AI Article Synopsis
- TRIB3, a pseudokinase, is found to be upregulated in retinoblastoma (RB) and promotes cell proliferation and invasion, revealing its potential role as an oncogene.
- The study utilized various assays to confirm that overexpression of TRIB3 increases the phosphorylation of the AKT and mTOR pathways, while knockdown reduces these effects.
- The findings suggest that targeting TRIB3 could be valuable for diagnosing and treating retinoblastoma.
Article Abstract
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.
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| http://dx.doi.org/10.3233/CBM-200050 | DOI Listing |
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