Abstract
Long non-coding RNAs (lncRNAs) have been linked to tumorigenesis. However, the role of LINC01210 in colorectal cancer (CRC) remains unclear. Relative levels of LINC01210 in CRC tissues and adjacent tissues were determined. Proliferative, migratory, and invasive abilities were examined in HCT116 cells and LoVo cells after silencing or overexpressing LINC01210. The interaction between LINC01210 and SRSF3 was explored by ChIP-PCR. Upregulated LINC01210 was associated with metastasis and advanced stage of CRC. Silencing LINC01210 attenuated proliferative, migratory, and invasive abilities in LoVo cells, while overexpressing LINC01210 promoted proliferative, migratory, and invasive abilities in HCT116 cells. Mechanism study revealed that LINC01210 increased the expression of SRSF3 by recruiting mixed lineage leukaemia protein-1, which upregulated the trimethylation of H3K4 me3 on SRSF3 promoter. Silencing SRSF3 reversed the effects of LINC01210 on CRC cells. In conclusions, LINC01210 accelerated proliferation and invasion in CRC cells through epigenetically upregulating SRSF3, and may be a potential therapeutic target for CRC treatment.