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作者:

Zhang, Li-Na (Zhang, Li-Na.) | Zhao, Lei (Zhao, Lei.) | Yan, Xin-Long (Yan, Xin-Long.) (学者:阎新龙) | Huang, Ying-Hui (Huang, Ying-Hui.)

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摘要:

Accumulating evidence suggests that Ras GTPase-activating protein SH3 domain-binding protein 1 (G3BP1) is very crucial to regulate tumorigenesis and metastasis. Recently, many research works have suggested that G3BP1 is overexpressed in many human cancers including esophageal cancer. Nevertheless, the functional roles of G3BP1 in esophageal cancer are still unknown. Here, the results suggested that silencing of G3BP1 inhibited proliferation, migration, and invasion of esophageal cancer cells, whereas overexpression of G3BP1 led to opposite effects on the growth and metastasis. Surprisingly, G3BP1-depletion had no effect on cell death but caused the arrest of cell cycle in the G(0)/G(1) phase and increased the levels of p53 and p21. In addition, loss of G3BP1 led to a significant elevation of E-cadherin and decrease of N-cadherin, Vimentin, Snail, MMP-9, and MMP-2. Mechanistically, loss of G3BP1 dramatically suppressed Wnt-stimulated T-cell factor/lymphoid enhancer factor (TCF/LEF) transcription factor activity and downregulated its target genes including c-Myc, Axin2, and cyclin D1. Moreover, knockdown of G3BP1 downregulated the expression levels of p-PI3K, p-AKT, and p-GSK-3 beta, but the total PI3K, AKT, and GSK-3 beta were not changed. Furthermore, our data proved that the promoting effects of G3BP1-overexpression on cell proliferation, migration, and invasion could be rescued by PI3K inhibitor LY294002 treatment. Collectively, our results here elucidate that G3BP1-depletion suppresses proliferation, migration, and invasion capabilities of esophageal cancer cells via the inactivation of Wnt/beta-catenin and PI3K/AKT signaling pathways. Furthermore, our findings imply that G3BP1 can participate in the regulation of esophageal cancer progression, and will be taken as a promising target to treat esophageal cancer.

关键词:

esophageal cancer Wnt/beta-catenin PI3K/AKT G3BP1 epithelial-mesenchymal transition (EMT)

作者机构:

  • [ 1 ] [Zhang, Li-Na]Beijing Univ Technol, Beijing Int Sci & Technol Cooperat Base Antivirus, Coll Life Sci & Bioengn, Beijing 100124, Peoples R China
  • [ 2 ] [Zhao, Lei]Beijing Univ Technol, Beijing Int Sci & Technol Cooperat Base Antivirus, Coll Life Sci & Bioengn, Beijing 100124, Peoples R China
  • [ 3 ] [Yan, Xin-Long]Beijing Univ Technol, Beijing Int Sci & Technol Cooperat Base Antivirus, Coll Life Sci & Bioengn, Beijing 100124, Peoples R China
  • [ 4 ] [Huang, Ying-Hui]Beijing Univ Technol, Beijing Int Sci & Technol Cooperat Base Antivirus, Coll Life Sci & Bioengn, Beijing 100124, Peoples R China

通讯作者信息:

  • [Zhang, Li-Na]Beijing Univ Technol, Beijing Int Sci & Technol Cooperat Base Antivirus, Coll Life Sci & Bioengn, Beijing 100124, Peoples R China

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来源 :

JOURNAL OF CELLULAR PHYSIOLOGY

ISSN: 0021-9541

年份: 2019

期: 11

卷: 234

页码: 20469-20484

5 . 6 0 0

JCR@2022

ESI学科: MOLECULAR BIOLOGY & GENETICS;

ESI高被引阀值:259

JCR分区:1

被引次数:

WoS核心集被引频次: 57

SCOPUS被引频次: 59

ESI高被引论文在榜: 0 展开所有

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中文被引频次:

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