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内源性血管生成素沉默诱导肝癌细胞程序性死亡。

Endocan silencing induces programmed cell death in hepatocarcinoma.

作者信息

Yang Jinghui, Sheng Shihou, Yang Qiwei, Li Li, Qin Shaoyou, Yu Shan, Zhang Xuewen

机构信息

Department of Hepatopancreatobiliary Surgery, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China.

Department of Colorectal & Anal Surgery, China-Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China.

出版信息

Oncol Lett. 2017 Nov;14(5):5333-5339. doi: 10.3892/ol.2017.6857. Epub 2017 Aug 31.

DOI:10.3892/ol.2017.6857
PMID:29113167
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5661370/
Abstract

Hepatocarcinoma is a type of high-grade malignant carcinoma identified worldwide. Its rapid development and late diagnosis prevents effective tumor resection in the majority of patients, and therefore recent studies have targeted metabolic signaling pathways and the tumor microenvironment for potential treatments. To investigate whether endocan may be a gene target for hepatocarcinoma treatment, the present study employed the following measures: MTT and Transwell assays, flow cytometry, western blotting and an mRFP-GFP-LC3 double fluorescence system. Following endocan gene silencing, cell proliferation was significantly inhibited and the number of invasive cells in the endocan siRNA-treated group was reduced compared with the control-siRNA treated-group. Furthermore, the apoptosis rate was 15% and autophagy was detected in the endocan short interfering (si)RNA-treated group compared with the control-siRNA treated-group. Using western blotting to detect NF-κB expression in the nucleus, the NF-κB expression was identified to be significantly reduced in the siRNA-treated group compared with the control groups. Endocan gene silencing inhibited hepatocarcinoma cell viability and invasion, whilst inducing apoptosis and autophagy. The results of the present study suggest that the effect of endocan gene silencing on cell survival was mediated via the NF-κB signaling pathway.

摘要

肝癌是一种在全球范围内被确认的高级别恶性肿瘤。其快速发展和晚期诊断使得大多数患者无法进行有效的肿瘤切除,因此最近的研究针对代谢信号通路和肿瘤微环境进行潜在治疗。为了研究内皮糖蛋白是否可能成为肝癌治疗的基因靶点,本研究采用了以下方法:MTT和Transwell实验、流式细胞术、蛋白质免疫印迹法以及mRFP-GFP-LC3双荧光系统。在内皮糖蛋白基因沉默后,与对照小干扰RNA(siRNA)处理组相比,内皮糖蛋白siRNA处理组的细胞增殖受到显著抑制,侵袭细胞数量减少。此外,与对照siRNA处理组相比,内皮糖蛋白小干扰RNA处理组的凋亡率为15%,并检测到自噬现象。通过蛋白质免疫印迹法检测细胞核中核因子κB(NF-κB)的表达,发现与对照组相比,siRNA处理组的NF-κB表达显著降低。内皮糖蛋白基因沉默抑制了肝癌细胞的活力和侵袭,同时诱导了凋亡和自噬。本研究结果表明,内皮糖蛋白基因沉默对细胞存活的影响是通过NF-κB信号通路介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64e8/5661370/5e494ff11239/ol-14-05-5333-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64e8/5661370/86cb9c5d91b5/ol-14-05-5333-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64e8/5661370/1523f9a9f94d/ol-14-05-5333-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64e8/5661370/10e706c20df0/ol-14-05-5333-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64e8/5661370/6003b3b3ae8a/ol-14-05-5333-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64e8/5661370/5e494ff11239/ol-14-05-5333-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64e8/5661370/86cb9c5d91b5/ol-14-05-5333-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64e8/5661370/1523f9a9f94d/ol-14-05-5333-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64e8/5661370/10e706c20df0/ol-14-05-5333-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64e8/5661370/6003b3b3ae8a/ol-14-05-5333-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64e8/5661370/5e494ff11239/ol-14-05-5333-g04.jpg

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