Conclusions
MALAT1 knockdown depleted migration and invasion by inhibiting autophagy through MALAT1/miR-384/GOLM1 axis in glioma in vitro and in vivo. The MALAT1/miR-384/GOLM1 axis was first proposed in our report, enriching the action mechanism of MALAT1 in glioma.
Methods
The expression of MALAT1, microRNA-384 (miR-384) and Golgi membrane protein 1 (GOLM1) was detected by quantitative Real-time polymerase chain reaction (qRT-PCR). The protein levels of GOLM1, light chain3 (LC3-II/LC3-I), p62, Vimentin and E-cadherin were proved by Western blot. Cell migration and invasion were monitored using the transwell assay. Bioinformatics tool starBase was used to predict target genes and associated binding sites. RNA immunoprecipitation assay (RIP) and dual-luciferase reporter assay were utilized to verify the relationship between miR-384 and MALAT1 or GOLM1. Tumor formation analysis in nude mice was conducted to ascertain the role of MALAT1 in vivo.
Objective
Glioma is characterized by high metastasis with poor outcomes. Long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) was well-explored in numerous human cancers, including glioma. This study aimed to provide a novel action mechanism of MALAT1 in glioma. Materials and
Results
MALAT1 was highly expressed in glioma tissues and cells. MALAT1 knockdown inhibited autophagy, migration and invasion of glioma cells. MiR-384 was a target of MALAT1, and miR-384 inhibition reversed the effects of MALAT1 knockdown in glioma cells. GOLM1 was a target of miR-384, and miR-384 inhibition eliminated the function of GOLM1 downregulation in glioma cells. In addition, GOLM1 was regulated by MALAT1 through miR-384. Moreover, MALAT1 knockdown blocked tumor growth and development in vivo. Conclusions: MALAT1 knockdown depleted migration and invasion by inhibiting autophagy through MALAT1/miR-384/GOLM1 axis in glioma in vitro and in vivo. The MALAT1/miR-384/GOLM1 axis was first proposed in our report, enriching the action mechanism of MALAT1 in glioma.