LncRNA CCAT1 Promotes Colorectal Cancer Tumorigenesis Via A miR-181b-5p/TUSC3 Axis.

AIM

The aim was to determine the function and molecular mechanism of long non-coding RNA colon cancer associated transcript-1(lncRNA CCAT1) in the development of colorectal cancer (CRC).

METHODS

CCAT1 mRNA expression levels were determined in CRC tissues and cells using reverse transcription-quantitative polymerase chain reaction. Cell Counting Kit-8 and colony formation assays were used to examine the effects of CCAT1 on the proliferation of CRC cells. Luciferase reporter gene analysis was used to confirm the target gene of microRNA-181b-5p (miR-181b-5p) in CRC cells. Tumor xenografts were subsequently used to investigate the role of CCAT1 in CRC growth in vivo.

RESULTS

The relative mRNA expression levels of CCAT1 were significantly higher in CRC tissues and cell lines compared with the normal tissues or cells. CCAT1 knockdown significantly inhibited CRC cell proliferation in vitro and in vivo. Bioinformatics and luciferase reporter assays showed that miR-181b-5p was a direct target of CCAT1, and the expression of miR-181b-5p was negatively correlated with the expression of CCAT1 in CRC tissues. Furthermore, CCAT1 positively regulated the level of tumor suppressor candidate 3 (TUSC3) by competing with miR-181b-5p in CRC cells.

CONCLUSION

These data suggested that lncRNA CCAT1 promoted colorectal cancer tumorigenesis via a miR-181b-5p/TUSC3 axis.