Long non-coding RNAs (lncRNAs) have appeared as vital regulatory factors in different pathological processes, particularly in tumorigenesis. Increasing number of evidence has demonstrated that long intergenic non-coding RNA 00662 (LINC00662) is overexpressed in several types of cancers and promotes cancer initiation and development. However, whether LINC00662 participates in colorectal cancer (CRC) remains unclear. This study was aimed to explore the expression, biological function and regulatory mechanism of LINC00662 in CRC. Here, we found that LINC00662 expression was obviously upregulated in CRC tissues and cell lines. Down-regulation of LINC00662 dramatically inhibited the growth of CRC cells and increased CRC cell apoptosis.MicroRNA-145 (miR-145) was speculated as a target miRNA of LINC00662 by bioinformatics analysis. Luciferase reporter assays and RNA pull-down assays verified that LINC00662 directly interacted with miR-145. Expression of miR-145 was downregulated in CRC tissues and cell lines. Up-regulation of miR-145suppressed cell growth and promoted apoptosis in CRC cells. Suppression of miR-145markedly reversed the suppressive function of LINC00662 knockdown on CRC cell growth. In addition, c-myc was confirmed as a target gene of miR-145 in CRC cells.  Recover of c-myc expression partially reversed suppression effect mediated by LINC00662 downexpression or miR-145overexpressionon CRC cell growth. Taken together, our results indicate that LINC00662lead to the malignant behavior of CRC cells by upregulating c-myc via sponging miR-145, underlining the essential role of the LINC00662/miR-145/c-myc axis in regulating the growth of CRC cells.

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