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下调血管生成素样蛋白 2 通过抑制 ERK/MAPK 信号通路抑制胶质瘤细胞的增殖和侵袭。

Knockdown of Angiopoietin-Like Protein 2 Inhibits Proliferation and Invasion in Glioma Cells via Suppressing the ERK/MAPK Signaling Pathway.

出版信息

Oncol Res. 2017 Sep 21;25(8):1349-1355. doi: 10.3727/096504017X14874337324615. Epub 2017 Feb 28.

Abstract

Angiopoietin-like protein 2 (ANGPTL2), a member of the glycoprotein family, is mainly secreted by adipose tissues under normal conditions. Recently, ANGPTL2 has been found to be upregulated in some types of cancers and is considered to be a tumor promoter. However, the functional significance of ANGPTL2 in glioma has not yet been elucidated. In this study, we investigated the specific role of ANGPTL2 in glioma. The results showed that ANGPTL2 was highly expressed in glioma tissues and cell lines. Knockdown of ANGPTL2 reduced the proliferative and invasive abilities of glioma cells. Moreover, the tumorigenesis assay showed that ANGPTL2 knockdown inhibited glioma tumor growth in vivo. We also found that ANGPTL2 knockdown decreased the protein levels of p-ERK1/2 in glioma cells and thus blocked the activity of the ERK/MAPK signaling pathway. Taken together, our study provided the first evidence that ANGPTL2 played an oncogenic role in glioma development and might be considered as a new therapeutic target for glioma treatment.

摘要

血管生成素样蛋白 2(ANGPTL2)是糖蛋白家族的一员,在正常情况下主要由脂肪组织分泌。最近发现,ANGPTL2 在某些类型的癌症中上调,被认为是一种肿瘤促进因子。然而,ANGPTL2 在神经胶质瘤中的功能意义尚未阐明。在本研究中,我们研究了 ANGPTL2 在神经胶质瘤中的特定作用。结果表明,ANGPTL2 在神经胶质瘤组织和细胞系中高表达。ANGPTL2 的敲低降低了神经胶质瘤细胞的增殖和侵袭能力。此外,肿瘤发生测定表明,ANGPTL2 的敲低抑制了体内神经胶质瘤肿瘤的生长。我们还发现,ANGPTL2 的敲低降低了神经胶质瘤细胞中 p-ERK1/2 的蛋白水平,从而阻断了 ERK/MAPK 信号通路的活性。总之,我们的研究首次提供了证据表明 ANGPTL2 在神经胶质瘤的发展中发挥致癌作用,并且可能被认为是神经胶质瘤治疗的新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/178b/7841190/a4440f9f9aef/OR-25-1349-g001.jpg

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