Abstract
ABSTRACT Lung squamous cell carcinoma (LUSC) is a subtype of non-small cell lung cancer with poor prognosis. This study aimed to explore the role of KDM2B in the development of LUSC. The results of this study demonstrated that KDM2B was upregulated in LUSC tissues and cell lines. Knockdown of KDM2B reduced cell viability and colony forming ability in SK-MES-1 and NCI-H520 cells. KDM2B inhibition reduced glucose consumption, lactate production, ATP level, and also downregulated the expression of LDHA and GLUT1. KDM2B knockdown decreased the protein expression of LC3-I and p62, and increased LC3-II and Beclin-1. Furthermore, KDM2B silencing inhibited the phosphorylation of AKT, mTOR and P70S6K. KDM2B knockdown led to reduced tumor size in mouse model. In conclusion, KDM2B is upregulated in LUSC tissues and cell lines. KDM2B silencing inhibits glycolysis and promotes autophagy through inactivation of the PI3K/Akt/mTOR signaling pathway.
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