Lnc-SNHG1 Activates the TGFBR2/SMAD3 and RAB11A/Wnt/β-Catenin Pathway by Sponging MiR-302/372/373/520 in Invasive Pituitary Tumors.

Background/Aims: Long noncoding RNAs (IncRNAs) are critical regulators in various diseases including human cancer and could function as competing endogenous RNAs (ceRNAs) to regulate microRNAs (miRNAs). Methods: Quantitative real-time PCR (qRT-PCR) was used to analyze the expression of Inc-SNHG1 and miR-302/372/373/520 in pituitary tumor tissues and cell lines. Cell proliferation was investigated using MTT and cell count assays. The mechanisms by which Inc-SNHG1 affects pituitary tumor progression were investigated using Western blot assays, transwell migration assays, immunohistochemistry, immunofluorescence, luciferase reporter assays, tumor xenografts, and flow cytometry. Results: We found that Inc-SNHG1 was overexpressed in invasive pituitary tumor tissues and cell lines. Ectopic expression of Inc-SNHG1 promoted cell proliferation, migration, and invasion, as well as the epithelial-mesenchymal transition (EMT), by affecting the cell cycle and cell apoptosis in vitro and tumor growth in vivo. Further study indicated that overexpression of Inc-SNHG1 markedly inhibited the expression of miR-302/372/373/520 (miRNA-pool) which is down-regulated in invasive pituitary tumor cells. Moreover, overexpression of Inc-SNHG1 significantly promoted the expression of TGFBR2 and RAB11A, the direct targets of miR-302/372/373/520. Finally, Inc-SNHG1 activates the TGFBR2/SMAD3 and RAB11A/Wnt/beta-catenin pathways in pituitary tumor cells via sponging miR-302/372/373/520. Conclusions: Our data suggest that Inc-SNHG1 promotes the progression of pituitary tumors and is a potential therapeutic target for invasive pituitary tumor. (C) 2018 The Author(s) Published by S Karger AG, Basel