Long non-coding RNA HOTAIR as a competitive endogenous RNA to sponge miR-206 to promote colorectal cancer progression by activating CCL2.

Colorectal cancer (CRC) is one of the common malignant tumors, the incidence of which is on rise. LncHOTAIR, considered as an oncogene, contributed to the progression of a lot of cancers. However, the molecular mechanism and biological functions of the HOTAIR/miR-206/CCL2 axis have not been reported before. Here, our research aimed to explore HOTAIR/miR-206/CCL2 axis in CRC to demonstrate its role in predicting the poor prognosis of CRC. LncHOTAIR, miR-206 and CCL2 mRNA were detected in CRC tissues and cells by RT-PCR. The interactions among LncHOTAIR, miR-206 and CCL2 were explored by luciferase reporter assay, qRT-PCR, western blot and RNA interfere. Flow Cytometry Cell Analysis was performed to detect cell cycle and apoptosis as well as colony assay was prepared to test the cell proliferation. Immunohistochemical analysis was used to detect the CCL2 protein in CRC tissues. In our study, silence of LncHOTAIR by RNA interference could suppress the proliferation, migration and invasion of CRC cells. Mechanistically, LncHOTAIR downregulated miR-206 abundance which indicated that LncHOTAIR was considered as a competing endogenous RNA (ceRNA) by directly sponging miR-206 in CRC cells. In addition, further exploration suggested that miR-206 could inhibit the function of the downstream CCL2, the expression of which was repressed by LncHOTAIR/miR-206 signaling. Furthermore, we verified that the overexpression of CCL2 attenuated CRC cell proliferation, migration, invasion. Overall, this study firstly elucidated that LncHOTAIR played as oncogene in CRC via directly sponging miR-206 to activate the downstream CCL2, which would be considered as the novel therapeutic target in CRC.