Effects Of LncRNA-HOTAIR On Proliferation, Invasion And Radiosensitivity In Colorectal Cancer CCL244 Cells

Objective: To explore the effects of LncRNA-HOTAIR on proliferation, invasion, apoptosis and radiosensitivity in colorectal cancer CCL244 cells.Methods: The expression level of HOTAIR in 53 pairs of human CRC and adjacent noncancerous tissues were performed by real time RT-PCR. The expression level of HOTAIR in 5 cell lines including one normal colonic mucosal cell line(FHC) and 4 CRC cell lines(HCT116, CCL244, SW480, DLD-1) was determined by real time RT-PCR. CCL244 cells were transfected with siRNA against HOTAIR and the silencing of HOTAIR expression were detected by real time RT-PCR. MTT assay, colony-formation assay and cell cycle progression analysis were performed to further explore the role of HOTAIR silencing in CRC cell proliferation. Transwell matrigel invasion and wound healing assays were performed to further explore the participation of HOTAIR knockdown in CRC cell metastasis. Clonogenic survival assay was performed to explore the influence of HOTAIR knockdown on radiosensitivity of CCL244 CRC cells. Flow cytometry was used to detect the percentage of apoptotic cells in HOTAIR silencing CCL244 cells with or without irradiation. Western blot was performed to detect the expression of MMP2, MMP9 Bax and Bcl-2.Results: HOTAIR was highly expressed in 53 CRC tissues compared to their non-tumorous counterparts. The expression of HOTAIR in HCT116, CCL244, SW480 and DLD-1 cells was higher than that in FHC cells. HOTAIR silencing inhibited the proliferation, migration and invasion while promoted radiation-induced apoptosis and radiosensitivity of CRC CCL244 cells. Knock-down of HOTAIR inhibited the expression of anti-apoptotic protein Bcl-2 and promoted the expression of pro-apoptotic protein Bax. HOTAIR knockdown inhibited the expression level of MMP2 and MMP9.Conclusion: HOTAIR is over-expressed in CRC and HOTAIR silencing inhibits the proliferation and enhances the radiosensitivity in CCL244 cells.