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晚期胃癌中脑源性神经营养因子的上调通过诱导长链五聚体蛋白3促进骨转移性骨溶解。

Upregulation of brain-derived neurotrophic factor in advanced gastric cancer contributes to bone metastatic osteolysis by inducing long pentraxin 3.

作者信息

Choi Bongkun, Lee Eun-Jin, Shin Min-Kyung, Park Young Soo, Ryu Min-Hee, Kim Sang-Min, Kim Eun-Young, Lee Hyung Keun, Chang Eun-Ju

机构信息

Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.

Cell Dysfunction Research Center, University of Ulsan College of Medicine, Seoul, Korea.

出版信息

Oncotarget. 2016 Aug 23;7(34):55506-55517. doi: 10.18632/oncotarget.10747.

DOI:10.18632/oncotarget.10747
PMID:27458153
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5342432/
Abstract

The brain-derived neurotrophic factor (BDNF) activates its receptor, tropomyosin receptor kinase B (TrkB; also called NTRK2) that has been shown to promote the malignant progression of several cancers. In this study, we investigated the clinical and biological significance of the BDNF/TrkB axis in the progression of human gastric cancer. The increased co-expression of the BDNF/TrkB axis was significantly correlated with bone metastatic properties in advanced gastric cancers. BDNF acting via TrkB receptors increased the levels of long pentraxin 3 (PTX3) that was related to bone metastatic status of gastric cancer by enhancing gastric cancer-osteoblastic niche interactions. In bone metastatic gastric cancer, PTX3 knockdown using small interfering RNA significantly inhibited BDNF-induced interactions of cancer cells with osteoblasts. Moreover, BDNF-derived PTX3 induction supported subsequent osteoclastogenesis, and this effect was significantly reversed by PTX3 silencing. These findings suggest that a functional interaction between BDNF/TrkB and PTX3 enhances the osteolysis of bone metastatic gastric cancer, thereby providing potential prognostic factors for the development of bone metastasis of gastric cancer.

摘要

脑源性神经营养因子（BDNF）激活其受体——原肌球蛋白受体激酶B（TrkB，也称为NTRK2），已有研究表明该受体可促进多种癌症的恶性进展。在本研究中，我们调查了BDNF/TrkB轴在人类胃癌进展中的临床和生物学意义。BDNF/TrkB轴共表达增加与晚期胃癌的骨转移特性显著相关。通过TrkB受体起作用的BDNF通过增强胃癌-成骨细胞微环境相互作用，增加了与胃癌骨转移状态相关的长链五聚体蛋白3（PTX3）的水平。在骨转移性胃癌中，使用小干扰RNA敲低PTX3可显著抑制BDNF诱导的癌细胞与成骨细胞的相互作用。此外，BDNF诱导的PTX3生成促进了随后的破骨细胞生成，而PTX3沉默可显著逆转这种作用。这些发现表明，BDNF/TrkB与PTX3之间的功能性相互作用增强了骨转移性胃癌的骨溶解，从而为胃癌骨转移的发生提供了潜在的预后因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c72/5342432/b68ddd49a57a/oncotarget-07-55506-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c72/5342432/b0dc37e03ad4/oncotarget-07-55506-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c72/5342432/d1bfec8000d7/oncotarget-07-55506-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c72/5342432/686a8e0196e7/oncotarget-07-55506-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c72/5342432/46a272181f6d/oncotarget-07-55506-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c72/5342432/b68ddd49a57a/oncotarget-07-55506-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c72/5342432/b0dc37e03ad4/oncotarget-07-55506-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c72/5342432/d1bfec8000d7/oncotarget-07-55506-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c72/5342432/686a8e0196e7/oncotarget-07-55506-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c72/5342432/46a272181f6d/oncotarget-07-55506-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c72/5342432/b68ddd49a57a/oncotarget-07-55506-g005.jpg

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