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三叶因子3通过调节缺氧诱导因子-1α促进神经胶质瘤的恶性发展。

Trefoil factor 3 contributes to the malignancy of glioma via regulating HIF-1α.

作者信息

Diao Shuo, Zheng Qianqian, Gao Jian, Yao Yiqun, Ren Siyang, Liu Yongjian, Xu Yinghui

机构信息

Department of Neurosurgery, First Affiliated Hospital, Dalian Medical University, Dalian, People's Republic of China.

Department of Pathophysiology, Basic Medical College, China Medical University, Shenyang, People's Republic of China.

出版信息

Oncotarget. 2017 Aug 7;8(44):76770-76782. doi: 10.18632/oncotarget.20010. eCollection 2017 Sep 29.

DOI:10.18632/oncotarget.20010
PMID:29100347
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5652741/
Abstract

Trefoil factor 3 (TFF3) plays significant roles in several solid tumors. However, the expression pattern and function of TFF3 in glioblastoma (GBM) have not been reported. Here, we report that expression level of TFF3 significantly elevated in glioma and correlated with the prognosis of glioma patients. Then we found TFF3 promotes proliferation, invasion, and migration and inhibits apoptosis of glioma cells , and delayed tumor progression in subcutaneous xenograft nude mice, and prolonged the median survival time in orthotopic xenograft mice. Moreover, knockdown of TFF3 reduced the expression of HIF-1α through a hypoxia-independent manner. These findings suggest that targeting TFF3 may offer a novel strategy for therapeutic intervention of malignant gliomas.

摘要

三叶因子3（TFF3）在多种实体瘤中发挥重要作用。然而，TFF3在胶质母细胞瘤（GBM）中的表达模式和功能尚未见报道。在此，我们报告TFF3的表达水平在胶质瘤中显著升高，并与胶质瘤患者的预后相关。然后我们发现TFF3促进胶质瘤细胞的增殖、侵袭和迁移，并抑制其凋亡，在皮下异种移植裸鼠中延缓肿瘤进展，在原位异种移植小鼠中延长中位生存时间。此外，敲低TFF3以非缺氧依赖的方式降低HIF-1α的表达。这些发现表明，靶向TFF3可能为恶性胶质瘤的治疗干预提供一种新策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ce/5652741/e7376197d8f0/oncotarget-08-76770-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ce/5652741/6e6b44e08cbf/oncotarget-08-76770-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ce/5652741/fe55ebc71431/oncotarget-08-76770-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ce/5652741/f9df64adde93/oncotarget-08-76770-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ce/5652741/5acd7c363e8b/oncotarget-08-76770-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ce/5652741/6c751ad79a30/oncotarget-08-76770-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ce/5652741/e7376197d8f0/oncotarget-08-76770-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ce/5652741/6e6b44e08cbf/oncotarget-08-76770-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ce/5652741/fe55ebc71431/oncotarget-08-76770-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ce/5652741/f9df64adde93/oncotarget-08-76770-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ce/5652741/5acd7c363e8b/oncotarget-08-76770-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ce/5652741/6c751ad79a30/oncotarget-08-76770-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53ce/5652741/e7376197d8f0/oncotarget-08-76770-g006.jpg

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本文引用的文献

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Trefoil Factor-3 (TFF3) Stimulates De Novo Angiogenesis in Mammary Carcinoma both Directly and Indirectly via IL-8/CXCR2.三叶因子3（TFF3）通过白细胞介素-8/趋化因子受体2（IL-8/CXCR2）直接和间接刺激乳腺癌中的新生血管生成。
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脑肿瘤的免疫治疗
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