The long noncoding RNA(lncRNA) small nucleolar RNA host gene 3(SNHG3) has been reported to be upregulated in colorectal cancer (CRC). However, its biological role and underlying mechanisms in CRC have not been well studied. The expression levels of SNHG3 were measured in CRC tissues and cell lines by real time quantitative PCR. Functional assays, including the cell counting Kit-8, wound healing and transwell invasion assays, were used to determine the effect of SNHG3 on CRC cell proliferation, migration and invasion,respectively. Furthermore, bioinformatics analysis, dual-Luciferase reporter assays and RNA immunoprecipitation were applied to determine the mechanism of SNHG3 in CRC. Mice xenograft models were established to assess the role of SNHG3 in CRC tumorigenicity and metastasis in vivo.The expression of SNHG3 was significantly upregulated in CRC tissues compared to adjacent normal tissues, which was positively correlated with advanced clinical stage, distant metastasis and poor overall survival. Functional experiments revealed that SNHG3 knockdown significantly decreased CRC growth and metastasis both in vitro and in vivo. Mechanistically, SNHG3 could bind to miR-539, thereby up-regulating the expression of its target gene runt-related transcription factor 2 (RUNX2), and play an oncogenic role in CRC progression. Our works suggest that lncRNA SNHG3 promotes CRC growth and metastasis via regulating miR-539/RUNX2 axis, suggesting that the SNHG3 might be a potential therapeutic target for CRC.