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

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 the 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 constructs 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.

Automated summary

IGF2BP3 promotes the development of lung cancer cells by binding to the CERS6-AS1 promoter and down-regulating miR-1202, potentially leading to the upregulation of GDPD5. High expression of IGF2BP3, CERS6-AS1, and GDPD5, as well as low expression of miR-1202, were observed in lung cancer tissues. Inhibition of IGF2BP3, CERS6-AS1 or promotion of miR-1202 could suppress lung cancer progression.