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中期因子基因的抑制通过Notch信号通路的调节促进顺铂对人胃癌细胞系AGS的体内外抗肿瘤作用。

Suppression of midkine gene promotes the antitumoral effect of cisplatin on human gastric cancer cell line AGS in vitro and in vivo via the modulation of Notch signaling pathway.

作者信息

Tian Wenyan, Shen Jiaqing, Chen Weichang

机构信息

The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.

出版信息

Oncol Rep. 2017 Aug;38(2):745-754. doi: 10.3892/or.2017.5743. Epub 2017 Jun 22.

DOI:10.3892/or.2017.5743
PMID:28656262
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5562011/
Abstract

Midkine (MK) is reported to be associated with the clinical stages and distant metastases in gastric cancer, and to positively regulate the proliferation of human gastric cancer cells. However, the possible mechanisms of MK in the development of gastric cancer are still not fully clarified. In this study, the therapeutic effect of MK inhibition in gastric cancer in vivo and in vitro was investigated, by knock-down of MK expression with a small interfering RNA (siRNA). MK was expressed in gastric carcinoma tissues and cancer cells. The cytotoxic effect of cisplatin on AGS cells in vitro was attenuated by recombinant human MK, but was promoted by suppressing MK expression via downregulating the Notch signaling pathway-related proteins (Notch 1, Notch 2, Delta‑like 1 and Jagged 1). Suppression of MK expression also promoted the inhibitory effect of cisplatin on AGS cells in vivo. In concusion, suppression of midkine gene promoted the antitumoral effect of cisplatin on human gastric cell line AGS in vitro and in vivo via Notch signaling pathway.

摘要

据报道，中期因子（MK）与胃癌的临床分期和远处转移相关，并能正向调节人胃癌细胞的增殖。然而，MK在胃癌发生发展中的可能机制仍未完全阐明。在本研究中，通过小干扰RNA（siRNA）敲低MK表达，研究了MK抑制在体内外对胃癌的治疗作用。MK在胃癌组织和癌细胞中表达。重组人MK减弱了顺铂对体外AGS细胞的细胞毒性作用，但通过下调Notch信号通路相关蛋白（Notch 1、Notch 2、Delta样1和Jagged 1）抑制MK表达则增强了顺铂的细胞毒性作用。抑制MK表达也增强了顺铂在体内对AGS细胞的抑制作用。总之，抑制中期因子基因通过Notch信号通路在体内外增强了顺铂对人胃癌细胞系AGS的抗肿瘤作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/fa2d39860028/OR-38-02-0745-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/1f5ee2c12141/OR-38-02-0745-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/a72cf0dc6f8a/OR-38-02-0745-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/b6b88ef0913b/OR-38-02-0745-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/2a383ab57470/OR-38-02-0745-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/04feb921d9eb/OR-38-02-0745-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/f299387b38f9/OR-38-02-0745-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/fa2d39860028/OR-38-02-0745-g07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/1f5ee2c12141/OR-38-02-0745-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/a72cf0dc6f8a/OR-38-02-0745-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/b6b88ef0913b/OR-38-02-0745-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/2a383ab57470/OR-38-02-0745-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/04feb921d9eb/OR-38-02-0745-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/f299387b38f9/OR-38-02-0745-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1aaf/5562011/fa2d39860028/OR-38-02-0745-g07.jpg

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MiR-181a suppresses autophagy and sensitizes gastric cancer cells to cisplatin.miR-181a 抑制自噬并增强胃癌细胞对顺铂的敏感性。
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Notch increased vitronection adhesion protects myeloma cells from drug induced apoptosis.
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Midkine promotes breast cancer cell proliferation and migration by upregulating NR3C1 expression and activating the NF-κB pathway.中期因子通过上调 NR3C1 表达和激活 NF-κB 通路促进乳腺癌细胞增殖和迁移。
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