Long noncoding RNAs (lncRNA) have been implicated in variety human cancer but their mechanisms of function are mainly undocumented. In the present study, we investigated lncRNAs alteration that contributed to colorectal cancer (CRC) by utilizing TCGA RNA sequencing data and other publicly available lncRNAs expression profiling data. Here, We screened out the CRC-associated lncRNA LL22NC03-N64E9.1, a key regulator of CRC development and progression. We also revealed that knockdown of LL22NC03-N64E9.1 inhibited cell proliferation, colony formation, tumorigenicity and apoptosis promotion, both in vitro and in vivo. Mechanistically, LL22NC03-N64E9.1 repressed underlying target gene KLF2 transcription through binding to EZH2. Furthermore, rescue experiments revealed that LL22NC03-N64E9.1 oncogenic function may partially depend on repressing KLF2. Taken together, our results suggested that LL22NC03-N64E9.1 confered an oncogenic function in human CRC and may serve as a candidate prognostic biomarker and target for new therapies in this deadly disease.
Keywords: KLF2; LL22NC03-N64E9.1; colorectal cancer; lncRNA; proliferation.