کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5526884 | 1401554 | 2017 | 8 صفحه PDF | دانلود رایگان |
![عکس صفحه اول مقاله: Downregulation of β-arrestin 1 suppresses glioblastoma cell malignant progression vis inhibition of Src signaling Downregulation of β-arrestin 1 suppresses glioblastoma cell malignant progression vis inhibition of Src signaling](/preview/png/5526884.png)
- Expression of β-arrestin 1 was upregulated in GBM and contributed to poor outcome.
- Knockdown of β-arrestin 1 inhibited the proliferation and glycolysis of GBM cells.
- Knockdown of β-arrestin 1 decreased the activity of Src signaling and expressions of malignancy-related factors.
- Knockdown of β-arrestin 1 suppressed GBM growth in vivo.
Glioblastoma multiforme (GBM) is one of the most common brain malignancies worldwide and is typically associated with a dismal prognosis, yet the mechanisms underlying its aggressiveness remain unclear. Here, we revealed that β-arrestin 1 was overexpressed in GBM and contributed to poorer outcome. Knockdown of β-arrestin 1 suppressed the proliferation, invasiveness and glycolysis of GBM cells, and also enhanced temozolomide efficacy. Further, we discovered that knockdown of β-arrestin 1 decreased the activity of Src, and suppression of Src signaling was critically involved in β-arrestin 1 silencing-mediated suppression of GBM malignancies. Finally, we investigated the effect of β-arrestin 1 knockdown on the tumor growth and survival of xenograft models, and found that shβ-arrestin 1 apparently inhibited GBM growth in vivo and resulted in better survival of mice. Taken together, our findings suggest that knockdown of β-arrestin 1 can suppress GBM cell proliferation, invasion and glycolysis by inhibiting Src signaling. Thus, targeting β-arrestin 1 may be a potential therapeutic strategy for GBM treatment.
Journal: Experimental Cell Research - Volume 357, Issue 1, 1 August 2017, Pages 51-58