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The long noncoding RNA (lncRNA)  LUCAT1  was recently reported to be upregulated and to play an essential role in multiple cancer types, especially colorectal cancer (CRC), but the molecular mechanisms of  LUCAT1  in CRC are mostly unreported. Here, a systematic analysis of  LUACT1  expression is performed with data from TCGA database and clinic CRC samples.  LUCAT1  is identified as a putative oncogene, which is significantly upregulated in CRC and is associated with poor prognosis. Loss of  LUCAT1  restricts CRC proliferative capacities in vitro and in vivo. Mechanically, NCL is identified as the protein binding partner of  LUCAT1  by using chromatin isolation by RNA purification coupled with mass spectrometry (ChIRP-MS) and RNA immunoprecipitation assays. We also show that NCL directly binds to  LUCAT1  via its putative G-quadruplex-forming regions from nucleotides 717 to 746. The interaction between  LUCAT1  and NCL interferes NCL-mediated inhibition of MYC and promote the expression of MYC. Cells lacking  LUCAT1  show a decreased MYC expression, and NCL knockdown rescue  LUCAT1  depletion-induced inhibition of CRC cell proliferation and MYC expression. Our results suggest that  LUCAT1  plays a critical role in CRC cell proliferation by inhibiting the function of NCL via its G-quadruplex structure and may serve as a new prognostic biomarker and effective therapeutic target for CRC.

The long noncoding RNA LUCAT1 promotes colorectal cancer cell proliferation by antagonizing Nucleolin to regulate MYC expression