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Simple Summary: Lung adenocarcinoma (LUAD) is the most common histologic subtype of lung cancer. Studies have shown that P3H4 is a key gene underlying the malignant progression of LUAD. A potential biomarker and therapeutic target, P3H4 is involved in various cancers, but its molecular mechanism in LUAD remains unclear. Based on a series of experiments, we found that it significantly promoted the metastasis and proliferation of LUAD in vivo and in vitro. Lung cancer is associated with the greatest number of cancer-related deaths worldwide. Lung adenocarcinoma (LUAD) accounts for 85% of all cases of lung cancer. Despite recent advances in treatment, the 5-year survival rate remains less than 15%. Thus, the diagnostic and therapeutic role of LUAD remain to be further studied. The prolyl 3-hydroxylase family member 4 (P3H4) is involved in various cancers, but little is known about its role in LUAD. Our study demonstrated that the P3H4 gene was upregulated in LUAD. Clinically, the expression of P3H4 was positively correlated with an advanced TNM stage and shorter survival. Functionally, P3H4 plays a significant role in the metastasis and proliferation of LUAD both in vitro and in vivo. Mechanistically, P3H4 might interact with EGFR to regulate the metabolic substances. Our study indicated that P3H4 is a critical gene in the malignant progression of LUAD and represents a potential biomarker and therapeutic target. [ABSTRACT FROM AUTHOR]