These results implicate FoxO3a as a selective target of deletion in mouse lung adenocarcinomas

This suggests that FOXO3a is a potential suppressor of carcinogenic damage in carcinogen-induced lung adenocarcinoma.

We reveal a new mechanism that FOXO3a transcriptionally represses DNMT3B expression and this regulation can be attenuated by MDM2 overexpression in human lung cancer model.

High expression of FOXO3a is associated with lung adenocarcinomas.

miR-622 overexpression mediated by the transcription factor FOXO3a decreased the invasiveness of lung tumor cells by inhibiting HIF-1alpha via inactivation of ERK signaling.

Our findings indicate that FOXO3a is a significant factor in EGFR mutation-independent gefitinib resistance and the stemness of lung cancer, and suggest that targeting the NF-kappaB/miR-155/FOXO3a pathway has potential therapeutic value in lung cancer with the acquisition of resistance to EGFR-TKIs.

Shikonin induces apoptosis in some lung cancer cells via activation of FOXO3a/EGR1/SIRT1 signaling, and AKT and p300 negatively regulate this process via Bim upregulation.

Results indicate that cordycepin promotes caveolin-1 (CAV1)upregulation to enhance c-jun N-terminal kinase (JNK)/forkhead box O3A protein (Foxo3a) signaling pathway activation, inducing apoptosis in lung cancer cells.

miR-182 might account for radioresistance in lung cancer and that miR-182-FOXO3 provides a novel radiosensitizing target