PRRX2 predicts poor survival prognosis, and promotes malignant phenotype of lung adenocarcinoma via transcriptional activates PSMD1

INTRODUCTION: : Paired-related homeobox transcription factor 2 (PRRX2) has been proved involves in the pathogenesis of tumors, but the role of PRRX2 in lung adenocarcinoma (LUAD) is basically not clear. MATERIALS AND METHODS: : LUAD datasets were obtained from Gene Expression Omnibus datasets. Functional enrichment analyses were performed based on R language. Several online analysis tools were used for PRRX2 expression, survival curves, and immune cell infiltration analyses. CCK-8, flow cytometry assays were used to detect the cell proliferation and apoptosis. Dual luciferase reporter system and chromatin immunoprecipitation were used to explore the interaction of PRRX2 and Proteasome 26S subunit, non-ATPases 1 (PSMD1). Xenograft in nude mice was used to assess the function of PRRX2 regulation in vivo. RESULTS AND DISCUSSION: : Bioinformatics analyses found that PRRX2 was highly expressed in LUAD tissues and the high PRRX2 expression had a poor prognostic value. PRRX2 was highly expressed in LUAD clinical samples and cell lines. PRRX2 acted as a positive regulator of cell proliferation and a negative regulator of apoptosis. PRRX2 could bind with the PSMD1 promoter and regulate PSMD1 expression, thereby affected LUAD cells' malignant phenotype. Result of xenografts in nude mice confirmed that PRRX2 promotes LUAD tumor growth in vivo. Summary, our study results reveal the crucial roles for PRRX2 in the proliferation and apoptosis of LUAD progression and suggest that PRRX2 may regulate PSMD1 expression by combining with the PSMD1 promoter, thereby participating in the malignant behavior of LUAD.