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Bcl‑2 相关抗凋亡基因 4 促进胃癌细胞的增殖、迁移和侵袭。

Bcl‑2 associated athanogene 4 promotes proliferation, migration and invasion of gastric cancer cells.

机构信息

Department of Gastroenterology, Leshan People's Hospital, Leshan, Sichuan 614000, P.R. China.

Department of General Surgery Two, Nanchong Central Hospital, Nanchong, Sichuan 637000, P.R. China.

出版信息

Mol Med Rep. 2017 Oct;16(4):3753-3760. doi: 10.3892/mmr.2017.7073. Epub 2017 Jul 21.

DOI:10.3892/mmr.2017.7073
PMID:29067445
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5646952/
Abstract

Currently, with the increase of morbidity and mortality rate, gastric cancer (GC) is attracting increasing attention in China. Bcl‑2‑associated athanogene 4 (BAG4) has been identified as a tumor promoter in several tumors, but its role in GC remains unknown. The present study aimed to detect the expression of BAG4 and determine its function in the progression of GC. The results from reverse transcription‑quantitative polymerase chain reaction and western blotting revealed that BAG4 was markedly upregulated in highly metastatic cell lines (SGC7901 and MGC803), compared with the lower‑metastatic cell lines (AGS and BGC823). Through Cell Counting Kit‑8, cell cycle, apoptosis, Transwell and colony formation assays, BAG4 was demonstrated to promote the proliferation, migration and invasion of GC cells in vitro. Additionally, in vivo assays further certified that BAG4 can increase the proliferation and invasion of GC cells. In conclusion, these findings implicate BAG4 as a potential therapeutic target for GC.

摘要

目前,随着发病率和死亡率的增加,胃癌(GC)在中国越来越受到关注。Bcl-2 相关抗凋亡基因 4(BAG4)已被确定为多种肿瘤的肿瘤促进因子,但它在 GC 中的作用尚不清楚。本研究旨在检测 BAG4 的表达,并确定其在 GC 进展中的功能。逆转录-定量聚合酶链反应和 Western blot 的结果显示,BAG4 在高转移性细胞系(SGC7901 和 MGC803)中的表达明显上调,而在低转移性细胞系(AGS 和 BGC823)中的表达下调。通过细胞计数试剂盒-8、细胞周期、凋亡、Transwell 和集落形成实验,证明 BAG4 可促进 GC 细胞的体外增殖、迁移和侵袭。此外,体内实验进一步证实 BAG4 可增加 GC 细胞的增殖和侵袭。综上所述,这些发现提示 BAG4 可能是 GC 的一个潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8451/5646952/10cd15121298/MMR-16-04-3753-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8451/5646952/64eec2080804/MMR-16-04-3753-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8451/5646952/34316645fe68/MMR-16-04-3753-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8451/5646952/21bddee9df98/MMR-16-04-3753-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8451/5646952/3031da8274e7/MMR-16-04-3753-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8451/5646952/10cd15121298/MMR-16-04-3753-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8451/5646952/64eec2080804/MMR-16-04-3753-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8451/5646952/34316645fe68/MMR-16-04-3753-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8451/5646952/21bddee9df98/MMR-16-04-3753-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8451/5646952/3031da8274e7/MMR-16-04-3753-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8451/5646952/10cd15121298/MMR-16-04-3753-g04.jpg

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