TPI1 promotes MAPK/ERK‐induced EMT, cell migration and invasion in lung adenocarcinoma

Abstract

AbstractBackgroundTriosephosphate isomerase 1 (TPI1), as a widely involved glycolytic enzyme, plays a significant role in glucose metabolism and is highly expressed in various tumors. However, its role in lung adenocarcinoma (LUAD) remains incompletely understood.MethodsThrough bioinformatic analysis, we identified a positive association between high expression of TPI1 and metastasis in LUAD. Western blot, RT‐qPCR, wound healing assays and transwell experiments, were employed to investigate potential mechanisms.ResultsIn this study, bioinformatic analysis showed that high expression of TPI1 was associated with poor prognosis in LUAD patients. We examined the expression of TPI1 in 29 paired LUAD tissues and found that TPI1 expression was higher in LUAD tissues than in paired adjacent noncancerous tissues. Meanwhile, overexpression of TPI1 promoted the epithelial‐mesenchymal transition (EMT) process in LUAD cells, while silencing TPI1 weakened the EMT process. Furthermore, TPI1 was shown to regulate EMT through the MAPK/ERK signaling pathway.ConclusionTPI1 promotes LUAD metastasis by activating the MAPK/ERK signaling pathway.