Inhibition of inhibits proliferation in lung carcinoma cell lines.

BACKGROUND

Lung cancer is one of the most common human malignant tumors and the leading cause of cancer death worldwide. Biphenyl hydrolase-like () is a gene encoding the human enzyme, a serine hydrolase that catalyzes the hydrolytic activation of amino acid ester prodrugs of nucleoside analogs such as valacyclovir and valganciclovir. However, the role of in lung cancer is still unknown.

METHODS

In this study, we assessed the effect knockdown on the proliferation, apoptosis, colony formation, metastasis, and cell cycle of cancer cells. knockdown NCI-H1299 and A549 cells demonstrated decreased proliferation, as measured by Celigo cell counting. The MTT assay results were consistent with Celigo cell counting. Caspase 3/7 activity increased significantly in the NCI-H1299 and A549 cells after shBPHL knockdown. Decreased colony formation in the NCI-H1299 and A54 cells after shBPHL knockdown, as measured by crystal violet staining. Transmigration assay using a Transwell demonstrated that there were significantly fewer migrating cells in the lower chamber in the knockdown NCI-H1299 and A549 cells. Cell cycle analysis by Propidium Iodide (PI) staining and fluorescence activated cell sorter (FACS). We also explored the effect of knockdown on tumor growth in a mouse model of tumor implantation in nude mice.

RESULTS

We found that the knockdown of gene expression by short hairpin RNA (shRNA) leads to a decrease in proliferation, colony formation, and metastasis and an increase in apoptosis in two lung adenocarcinoma (LUAD) cell lines . knockdown induces decreased tumor growth, colony formation, and metastasis; increased apoptosis; and altered cell cycle destruction. knockdown results in decreased tumor growth . Moreover, knockdown A549 cells demonstrated slower growth compared to control cells upon implantation in nude mice, confirming the findings.

CONCLUSIONS

In this study, the data indicate that potentially promotes proliferation, inhibits apoptosis, and increases colony formation and metastasis in lung cancer. Overall, our study suggests that may be a gene that promotes tumor growth in lung cancer.