Objective Angiogenesis plays a key role in the tumorigenesis and progression of colorectal cancer (CRC). In this study, we investigated the effect of long noncoding RNA (lncRNA) GAS5 on the angiogenesis, invasion, and metastasis of CRC, and the involvement of the Wnt/β‐catenin signaling pathway. Methods CRC tissues and adjacent normal tissues were collected from 52 patients with CRC. GAS5 expression was determined in vivo and in vitro by real‐time quantitative polymerase chain reaction (RT‐qPCR). Then RT‐qPCR and Western blot were used to identify expression of key genes of Wnt/β‐catenin signaling pathway. CRC cells with lowest GAS5 expression were selected and subjected to si‐GAS5, oe‐GAS5, or XAV939 to validate the effect of GAS5 and Wnt/β‐catenin signaling pathway on CRC cell activities. The activation of Wnt/β‐catenin signaling pathway was determined in response to GAS5. Subcutaneous tumor growth and microvascular density were observed in nude mice, in which in vivo metastasis was observed following tail vein injection of CRC cells. Results Initially, poor expression of GAS5 was observed in CRC tissues and cells. Upregulated GAS5 repressed CRC cell invasion and migration in vitro, as well as subcutaneous tumor growth, angiogenesis, and liver metastases in vivo. Furthermore, the Wnt/β‐catenin signaling pathway was determined to be activated in CRC tissues and cells, while its activation was inhibited by GAS5. The Wnt/β‐catenin signaling pathway promoted the CRC cell invasion and migration in vitro, subcutaneous tumor growth, angiogenesis and, liver metastases in vivo. Conclusion Taken together, the results of the study conclude that lncRNA GAS5 inhibited the activation of the Wnt/β‐catenin signaling pathway, thereby suppressing the angiogenesis, invasion, and metastasis of CRC.

BackgroundmicroRNAs (miRNAs) have been implicated to play crucial roles in carcinogenesis. miR‐1249‐3p was reported to be abnormally expressed in multiple human cancers. However, its biological role and the associated underlying mechanisms in hepatocellular carcinoma (HCC) remain largely unknown.Methods miR‐1249‐3p expression level in HCC cell lines and normal cell line was measured by quantitative real‐time PCR. Role of miR‐1249‐3p on HCC cell proliferation, colony formation, and invasion was examined by cell counting kit‐8 assay, colony formation assay, and transwell invasion assay, respectively. Luciferase activity reporter assay and western blot were performed to validate whether heterogeneous nuclear ribonucleoprotein K (HNRNPK) was a direct target of miR‐1249‐3p. Effect of miR‐1249‐3p on overall survival of HCC patients was analyzed at KM Plotter website.ResultsWe found miR‐1249‐3p expression level was increased, while HNRNPK expression level was decreased in HCC cell lines compared with normal cell line. Knockdown miR‐1249‐3p expression inhibits HCC cell proliferation, colony formation, and cell invasion through regulating HNRNPK in vitro. We also showed high miR‐1249‐3p expression was a predictor for poor overall survival of HCC patients.ConclusionsThese findings about miR‐1249‐3p/HNRNPK pair provide a novel therapeutic method for HCC patients.