Background: Previously, we first identified the human tripartite motifcontaining
protein 45 (TRIM45) acts as a novel transcriptional repressor in mitogenactivated
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 by 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.