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One of the primary mechanisms of post-transcriptional gene regulation is the modulation of RNA stability. We recently discovered that  LINC00675 , a transcript annotated as a long noncoding RNA (lncRNA), is transcriptionally regulated by FOXA1 and encodes a highly conserved small protein that localizes to the endoplasmic reticulum, hence renamed as  FORCP  (FOXA1-regulated conserved small protein). Here, we show that the endogenous  FORCP  transcript is rapidly degraded and rendered unstable as a result of 3’UTR-mediated degradation. Surprisingly, although the  FORCP  transcript is a canonical nonsense-mediated decay (NMD) and microRNA (miRNA) target, we found that it is not degraded by NMD or miRNAs. Targeted deletion of an evolutionarily conserved region in the  FORCP  3’UTR using CRISPR/Cas9 significantly increased the stability of the  FORCP  transcript. Interestingly, this region requires the presence of an immediate downstream 55-nt-long sequence for transcript stability regulation. Functionally, colorectal cancer cells lacking this conserved region expressed from the endogenous  FORCP  locus displayed decreased proliferation and clonogenicity. These data demonstrate that the  FORCP  transcript is destabilized via conserved elements within its 3’UTR and emphasize the need to interrogate the function of a given 3’UTR in its native context.

An Evolutionarily Conserved AU-Rich Element in the 3' Untranslated Region of a Transcript Misannotated as a Long Noncoding RNA Regulates RNA Stability