Background
Pituitary adenoma (PA) is a common primary brain tumor with invasive properties. Despite that long noncoding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6) exerts oncogenic function in cancer cells and that miR-944 inhibits epithelial-mesenchymal transition (EMT) of cancer cells are well documented, few studies have explored the function and mechanism of SNHG6 and miR-944 in invasive pituitary adenoma (IPA). Materials and
Conclusions
This study authenticates that the SNHG6/miR-994/RAB11A axis plays a crucial role in regulating proliferation, migration, invasion, and EMT of IPA cells. SNHG6 and miR-994 can serve as novel valuable therapeutic targets for IPA.
Methods
Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expressions of SNHG6 and miR-944 in PA samples. Human PA cell line HP75 was used as a cell model. The biological effects of SNHG6 and miR-944 on HP75 cells were investigated with cell counting kit-8 (CCK-8) assay, Transwell assay, and scratch healing assay in vitro, respectively. Markers of EMT, including E-cadherin and vimentin, were detected by Western blot. Interactions between SNHG6 and miR-944, miR-944 and RAB11A were determined by bioinformatics analysis, qRT-PCR, and dual luciferase reporter assay.
Results
SNHG6 was significantly upregulated in IPA samples, whereas miR-944 was downregulated. SNHG6 markedly promoted viability, migration, invasion, and EMT of PA cells, whereas miR-944 transfection had the opposite effects. SNHG6 could downregulate miR-944, and there was a negative correlation between SNHG6 expression and miR-944 expression in IPA samples. Besides, it was confirmed that miR-944 could pair with the 3'-untranslated region of RAB11A and repress its expression. Conclusions: This study authenticates that the SNHG6/miR-994/RAB11A axis plays a crucial role in regulating proliferation, migration, invasion, and EMT of IPA cells. SNHG6 and miR-994 can serve as novel valuable therapeutic targets for IPA.