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IGF 信号通路对 EBV 阳性胃癌细胞增殖和侵袭的调控

Regulation of proliferation and invasion by the IGF signalling pathway in Epstein-Barr virus-positive gastric cancer.

机构信息

Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea.

Songdang Institute for Cancer Research, Yonsei University College of Medicine, Seoul, Korea.

出版信息

J Cell Mol Med. 2018 Dec;22(12):5899-5908. doi: 10.1111/jcmm.13859. Epub 2018 Sep 24.

DOI:10.1111/jcmm.13859
PMID:30247804
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6237558/
Abstract

Several carcinomas including gastric cancer have been reported to contain Epstein-Barr virus (EBV) infection. EBV-associated gastric cancer (EBVaGC) is classified as one of four molecular subtypes of gastric cancer by The Cancer Genome Atlas (TCGA) group with increased immune-related signatures. Identification of EBV-dependent pathways with significant biological roles is needed for EBVaGC. To compare the biological changes between AGS gastric epithelial cells and EBV-infected AGS (AGS-EBV) cells, proliferation assay, CCK-8 assay, invasion assay, cell cycle analysis, RT-PCR, Western blot and ELISA were performed. BI836845, a humanized insulin-like growth factor (IGF) ligand-neutralizing antibody, was used for IGF-related signalling pathway inhibition. AGS-EBV cells showed slower proliferating rate and higher sensitivity to BI836845 compared to AGS cells. Moreover, invasiveness of AGS-EBV was increased than that of AGS, and BI836845 treatment significantly decreased the invasiveness of AGS-EBV. Although no apoptosis was detected, entry into the S phase of the cell cycle was delayed in BI836845-treated AGS-EBV cells. In conclusion, AGS-EBV cells seem to modulate their proliferation and invasion through the IGF signalling pathway. Inhibition of the IGF signalling pathway therefore could be a potential therapeutic strategy for EBVaGC.

摘要

包括胃癌在内的几种癌症已被报道含有 Epstein-Barr 病毒 (EBV) 感染。EBV 相关胃癌 (EBVaGC) 被 The Cancer Genome Atlas (TCGA) 组归类为胃癌的四个分子亚型之一，具有增加的免疫相关特征。需要确定 EBV 依赖性途径与重要的生物学作用，以用于 EBVaGC。为了比较AGS 胃上皮细胞和 EBV 感染的 AGS（AGS-EBV）细胞之间的生物学变化，进行了增殖测定、CCK-8 测定、侵袭测定、细胞周期分析、RT-PCR、Western blot 和 ELISA。BI836845 是一种人源化胰岛素样生长因子 (IGF) 配体中和抗体，用于 IGF 相关信号通路抑制。与 AGS 细胞相比，AGS-EBV 细胞的增殖速度较慢，对 BI836845 更敏感。此外，AGS-EBV 的侵袭性高于 AGS，BI836845 处理显著降低了 AGS-EBV 的侵袭性。尽管未检测到细胞凋亡，但 BI836845 处理的 AGS-EBV 细胞进入 S 期的细胞周期被延迟。总之，AGS-EBV 细胞似乎通过 IGF 信号通路调节其增殖和侵袭。因此，抑制 IGF 信号通路可能是 EBVaGC 的一种潜在治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/830e/6237558/54b6e36c4f21/JCMM-22-5899-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/830e/6237558/336a0801faac/JCMM-22-5899-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/830e/6237558/1147e2c516a5/JCMM-22-5899-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/830e/6237558/7ec968ab341f/JCMM-22-5899-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/830e/6237558/356d2f12640c/JCMM-22-5899-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/830e/6237558/54b6e36c4f21/JCMM-22-5899-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/830e/6237558/336a0801faac/JCMM-22-5899-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/830e/6237558/1147e2c516a5/JCMM-22-5899-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/830e/6237558/7ec968ab341f/JCMM-22-5899-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/830e/6237558/356d2f12640c/JCMM-22-5899-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/830e/6237558/54b6e36c4f21/JCMM-22-5899-g005.jpg

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