Findings indicate that Cul4A is oncogenic in vivo and that Cul4A over-expression is associated with cisplatin resistance in lung cancer cells.

PR-Set7 is a direct target of Cul4A for degradation and involved in the formation of lung tumors in the conditional Cul4A transgenic mouse model.

We observed that knockdown of Cul4A was associated with increased sensitivity to gemcitabine through upregulation of TGFBI in lung cancer cells.

findings revealed that CUL4A and CUL4B are differentially associated with etiologic factors for pulmonary malignancies and are independent prognostic markers for the survival of distinct lung cancer subtypes

JMJD2C regulated the activities of lung cancer cells by directly controlling the expression of CUL4A in JMJD2C over-expression cell line.

These results suggest that different DDB1-CUL4 associated factors play distinct roles in human lung adenocarcinoma development.

miR-363-3p levels were significantly decreased in tumor tissues of non-small cell lung cancer (NSCLC) patients. CUL4A mRNA and protein levels were decreased in A549 cells transfected with miR-363-3p mimics. The Dual-Luciferase reporter assay results further suggested that CUL4A represents a target gene of miR-363-3p. Decreased miR-363-3p expression enhanced gemcitabine resistance in NSCLC cells via regulation of CUL4A.

Effect of CUL4A on the metastatic potential of lung adenocarcinoma to the bone.