Disrupting of IGF2BP3-stabilized HK2 mRNA by MYO16-AS1 competitively binding impairs LUAD migration and invasion

Abstract

Since invasive cancer is associated with poor clinical outcomes, exploring the molecular mechanism underlying LUAD progression is crucial to improve the prognosis of patients with advanced disease. Herein, we found that MYO16-AS1 is expressed mainly in lung tissue but is notably downregulated in LUAD tissues. Overexpression of MYO16-AS1 inhibited the migration and invasion of LUAD cells. Mechanistic studies indicated that H3 K27Ac modification mediated MYO16-AS1 transcription. Furthermore, we found that MYO16-AS1 competitively bound to the IGF2BP3 protein and in turn reduced IGF2BP3 protein binding to HK2 mRNA, decreasing HK2 mRNA stability and inhibiting glucose metabolism reprogramming and LUAD cell invasion in vitro and in vivo. The finding that the MYO16-AS1/IGF2BP3-mediated glucose metabolism reprogramming mechanism regulates HK2 expression provides novel insight into the process of LUAD invasion and suggests that MYO16-AS1 may be a therapeutic target for LUAD.

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