LINC00707 promotes cell proliferation and invasion of colorectal cancer via miR-206/FMNL2 axis.

Abstract

Long non-coding RNAs (lncRNAs) have been verified to participate in the regulation of colorectal cancer (CRC). However, the role of LINC00707 in CRC still remains unknown. Here, we aim to study the role of LINC00707 in CRC. LINC00707 expression in 97 pairs of CRC tissues and adjacent normal tissues was determined by the quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). LINC00707 overexpression or knockdown in SW620 or HCT116 cells was achieved by lentivirus transfection. The proliferation and cell circle progression of established cells were detected by cell counting kit-8 (CCK-8) assay and flow cytometry, respectively. Cell invasion and migration abilities were studied by transwell assay. Dual-luciferase assay and Western blot was used to verify the underlying mechanism of LINC00707 in CRC. Nude mice were obtained to identify the in vivo function of LINC00707 in CRC. LINC00707 was significantly over-expressed in CRC tissues and cell lines. Up-regulation of LINC00707 promoted cell proliferation, cell cycle progression, invasion, and migration of SW620 cells. Conversely, down-regulation of LINC00707 reduced cell growth and metastasis of HCT116 cells. MiR-206 was verified as a direct target of LINC00707, and its function was inhibited by LINC00707. FMNL2 was a target for miR-206 in CRC cells. Meanwhile, LINC00707 promoted tumor growth of CRC in vivo. LINC00707 was up-regulated in CRC tissues and cells, which promoted cell proliferation and metastasis via sponging miR-206 to increase FMNL2 expression. This might provide a novel target for the biological treatment of CRC.