Objectives: This study aims to investigate the role of topoisomerase II binding protein 1-interacting checkpoint and replication regulator (TICRR) on the proliferation of lung adenocarcinoma (LUAD) and its potential molecular mechanism as well as to provide a new strategy to improve LUAD treatment. Material and Methods: The expression level of TICRR in patients with LUAD was analyzed on the basis of the Cancer Genome Atlas program database, and loss- and gain-of-function experiments were conducted to validate whether TICRR promoted the proliferation of LUAD cells. Then, pathway enrichment analysis and luciferase reporter assays were performed to dissect the potential mechanism. Results: Overexpression of TICRR in patients with LUAD was associated with poor survival ( P < 0.001). In addition, overexpression of TICRR aggravated LUAD cell proliferation, which was ameliorated by TICRR depletion. In addition, TICRR could activate the myelocytomatosis oncogene (MYC) signaling pathway by regulating Bcl-2-associated X protein and Cyclin B1, which are the pivotal effectors of the MYC signaling pathway. Conclusion: TICRR plays a critical role in fostering the progression of LUAD by regulating the MYC signaling pathway.
Zhao et al. (Wed,) studied this question.
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