ADPGK-AS1 promotes the progression of colorectal cancer via sponging miR-525 to upregulate FUT1.

OBJECTIVE

We sought to uncover the potential role of long non-coding RNA (lncRNA) ADPGK-AS1 in colorectal cancer (CRC).

PATIENTS AND METHODS

ADPGK-AS1 levels in 58 pairs of CRC tissues and paracancerous tissues and 30 normal colorectal tissues were determined. The in vitro level of ADPGK-AS1 in CRC cell lines was tested as well. The regulatory effects of ADPGK-AS1 on the proliferative, migratory, and invasive properties of HCT116 and SW480 cells were assessed. Using a Dual-Luciferase reporter gene assay, the interaction among ADPGK-AS1/miR-525/FUT1 was identified. Finally, potential influences of the regulatory loop ADPGK-AS1/miR-525/FUT1 on the phenotypes of CRC cells were explored.

RESULTS

ADPGK-AS1 was upregulated in CRC tissues and cells. Knockdown of ADPGK-AS1 attenuated the proliferative, migratory, and invasive abilities of CRC cells. Meanwhile, miR-525 was confirmed to be the target of ADPGK-AS1 and FUT1 was the downstream gene binding miR-525. The regulatory loop ADPGK-AS1/miR-525/FUT1 was found to aggravate the malignant progression of CRC.

CONCLUSIONS

ADPGK-AS1 is upregulated in CRC. The regulatory loop ADPGK-AS1/miR-525/FUT1 exacerbates the progression of CRC by promoting the proliferation, migration, and invasion of tumor cells.