TRIM11 promotes tumor angiogenesis via activation of STAT3/VEGFA signaling in lung adenocarcinoma.

Tripartite motif containing 11 (TRIM11) plays important roles in the regulation of lung cancer behaviors. However, the mechanisms of action of TRIM11 in tumor angiogenesis remain unclear. In this study, we found that TRIM11 expression is higher in lung adenocarcinoma (ADC) than in normal lung tissues. High TRIM11 expression was found to be associated with advanced progression and a poor prognosis of lung ADCs. Functional assays demonstrated that TRIM11 promoted tumor growth and angiogenesis in vivo and enhanced migration of (and tube formation by) human umbilical vein endothelial cells (HUVECs). Mechanistically, TRIM11 was found to regulate angiogenesis through the signal transducer and activator of transcription 3 (STAT3)/vascular endothelial growth factor A (VEGFA) pathway. Moreover, in clinical samples, VEGFA expression was much higher in cancer tissue samples and positively correlated with TRIM11 expression. TRIM11-overexpressing samples showed higher CD31 staining and microvessel density. Thus, we provide evidence that TRIM11 is a proangiogenic factor in lung ADC and may serve as a therapeutic target for lung ADC treatment. AJCR