Alkaline phosphatase downregulation promotes lung adenocarcinoma metastasis via the c-Myc/RhoA axis

Abstract Background Lung adenocarcinoma (LUAD) metastasis significantly reduces patient survival; hence inhibiting the metastatic ability of lung cancer cells will greatly prolong survival. Alkaline phosphatase (ALPL), a homodimeric cell surface phosphohydrolase, is reported to play controversial role in prostate and ovarian migration; however, function ALPL LUAD related mechanisms remain unclear. Methods TCGA database was used analysis expression ALPL, further verification performed cohort 36 samples by qPCR western blot. Soft-agar assay, transwell assay were employed detect progression. The qPCR, luciferase promoter reporter blot clarify molecular promoting LUAD. Results downregulated LUAD, disease-free survival rate patients with low reduced. Further studies showed that overexpression lines did not affect proliferation, but it attenuate mouse model. downregulation led decrease amount phosphorylated (p)-ERK. Because p-ERK promotes classical c-Myc degradation pathway, accumulation therefore an increase RhoA transcription, which enhanced metastasis. Conclusion specially inhibits affecting p-ERK/c-Myc/RhoA axis, providing theoretical basis for targeted therapy clinical