LINC00365 promotes colorectal cancer cell progression through the Wnt/β‐catenin signaling pathway

In the past decade, substantial evidence established that long noncoding RNAs are serious about mediating the evolution of malignancies. In previous studies, LINC00365, which has not been reported in colorectal cancer (CRC), was selected using the bioinformatics analysis in GSE109454 and GSE41655 data sets. However, the function and mechanism of LINC00365 are still obscure. In our study, LINC00365 was found upregulated in CRC specimens and intimately connected with the prognosis of patients with CRC. In addition, LINC00365 overexpression enhances the cell abilities of proliferation, migration, and invasion in vitro. Meanwhile, mechanistic studies showed that LINC00365 might involve in CRC cell progression by mediating the Wnt/β‐catenin pathway. Furthermore, LINC00365 upregulation increased CDK1 protein expression. In conclusion, this study suggests that LINC00365 acts as a vital part in facilitating CRC progression and might play as a therapeutic target for patients with CRC. In this study, we identified LINC00365 was upregulated in colorectal cancer (CRC) and it might promote CRC cell progression via Wnt/β‐catenin signaling pathway. Our study indicated that LINC00365 played a cruial role as an oncogenes and promoted tumor progression, and it might serve as a potential therapeutic target for CRC.