Long non-coding RNA MIR22HG inhibits the proliferation and migration, and promotes apoptosis by targeting microRNA-9-3p/ SOCS1 axis in small cell lung cancer cells

Background: This study aims to determine the role of long non-coding RNA (LncRNA) MIR22HG in small cell lung cancer (SCLC), and to explore its relevant mechanism.

Methods and results: The expressions of genes and proteins in SCLC cells were examined applying qRT-PCR and western blot. Cell proliferation estimation was implemented utilizing cell counting kit-8 (CCK-8) and colony formation assays; the assessment of cell migration and invasion was operated employing Wound healing and Transwell; apoptosis evaluation was conducted adopting flow cytometric assay. Binding relationships was confirmed by luciferase reporter assay. Moreover, SCLC animal model was established to explore the role of MIR22HG in vivo. It was found that MIR22HG was declined and miR-9-3p was elevated in five SCLC cell lines (NCI-H446, NCI-H69, SHP-77, DMS79 and NCI-H345) in comparison with normal human bronchial epithelial cell line (NHBE). More interestingly, overexpression of MIR22HG resulted in decreased cell viability, declined colony formation, diminished capacities of cell migration and invasion in NCI-H446 and NCI-H345 cells but induced more apoptotic cells. However, these impacts were reversed by miR-9-3p upregulation. Meanwhile, MIR22HG could bind to miR-9-3p and negatively regulate its expression in SCLC. What's more, LncRNA MIR22HG overexpression was also testified to elevate SOCS1 via downregulating miR-9-3p expression. Furthermore, in vivo study further confirmed the role of MIR22HG/miR-9-3p in tumor regulation of SCLC.

Conclusions: In conclusion, MIR22HG in SCLC was found to modulate miR-9-3p level and might act as a possible biomarker for SCLC treatment.