Background:Increasing evidence proves that long non-coding RNAs (lncRNAs) play a
key role in the occurrence and development of colorectal cancer. However, the function and
molecular mechanism of LINC01836 in CRC are still unknown.Methods:The differentially expressed lncRNAs in colorectal cancer were obtained from the RNA
sequencing data. The effects of LINC01836 on colorectal cancer cells were tested in in vitro
experiments. The mechanism of LINC01836 action was investigated through western blot, RNA
immunoprecipitation assay and luciferase reporter assay. Moreover, the xenograft mouse model
was conducted to examine the effects of LINC01836 in vivo.Results:In this study, we showed that LINC01836 was significantly elevated in colorectal cancer
tissues and cells. Elevated LINC01836 expression significantly correlated with larger tumor size,
positive lymph node metastasis, distant metastasis, advanced tumor-node-metastasis (TNM) stage,
and poor prognosis. Furthermore, decreased expression of LINC01836 repressed proliferation,
migration, and invasion in vitro and vivo, and high LINC01836 expression displayed the opposite
effect. Further analysis revealed that LINC01836 could regulate the expression of SLC17A9 by
competing with miR-‐1226-3p. Furthermore, down-regulation of LINC01836 or increased
expression of miR-‐1226-3p markedly reversed the effects of SLC17A9 overexpression on
colorectal cancer cells.Conclusion:This study showed that LINC01836 regulated the expression of SLC17A9 through
sponge miR-1226-3p by acting as a competitive endogenous RNA (ceRNA), promoted the
progression of colorectal cancer, and suggested a new prognostic biomarker and potential cancer
treatment target for colorectal cancer.