Our data indicated that USP22 may promote lung adenocarcinoma cell invasion by the induction of EMT.

Downregulation of USP22 in ATC cells impeded tumor growth and lung metastasis in vivo.

these findings suggest that miR-30e-5p suppresses non-small cell lung cancer (NSCLC) tumorigenesis by downregulating USP22-mediated Sirt1/JAK/STAT3 signaling.

Targeting USP22 represents a potential therapeutic approach to suppress cancer-initiating cells (CIC) in lung adenocarcinoma partially through downregulation of ALDH1A3 expression.

Results showed that USP22 promotes cell proliferation, migration and invasion, and contributes to resistance to EGFR-TKIs in EGFR mutant lung adenocarcinoma cells. Mechanistically, USP22 deubiquitinates EGFR localized on late endosomes, prevents ubiquitination mediated EGFR degradation and enhances recycling of EGFR after EGF stimulation.

USP22 and CCND1 levels correlate in patient lung and colorectal cancer samples and our preclinical studies indicate that targeting USP22 in combination with CDK inhibitors may offer an approach for treating cancer patients whose tumors exhibit elevated CCND1.

Ubiquitin-specific protease 22 is critical to in vivo angiogenesis, growth and metastasis of non-small cell lung cancer.

USP22 promotes development of lung adenocarcinoma through ubiquitination and immunosuppression.

circRNA circFAT1(e2) Elevates the Development of Non-Small-Cell lung cancer by Regulating miR-30e-5p and USP22.