TRIM45 Suppresses the Development of Non-small Cell Lung Cancer

Background: Previously, we first identified the human tri-partite motif-containing protein 45 (TRIM45) acts as a novel transcriptional repressor in mitogen-activated protein kinase (MAPK) signaling pathway. After that, the inhibitory role of TRIM45 in the development of tumor was gradually unveiled. However, the function of TRIM45 in the tumorigenesis of lung cancer has not been characterized. Results: In this study, we found that TRIM45 was up-regulated in early-stage human non-small-cell lung cancer (NSCLC) tissues. Overexpression of TRIM45 in lung cancer cells induces G1 arrest and promotes apoptosis, which accompanied with up-regulated expression of RB, p16, p53, p27Kip1 and Caspase3 and down-regulated expression of CyclinE1 and CyclinE2. Further detection of the expression of the molecules in the MAPK signaling pathway revealed that overexpression of TRIM45 in lung cancer cells promotes phosphorylated p38 (p-p38) activation and inhibits phosphorylated ERK (p-ERK) activation. In accordance with this, p-p38 is increased while p-ERK is decreased in lung cancer tissues. Conclusion: These findings indicate that TRIM45 plays an inhibitory role in the tumorigenesis of lung cancer. High-level expression of TRIM45 in lung cancer tissue may promote cell apoptosis by activating p38 signal and inhibit proliferation by down-regulating p-ERK, which provides a new clue for understanding the tumorigenesis of lung cancer.