu M，Yu J，Wang D，et al. Epigenetically upregulated microRNA-602 is involved in a negative feedback loop with FOXK2 in esophageal squamous cell carcinoma [J]. Mol Ther，2019，27（10）：1796-1809.
[2] Kiuchi J，Komatsu S，Imamura T，et al. Low levels of tumour suppressor miR-655 in plasma contribute to lymphatic progression and poor outcomes in oesophageal squamous cell carcinoma [J]. Mol Cancer，2019，18（1）：2.
[3] Junker F，Chabloz A，Koch U，et al. Dicer1 imparts essential survival cues in Notch-driven T-ALL via miR-21-mediated tumor suppressor Pdcd4 repression [J]. Blood，2015，126（8）：993-1004.
[4] Wang P，Guan Q，Zhou D，et al. miR-21 inhibitors modulate biological functions of gastric cancer cells via PTEN/PI3K/mTOR pathway [J]. DNA Cell Biol，2018，37（1）：38-45.
[5] Zhang Z，Zha Y，Hu W，et al. The autoregulatory feedback loop of microRNA-21/programmed cell death protein 4/activation protein-1 （MiR-21/PDCD4/AP-1） as a driving force for hepatic fibrosis development [J]. J Biol Chem，2013，288（52）：37082-37093.
[6] 杨鲸蓉，吴波.microRNA-21在食管癌中的研究进展[J].中国医药导报，2017，14（16）：40-43.
[7] Irimie-Aghiorghiesei AI，Pop-Bica C，Pintea S，et al. Prognostic value of miR-21：an updated meta-analysis in head and neck squamous cell carcinoma （HNSCC） [J]. J Clin Med，2019，8（12）：E2041.
[8] Zhang N，Hu Z，Qiang Y，et al. Circulating miR-130b- and miR-21-based diagnostic markers and therapeutic targets for hepatocellular carcinoma [J]. Mol Genet Genomic Med，2019，7（12）：e1012.
[9] Hu Y，Rao SS，Wang ZX，et al. Exosomes from human umbilical cord blood accelerate cutaneous wound healing through miR-21-3p-mediated promotion of angiogenesis and fibroblast function [J]. Theranostics，2018，8（1）：169-184.
[10] Liu Y，Ren L，Liu W，et al. MiR-21 regulates the apoptosis of keloid fibroblasts by caspase-8 and the mitochondria-mediated apoptotic signaling pathway via targeting FasL [J]. Biochem Cell Biol，2018，96（5）：548-555.
[11] Wang F，Gao X，Zhang R，et al. LncRNA TUG1 ameliorates diabetic nephropathy by inhibiting miR-21 to promote TIMP3-expression [J]. Int J Clin Exp Pathol，2019， 12（3）：717-729.
[12] 姜艳，杨大群，王聪洋，等.抑癌基因PDCD4与肿瘤关系的研究进展[J].现代肿瘤医学，2015，23（22）：3363-3366.
[13] Liu T，Liu Q，Zheng S，et al. MicroRNA-21 promotes cell growth and migration by targeting programmed cell death 4 gene in Kazakh′s esophageal squamous cell carcinoma [J]. Dis Markers，2014，2014：232837.
[14] Fassan M，Pizzi M，Battaglia G，et al. Programmed cell death 4 （PDCD4） expression during multistep Barrett′s carcinogenesis [J]. J Clin Pathol，2010，63（8）：692-696.
[15] 张建东，贺利民，马磊，等.miR-21、PDCD4表达对Ⅱ期食管鳞癌术后患者生存期的影响[J].肿瘤学杂志，2017， 183（12）：5-12.
[16] Zhang J，Ma L，Shi D，et al. Prognostic significance of miR-21 and PDCD4 in patients with stage Ⅱ esophageal carcinoma after surgical resection [J]. J Cell Biochem，2018，119（6）：4783-4791.
[17] 虞勇，虞莹，刘桂剑，等.miR21对心脏微血管内皮细胞PDCD4/AP1通路的调节作用[J].中国分子心脏病学杂志，2015，15（6）：1534-1538.
[18] Zhu Q，Wang Z，Hu Y，et al. miR-21 promotes migration and invasion by the miR-21-PDCD4-AP-1 feedback loop in human hepatocellular carcinoma [J]. Oncol Rep，2012，27（5）：11660-11668.
[19] Chang CR，Wang HY，Liu JC，et al. Porphyromonas gingivalis infection promoted the proliferation of oral squamous cell carcinoma cells through the miR-21/PDCD4/AP-1 negative signaling pathway [J]. ACS Infect Dis，2019，5（8）：1336-1347.
[20] Talotta F，Cimmino A，Matarazzo MR，et al. An autoregulatory loop mediated by miR-21 and PDCD4 controls the AP-1 activity in RAS transformation [J]. Oncogene，2009，28（1）：73-84.