CFIm25-regulated lncRNA acv3UTR promotes gastric tumorigenesis via miR-590-5p/YAP1 axis

Accumulating evidences indicate that 3ʹUTR of the coding gene can act as crucial regulators in gastric cancer (GC). However, the detailed mechanisms and responsive targets are not well established. Here, we found that acvr1b gene 3ʹUTR ( acv 3UTR) was elevated in GC tissue, the expression of which was significantly correlated with advanced pTNM-stage and poor outcome in clinical patients. Forced expression of acv 3UTR promoted GC cells growth in vitro and in vivo. Mechanistically, our results suggested that acv 3UTR functioned as an oncogenic competing endogenous RNA via sponging miR-590-5p and enhancing YAP1 level. Tumor suppressor miR-590-5p was a molecular module in acv 3UTR regulatory axis, the forced expression of which led to impairing of oncogenic potential of acv 3UTR. The positive correlation of acv 3UTR and YAP1 expression, and the negative correlation of acv 3UTR and miR-590-5p expression, were verified in GC patients. Moreover, CFIm25 was identified as a key regulator contributing to acv 3UTR aberrant expression in GC binding to UGUA-264 motif. Overall, our finding defines a mechanism for understanding the potential role of acv 3UTR transcription in GC tumorigenesis, and indicates a correlation between 3ʹUTR trans -regulatory effect and GC development.