Epithelial-mesenchymal transition (EMT) has been shown to facilitate lung adenocarcinoma (LUAD) progress, and KLF13 inhibits tumor progression in various cancers. We intended to explore the mechanisms of KLF13 on EMT in LUAD. The biological functions (including cell viability, invasion, migration, and EMT) were checked using CCK-8, Transwell, and wound healing. The KLF13 and EMT markers levels were detected by immunohistochemistry. Interaction between KLF13 and TROAP promoter was probed by ChIP and dual luciferase reporter gene assay. The association between FBXW5 and KLF13 was verified by CoIP. RT-qPCR or Western blot was employed to check the expressions of FBXW5, KLF13, TROAP, and EMT markers. A xenograft tumor model was constructed to determine the growth of LUAD cells. KLF13 was lowly expressed in LUAD tissues and cells. KLF13 inhibited the invasion, migration, and EMT of LUAD cells. KLF13 suppressed TROAP transcription, and overexpression of TROAP reversed the inhibitory effect of KLF13 on the biological functions of LUAD cells. FBXW5 promoted KLF13 ubiquitinated degradation, and the knockdown of FBXW5 promoted KLF13 to inhibit LUAD cell progression. FBXW5 promoted KLF13 ubiquitinated degradation, which downregulated KLF13 to increase TROAP transcription, thereby facilitating EMT in LUAD.
Keywords: EMT; FBXW5; KLF13; LUAD; TROAP.
© 2025 Wiley Periodicals LLC.