Long non‐coding <scp>RNA FAL</scp>1 functions as a ce<scp>RNA</scp> to antagonize the effect of miR‐637 on the down‐regulation of <scp>AKT</scp>1 in Hirschsprung's disease

Abstract

These results illuminated that FAL1 may work as a ceRNA to modulate AKT1 expression via competitively binding to miR-637 in HSCR, suggesting that it may be clinically valuable as a biomarker of HSCR.