Study on the expression and function of macrophage stimulating 1 in ovarian cancer
10.3760/cma.j.cn.115807-20200825-00256
- VernacularTitle:巨噬细胞刺激1在卵巢癌中的表达及作用研究
- Author:
Jia CHEN
;
Xiaojuan WU
;
Juan GUO
;
Yadong WANG
- From:
Chinese Journal of Endocrine Surgery
2021;15(1):98-102
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the expression of MST1 in ovarian cancer (OV) , its relationship with the clinicopathological characteristics, and the potential molecular mechanism.Methods:62 OV patients admitted to Chongqing Emergency Medical Center and the Fifth People’s Hospital of Chongqing from Mar. 2016 to Feb. 2020 were selected. The expression levels of mRNA were detected by quantitative real-time polymerase chain reaction. [MST1 over-expression group: 24 h: (0.31±0.02) , 48 h: (0.44±0.03) , 72 h: (0.62±0.02) ; Blank group:24 h: (0.32±0.02) , (0.55±0.02) , (0.74±0.02) ;MST1 empty vector group:24 h: (0.32±0.03) , 48 h: (0.56±0.02) , 72 h: (0.77±0.02) ]Results:The expression of MST1 was lower in OV than in adjacent tissues[ (0.52±0.12) vs (1.18±0.21) ]. MST1 expression level was not related to age, but significantly correlated with the size of the tumors[ (0.46±0.12) vs (0.58±0.10) , P=0.00], TNM[ (0.57±0.10) vs (0.43±0.12) , P=0.00], TNM stage 9 (0.57±0.10) vs (0.43±0.12) , P=0.00] and lymph node metastasis[ (0.47±0.14) vs (0.56±0.09) , P=0.003]. Over-expression of MST1 obviously inhibited cellular proliferation in OV (MST1 over-expression group: 24 h: 0.31±0.02, 48 h: 0.44±0.03, 72 h: 0.62±0.02; blank group: 24 h: 0.32±0.02, 0.55±0.02, 0.74±0.02; empty vector group: 24 h: 0.32±0.03, 48 h: 0.56±0.02, 72 h: 0.77±0.02) . MST1 over-expression could promote FOXO3 expression, ,the expression level of FOXO3 in Mst1 overexpression group and control group were[ (0.61±0.04) vs (0.41±0.03) ]. MST1 inhibited proliferation of OV cells through upregulating the expression of FOXO3. Conclusions:The expression of MST1 is closely related to the clinicopathological features of OV patients, and MST1 may restrain OV by positively regulating FOXO3 expression.
