We tested the hypothesis that <b>N</b>uclear <b>E</b>nriched <b>A</b>bundant sh-NEAT1 knock-down ranscript 1 (NEAT1) is involved in the pathogenesis of PTC <i>in vitro</i> and <i>in vivo</i>.
NEAT1 was over-expressed in RAI-resistant PTC tissues and cell lines and could resist RAI by accelerating proliferation accompanied by suppressing apoptosis.