Background
Long non-coding RNAs are reportedly endowed with the function of promoting or inhibiting cancer occurrence and development. The emphasis of this study was placed on the effect of lncRNA HLA complex group 11 (HCG11) on glioma progression, as well as its mechanism.
Conclusions
HCG11 suppresses glioma cells proliferation and migration through regulating the miR-590-3p/CADM2 molecular axis.
Methods
Quantitative real-time polymerase chain reaction was utilized for detecting HCG11, miR-590-3p, and CAMD2 mRNA expression levels in glioma tissues. Western blot was adopted to examine cell adhesion molecule (CADM2) protein expression. Cell counting kit-8, BrdU, Transwell and wound healing assays were employed for investigating the malignant biological behaviors of glioma cells. RNA immunoprecipitation assay and dual-luciferase reporter assay were performed to prove the relationship between miR-590-3p and HCG11, as well as CADM2 and miR-590-3p.
Results
HCG11 expression was lower in glioma tissues compared with that in paracancerous tissues, and its expression level was negatively correlated with WHO tumor stage. In addition, compared with in astrocyte cell line, the expression of HCG11 was lower in glioma cells. Functional experiments showed that HCG11 inhibited glioma cells migration and proliferation, while miR-590-3p facilitated these processes. Acting as a competitive endogenous RNA, HCG11 adsorbed miR-590-3p and upregulated the expression of CADM2, the target gene of miR-590-3p. Conclusions: HCG11 suppresses glioma cells proliferation and migration through regulating the miR-590-3p/CADM2 molecular axis.