Background: Long intergenic non-protein coding RNA 239  (LINC00239 ) is an oncogenic long non-coding RNA in acute myeloid leukemia. We aimed to determine LINC00239  expression in colorectal cancer (CRC) and examine the influences of LINC00239  on tumor behaviors of CRC cells. Furthermore, the mechanism underlying the actions of LINC00239  in CRC was unveiled in detail.
Materials and Methods: Quantitative real-time polymerase chain reaction was used to detect LINC00239  expression in CRC tissues and cell lines. CRC cell proliferation, apoptosis, migration, and invasion were investigated by cell counting kit-8 assays, flow cytometry, and cell migration and invasion assays, respectively. Tumor xenograft experiments were performed to evaluate the tumor growth of CRC cells in vivo. The interactions among LINC00239 , microRNA-484 (miR-484), and kruppel-like factor 12  (KLF12 ) were analyzed by bioinformatics prediction, RNA immunoprecipitation and luciferase reporter assay.
Results: LINC00239  was upregulated in CRC tissues and cell lines. LINC00239  knockdown impaired CRC cell proliferation, migration, and invasion and promoted apoptosis in vitro. Additionally, LINC00239  deficiency inhibited CRC growth in vivo. Mechanistically, LINC00239  functioned as a competing endogenous RNA by directly sponging miR-484, thereby enhancing KLF12  expression. Rescue experiments further corroborated that miR-484 inhibition or KLF12  overexpression reversed the inhibitory actions of LINC00239  knockdown in CRC cells.
Conclusion: The LINC00239/miR-484/KLF12 pathway executed critical roles in CRC oncogenicity and may provide potential targets for CRC treatments.
Keywords: long intergenic non-protein coding RNA 239, kruppel-like factor 12, CRC, miRNA sponge