GTPBP4: A New Therapeutic Target Gene Promotes Tumor Progression in Non-Small Cell Lung Cancer via EMT.
Junlu WuGuofei ChenWeiwei WangYang YangYuan YiAnquan ShangWenqiang QuanLixin WangPublished in: Journal of oncology (2022)
Lung cancer has a complex etiology involving multiple regulatory systems. Uncertainty about the biology and evolution of lung cancer has made it difficult to improve its poor prognosis. To create efficient therapeutic targets and optimal molecular screening tools for lung cancer, the most important task seems to be to understand how it develops and progresses. The expression and regulation of GTPBP4 in non-small cell lung cancer (NSCLC) are not well understood. Using methods such as knocking down GTPBP4 in lung cancer cells and establishing a mouse lung cancer model, we found that the expression of GTPBP4 was upregulated in human lung adenocarcinoma cells and tissues, and that knocking down the expression of the GTPBP4 gene in A549 and Calu-1 lung adenocarcinoma cells can inhibit the proliferation of lung adenocarcinoma cells and reduce their invasion ability. The results of the mouse lung cancer model showed that the lung weight and the number of lung surface nodules decreased significantly in the LLC-GTPBP4 KO group. The mechanism by which GTPBP4 regulation affects the progression of lung adenocarcinoma may be related to the regulation of EMT. From this study, new research ideas emerge to explore GTPBP4 as a biomarker and therapeutic target for early diagnosis and treatment of lung cancer.
Keyphrases
- poor prognosis
- long non coding rna
- induced apoptosis
- cell cycle arrest
- epithelial mesenchymal transition
- small cell lung cancer
- gene expression
- endothelial cells
- endoplasmic reticulum stress
- physical activity
- signaling pathway
- dna methylation
- advanced non small cell lung cancer
- weight loss
- transcription factor
- cell migration
- pluripotent stem cells