lncRNA-SNHG17 promotes colon adenocarcinoma progression and serves as a sponge for miR-375 to regulate CBX3 expression.

Long non-coding RNA (lncRNA) has been reported could regulate initiation and progression of colon adenocarcinoma (COAD) tumorigenesis in recent years. Small nucleolar RNA host gene 17 (SNHG17) was found play crucial roles in cancer progression but its role in COAD remains unclear. In this work, qRT-PCR was performed to detect SNHG17 expression level in COAD cell lines. Roles of SNHG17 on COAD cell behaviors were analyzed with gain and loss-of-function experiments. Luciferase activity assay, RNA pull-down assay, and RNA immunoprecipitant assay were performed to analyze the association of SNHG17 or chromobox 3 (CBX3) with microRNA-375 (miR-375). Effects of SNHG17 on miR-375/CBX3 axis were analyzed by rescue experiments. We showed SNHG17 was upregulated expression in COAD tissues and cells. Functionally, SNHG17 could promote COAD cell proliferation, colony formation, migration, and invasion in vitro. Further investigations showed SNHG17 serves as competing endogenous RNA (ceRNA) for miR-375 to regulate CBX3 expression. Additionally, we showed the roles of SNHG17 on COAD cell behaviors were exerted via miR-375/CBX3 axis. In conclusion, we demonstrated a novel SNHG17/miR-375/CBX3 triplets that participates in COAD progression, which may provide promising therapeutic targets for COAD.