Abstract
BACKGROUND: Proline dehydrogenase (PRODH) encodes a mitochondrial protein that catalyzes the first step of proline degradation and is related to angiogenesis. Angiogenesis is a critical process in the development and progression of tumors, including lung adenocarcinoma (LUAD), as tumor growth and metastasis are dependent on angiogenesis. The mitochondria and their associated genes thus play a vital role in tumor therapy. However, the specific mechanism of action of PRODH in LUAD is not yet clear. The aim of this study was thus to clarify the specific mechanism of PRODH as a mitochondrial gene in LUAD. METHODS: This study identified genes related to mitochondria and angiogenesis in LUAD. Based on the high and low expression of the genes in LUAD, we grouped them and conducted relevant bioinformatics analysis on the differentially expressed genes. RESULTS: We screened genes related to mitochondria and angiogenesis in the differential genes of LUAD, and identified PRODH as a gene of interest. The expression of PRODH was associated with the survival outcome of patients with LUAD. Additionally, PRODH was found to be associated with immune cell infiltration and tumor mutations. CONCLUSIONS: Mitochondrial metabolism and angiogenesis may have significant therapeutic ramifications for patients with LUAD. We identified PRODH, a gene exerts a dual role in cancer. PRODH may be a prospective therapeutic target in LUAD and a possible diagnostic and prognostic biomarker associated with immune infiltration and tumor mutational burden.