IGF2BP3 Worsens Lung Cancer through Modifying Long Non-coding RNA CERS6-AS1/microRNA-1202 Axis

Abstract

Background: Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3) can epigenetically regulate lung cancer progression, but its regulatory mechanism in the disease lacks sufficient exploration. Objective: The study was conducted to probe the regulatory function of IGF2BP3 in lung cancer via modulating long non-coding RNA CERS6-AS1/microRNA-1202 (CERS6-AS1/miR-1202) axis. Methods: Clinical samples were collected to evaluate IGF2BP3, CERS6-AS1, miR-1202 and glycerophosphodiester phosphodiesterase domain containing 5 (GDPD5) levels. The interactions among IGF2BP3, CERS6-AS1, miR-1202 and GDPD5 were assessed. IGF2BP3-, CERS6-AS1-, and miR-1202-related vectors were transfected into lung cancer cells to determine cell biological functions. Cell tumor formation ability was further detected in vivo. Results: High expression of IGF2BP3, CERS6-AS1 and GDPD5, and low expression of miR-1202 levels were witnessed in lung cancer tissues. Suppression of IGF2BP3 restrained lung cancer progression. IGF2BP3 positively modulated CERS6-AS1 to regulate miR-1202-targeted GDPD5. Inhibition of CERS6-AS1 or promotion of miR-1202 depressed lung cancer aggravation. CERS6-AS1 silencing or miR-1202 overexpression reversed the impacts induced by IGF2BP3 on lung cancer. Conclusion: IGF2BP3 facilitates the development of lung cancer cells via binding to the CERS6-AS1 promoter and down-regulating miR-1202, which may be related to GDPD5 upregulation.