Abstract
It has been well established that mammalian sterile 20-like 1 (MST1) functions as a suppressor via regulating cell progression in many tumors. However, the molecular mechanism of MST1 on regulating glioma progression remains unclear. Here, we discovered that MST1 was robustly down-regulated in glioma tissues and cells. Functional analysis showed that over-expression of MST1 downregulated viability and colony formation and promoted apoptosis of glioma cells. Our results also identified that MST1 positively regulated expression of SIRT6 (Sirtuin 6) via transcriptional factor FOXO3a (Forkhead box O3a). Furthermore, the functional role of MST1 in glioma cell viability (or apoptosis) were significantly reversed after knocking down of SIRT6. Our research indicates that MST1 is a potential biomarker for the prognosis and diagnosis of glioma and provides new direction on the molecular mechanism of glioma progression and development.
Highlights
Glioma comprises 30% of all brain tumors and central nervous system tumors, and accounting for 80% of all malignant brain tumors (Goodenberger and Jenkins, 2012)
3.2 Over-expression of mammalian sterile 20-like 1 (MST1) inhibited cell viability and colony formation and induced cell apoptosis of glioma cells MST1 expression profiles were detected in three independent glioma cell lines (A-172, U-138 MG and U-251 MG) and human embryonic brain cell line (HEB)
The results showed that the mRNA (Fig. 2A) and protein (Fig. 2B) expression of MST1 in glioma cell lines were significantly down-regulated as compared with that in Human embryonic brain cells (HEB) cells
Summary
Glioma comprises 30% of all brain tumors and central nervous system tumors, and accounting for 80% of all malignant brain tumors (Goodenberger and Jenkins, 2012). Glioma is characterized by uncontrolled proliferation, invasion and angiogenesis (Chang et al, 2017). The average survival time of glioma is generally ranging from 12 to 15 months (Huse et al, 2011; Grossman et al, 2010). A common treatment method is a combination of surgery, radiation therapy, and chemotherapy (Sun et al, 2013; Zach et al, 2009). After use of this method the postoperative survival rate have shown to be unsatisfactory due to high risk for metastasis and invasion (Wu et al, 2017; Bohman et al, 2009). Finding new targets and elucidating the molecular mechanisms of glioma remains necessary
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