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.
Methods and Results:
In this study, we found that TRIM45 was up-regulated in earlystage
human non-small-cell lung cancer (NSCLC) tissues. Overexpression of TRIM45 in
lung cancer cells induces G1 arrest and promotes apoptosis, which accompanied by upregulated
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.
CARMA3 regulates the invasion, migration, and apoptosis of non-small cell lung cancer cells by activating NF-кB and suppressing the P38 MAPK signaling pathway