is activated by and promotes lung adenocarcinoma development via the Wnt pathway.

Background: The effects and mechanism of 6-pyruvoyl-tetrahydropterin synthase () on lung adenocarcinoma (LUAD) were studied in LUAD cells and mice with subcutaneously transplanted tumors.

Methods: level in tissues and cells was tested by immunohistochemistry, western blot, and quantitative real-time polymerase chain reaction (qRT-PCR). The impacts of on cell viability, proliferation, apoptosis, invasion, and migration were determined by Cell Counting Kit-8 (CCK-8), colony formation assay, flow cytometry, transwell assay, and wound healing assay, respectively. The Cancer Genome Atlas (TCGA) analysis and dual luciferase assay were conducted to predict and verify the relationship between and activating transcription factor 4 (). A mouse model was established by subcutaneous injection with cancer cells. Tumor volume was calculated as V = ab/2. Ki67 and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining were used to measure cell proliferation and apoptosis in tumors.

Results: was highly expressed in LUAD. Higher level was correlated with late clinical stages and poor survival of patients. Down-regulation of PTS inhibited the viability and proliferation and induced apoptosis of LUAD cells. was activated by , and up-regulation of reversed the inhibitory effect of silencing on LUAD cells. Silencing of inhibited the Wnt pathway. Down-regulation of inhibited tumor growth in mice.

Conclusions: was highly expressed in LUAD. PTS was activated by and promoted LUAD development via the Wnt pathway.