Colorectal Cancer

LINC00239[LncRNA]

miR-484[miRNA]

KLF12[mRNA]

Colorectal Cancer cells

Homo sapiens (human)

Onco Targets Ther. 2020 Nov 23;13:12067-12081. doi: 10.2147/OTT.S278582. eCollection 2020.

Long Non-Coding RNA LINC00239 Functions as a Competitive Endogenous RNA by Sponging microRNA-484 and Enhancing KLF12 Expression to Promote the Oncogenicity of Colorectal Cancer.

Cell migration and invasion assay;RNA immunoprecipitation;Flow Cytometry assay;Luciferase reporter assay;RNA immunoprecipitation;

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.