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整合素β样蛋白1(ITGBL1)通过Akt信号通路促进胃癌细胞的增殖和侵袭。

ITGBL1 promotes gastric cancer cell proliferation and invasion via Akt signal pathway.

作者信息

Yin Feng-Yan, Qi Huan-Peng, Qiao Hui, Lv Xiao-Hong, Tan Hai-Hua

机构信息

Department of Thyroid Surgery, Taian Central Hospital, Taian, Shandong,271000, PR China.

Department of Oncology, Taian Central Hospital, Taian, Shandong, 271000, PR China.

出版信息

Front Biosci (Landmark Ed). 2021 Jan 1;26(4):682-691. doi: 10.2741/4912.

DOI:10.2741/4912
PMID:33049688
Abstract

Integrin beta- like 1 (ITGBL1), an extracellular matrix protein, plays an oncogenic role in diverse forms of cancers. To this end, we examined the importance of ITGBL1 in gastric cancer (GC). The upregulated expression of ITGBL1 in GC was associated with a poor prognosis. Moreover, upregulation of ITGBL1 enhanced cell mobility while silencing it exerted an opposite effect. Up-regulation of ITGBL1 significantly promoted phosphorylation of Akt, decreased the ratio of phosphorylated Akt in AGS/ITGBL1-shRNA and N87/ITGBL1-shRNA cells, enhanced cell mobility and proliferation. Silencing ITGBL1 had an opposite effect on Akt phosphorylation, cell mobility, and proliferation. These findings show that ITGBL1 regulates mobility and proliferation of GC likely through activation of Akt signaling.

摘要

整合素β样蛋白1(ITGBL1)是一种细胞外基质蛋白,在多种癌症中发挥致癌作用。为此,我们研究了ITGBL1在胃癌(GC)中的重要性。GC中ITGBL1的表达上调与预后不良相关。此外,ITGBL1的上调增强了细胞迁移能力,而沉默ITGBL1则产生相反的效果。ITGBL1的上调显著促进了Akt的磷酸化,降低了AGS/ITGBL1-shRNA和N87/ITGBL1-shRNA细胞中磷酸化Akt的比例,增强了细胞迁移和增殖能力。沉默ITGBL1对Akt磷酸化、细胞迁移和增殖产生相反的影响。这些发现表明,ITGBL1可能通过激活Akt信号通路调节GC的迁移和增殖。

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