Colorectal cancer (CRC) is one of the most lethal human cancers all over the world. Moreover, it ranks fourth for cancer-related deaths among males. Although many efforts have been made to cure CRC, the effect remains limited. It has been reported that lncRNA five prime to Xist (FTX) was upregulated in CRC. However, the mechanism by which lncRNA FTX regulates the progression of CRC remains largely unknown. In this study, qRT-PCR was performed to detect the expression of FTX, miR-590-5p and Recombination signal binding protein for immunoglobulin kappa J region (RBPJ) in CRC tissues or cells. Protein expression in cells was measured by western blot. MTT assay was used to test the cell viability. Moreover, tran... More
Colorectal cancer (CRC) is one of the most lethal human cancers all over the world. Moreover, it ranks fourth for cancer-related deaths among males. Although many efforts have been made to cure CRC, the effect remains limited. It has been reported that lncRNA five prime to Xist (FTX) was upregulated in CRC. However, the mechanism by which lncRNA FTX regulates the progression of CRC remains largely unknown. In this study, qRT-PCR was performed to detect the expression of FTX, miR-590-5p and Recombination signal binding protein for immunoglobulin kappa J region (RBPJ) in CRC tissues or cells. Protein expression in cells was measured by western blot. MTT assay was used to test the cell viability. Moreover, transwell was performed to examine the cell migration and invasion. Luciferase report assay was performed to verify the relation between miR-590-5p and FTX or RBPJ. It was found that FTX was upregulated in CRC tissues and cells. Knockdown of FTX or overexpression of miR-590-5p can inhibit the proliferation, migration, and invasion of CRC cells. Besides, silencing of FTX could inhibit the expression of migration and invasion-related proteins in CRC cells. Meanwhile, miR-590-5p was the target of FTX, and RBPJ was the direct target of miR-590-5p. Inhibition of miR-590-5p could reverse the inhibitory effect of FTX on the progression of CRC. These findings suggested that knockdown of FTX could inhibit the tumorigenesis of CRC in vitro, which may serve as a potential novel strategy for treatment of CRC.
