Long non-coding RNAs (lncRNAs) play critical functions in various
cancers. Firre intergenic repeating
RNA element (FIRRE), a
lncRNA located in the nucleus, was overexpressed in
colorectal cancer (CRC). However, the detailed mechanism of FIRRE in CRC remains elusive. Results of RNA sequence and qPCR illustrated overexpression of FIRRE in CRC cell lines and tissues. The aberrant expression of FIRRE was correlated with the migration, invasion, and proliferation in cell lines. In accordance, it was also associated with
lymphatic metastasis and distant
metastasis in patients with CRC. FIRRE was identified to physically interact with
Polypyrimidine tract-binding protein (PTBP1) by
RNA pull-down and
RNA immunoprecipitation (RIP). Overexpression of FIRRE induced the translocation of PTBP1 from nucleus to cytoplasm, which was displayed by immunofluorescence and western blot. In turn, delocalization of FIRRE from nucleus to cytoplasm is observed after the loss of PTBP1. The
RNA-
protein complex in the cytoplasm directly bound to BECN1
mRNA, and the binding site was at the 3' end of the
mRNA. Cells with FIRRE and PTBP1 depletion alone or in combination were treated by
Actinomycin D (ACD). Results of qPCR showed FIRRE stabilized BECN1
mRNA in a PTBP1-medieated manner. In addition, FIRRE contributed to autophagy activity. These findings indicate FIRRE acts as an oncogenic factor in CRC, which induces
tumor development through stabilizing BECN1
mRNA and facilitating autophagy in a PTBP1-mediated manner.