LncRNA PSMA3-AS1 promotes cell proliferation, migration, and invasion in ovarian cancer by activating the PI3K/Akt pathway via the miR-378a-3p/GALNT3 axis

被引:20
作者
Xu, Zhihong [1 ]
Jin, Hui [1 ]
Duan, Xiaoyang [1 ]
Liu, Hong [2 ]
Zhao, Xiwa [2 ]
Fan, Shaoshuang [1 ]
Wang, Yan [3 ]
Yao, Tiezhu [4 ]
机构
[1] Hebei Med Univ, Dept Oncol, Hosp 4, Shijiazhuang, Hebei, Peoples R China
[2] Hebei Med Univ, Dept Gynecol, Hosp 4, Shijiazhuang, Hebei, Peoples R China
[3] Hebei Med Univ, Dept Thorac Surg, Hosp 4, Shijiazhuang, Hebei, Peoples R China
[4] Hebei Med Univ, Dept Cardiol, Hosp 4, Shijiazhuang, Hebei, Peoples R China
关键词
GALNT3; miR-378a-3p; ovarian cancer; PI3K; Akt pathway; PSMA3-AS1; LONG NONCODING RNA; EXPRESSION; PROGRESSION; PROGNOSIS; REVEALS; GROWTH;
D O I
10.1002/tox.23370
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
The crucial roles of the long noncoding RNAs (lncRNAs) in the development of ovarian cancer (OC) have been extensively studied. According to the prediction result from the Kaplan-Meier Plotter database, high expression of lncRNA proteasome subunit alpha type-3 antisense RNA1 (PSMA3-AS1) is associated with the poor prognosis in patients with OC. Thus, the study aimed to investigate the role of lncRNA PSMA3-AS1 in OC. Reverse transcription quantitative polymerase chain reaction analysis revealed that PSMA3-AS1 expression was significantly upregulated in OC cells and tissues. PSMA3-AS1 silencing inhibited OC cell proliferation, migration, and invasion, as shown by results of cell counting kit-8, colony formation, wound healing, and Transwell assays, respectively. Additionally, PSMA3-AS1 deficiency suppressed tumor growth in vivo. Mechanistically, luciferase reporter and RNA pulldown assays implied that PSMA3-AS1 served as a competing endogenous RNA for miR-378a-3p to upregulate the expression of polypeptide N-acetylgalactosaminyltransferase 3 (GALNT3). GALNT3 was a target gene of miR-378a-3p in OC. Moreover, PSMA3-AS1 activated the PI3K/Akt pathway by upregulating GALNT3 expression. Overall, PSMA3-AS1 promotes OC cell proliferation, migration, invasion, and xenograft tumor growth by activating the PI3K/Akt pathway via the miR-378a-3p/GALNT3 axis.
引用
收藏
页码:2562 / 2577
页数:16
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