Peptidyl-prolyl isomerase F as a prognostic biomarker associated with immune infiltrates and mitophagy in lung adenocarcinoma.

BACKGROUND

Lung adenocarcinoma (LUAD) is among the most prevalent malignancies worldwide, with unfavorable treatment outcomes. Peptidyl-prolyl isomerase F () is known to influence the malignancy traits of tumor progression by modulating the bioenergetics and mitochondrial permeability in cancer cells; however, its role in LUAD remains unclear. Our study seeks to investigate the clinical significance, tumor proliferation, and immune regulatory functions of in LUAD.

METHODS

The expression of in LUAD tissues and cells was assessed using bioinformatics analysis, immunohistochemistry (IHC), and Western blotting. Survival curve analysis was conducted to examine the prognostic association between expression and LUAD. The immunomodulatory role of in LUAD was assessed through the analysis of expression and immune cell infiltration. A series of gain- and loss-of-function experiments were conducted on to investigate its biological functions in LUAD both and . The mechanisms underlying 's effects on LUAD were delineated through functional enrichment analysis and Western blotting assays.

RESULTS

exhibited overexpression in LUAD tissues compared to normal controls. Survival curve analysis revealed that patients with LUAD exhibiting higher expression demonstrated decreased overall survival and a shorter progression-free interval. was implicated in modulating immune cell infiltration, particularly in regulating the T helper 1-T helper 2 cell balance. Functionally, was discovered to promote tumor cell proliferation and advance cell-cycle progression. Furthermore, could impede mitophagy by targeting the FOXO3a/PINK1-Parkin signaling pathway.

CONCLUSIONS

The findings of this study indicate that the prognosis-related gene may have a significant role in the regulation of LUAD cell proliferation, tumor-associated immune cell infiltration, and mitophagy, and thus may be a promising therapeutic target of LUAD.