Long non-coding RNA H19 knockdown inhibits the cell viability and promotes apoptosis of thyroid cancer cells through regulating the PI3K/AKT pathway.

Certain long non-coding (lnc)RNAs have been reported to serve important roles in the genesis and progression of thyroid cancer (TC). Recent studies have demonstrated that the expression of lncRNA H19 is upregulated in TC tissues; however, knowledge of the associated molecular mechanisms is limited. Therefore, the present study aimed to clarify the roles of H19 in TC. The mRNA expression of lncRNA H19 in TC tissues was determined using reverse transcription-quantitative polymerase chain reaction analysis, and the effects of H19 knockdown on cell viability and apoptosis in vitro were assessed using MTT and flow cytometric assays, respectively. Finally, the signaling pathways involved in the effects of H19 were examined. The results indicated that H19 was upregulated in TC tissues. Silencing of H19 inhibited the cell viability and promoted apoptosis of FTC-133 and TPC-1 TC cells, accompanied by an increased expression of B-cell lymphoma 2 (Bcl-2)-associated X protein and caspase 3, and repressed expression of Bcl-2. The results of western blot analysis suggested that the levels of phosphorylated phosphoinositide-3 kinase (PI3K) and phosphorylated AKT were attenuated by H19 silencing. These results suggest that lncRNA H19 exerts an oncogenic function in TC, in part through the PI3K/AKT pathway.