TRIB3 promotes proliferation, migration, and invasion of retinoblastoma cells by activating the AKT/mTOR signaling pathway

被引:6
|
作者
Bao, Xian-Yi [1 ]
Sun, Ming [1 ]
Peng, Ting-Ting [1 ]
Han, Dong-Mei [2 ]
机构
[1] Wuhan Univ, Dept Cataract, Aier Eye Hosp, Wuhan, Hubei, Peoples R China
[2] Huainan Chenguang Eye Hosp, Dept Fundus Dis, 168 Guoqing East Rd, Huainan 232007, Anhui, Peoples R China
关键词
TRIB3; retinoblastoma; proliferation migration invasion; AKT; CANCER; CHALLENGES; MANAGEMENT;
D O I
10.3233/CBM-200050
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
BACKGROUND: Tribbles pseudokinase 3 (TRIB3) is a member of the tribbles-related family, which has been determined in various cancers, including renal cell carcinoma, acute promyelocytic leukemia, colorectal cancer, endometrial cancer, and glioma. However, its role in retinoblastoma (RB) has not yet been explored. METHODS: The expression level of TRIB3 was detected in RB tissues and cell lines using qRT-PCR. The effects of TRIB3 on cell proliferation and invasion capacities were analyzed with MTT, crystal violet, and transwell assays. Western blot and rescue assays were conducted to explore the underlying mechanism. RESULTS: This study found that TRIB3 was upregulated in human RB tissues compared to adjacent normal tissues both at the mRNA and protein levels. Overexpression of TRIB3 significantly promoted cell proliferation and invasion of RB cells, while TRIB3 knockdown inhibited these processes. Moreover, the mechanism deciphering experiments showed that TRIB3 overexpression can increase AKT and mTOR phosphorylation. Conversely, TRIB3 knockdown decreased the phosphorylation of AKT and mTOR. Additionally, MK2206, a potent AKT inhibitor, blocked the promotive effects of TRIB3 in RB cells. CONCLUSION: This study demonstrated that TRIB3 acts as an oncogene and plays a crucial role in the proliferation and invasion of RB cells via regulating the AKT/mTOR signaling pathway. Therefore, TRIB3 may serve as a potential target in the diagnosis and/or treatment of RB.
引用
收藏
页码:307 / 315
页数:9
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