Roles of the SNHG7/microRNA-9-5p/DPP4 ceRNA network in the growth and 131I resistance of thyroid carcinoma cells through PI3K/Akt activation

Radioactive iodine (RAI, I-131) therapy is the main treatment for thyroid carcinoma (TC). Long noncoding RNA (lncRNA)/microRNA (miR) competing endogenous RNA (ceRNA) networks have aroused great interest for their roles in gene expression. The present study aimed to investigate the effect of lncRNA SNHG7 on the growth and I-131 resistance of TC. Differentially expressed lncRNAs in TC and paracancerous tissues were analyzed. The binding of miR-9-5p with small nucleolar RNA host gene 7 (SNHG7) and dipeptidyl-peptidase 4 (DPP4) was identified. Gain- and loss-of-function analyses of SNHG7 and miR-9-5p were performed to determine their effects on the growth and I-131 resistance of TC cells. The activity of the PI3K/Akt pathway was evaluated. Consequently, upregulated SNHG7 was revealed in TC tissues and correlated with I-131 resistance. Silencing of SNHG7 or overexpressing miR-9-5p inhibited the growth and I-131 resistance of TC cells. SNHG7 acted as a ceRNA of miR-9-5p to enhance DPP4 expression. Overexpressed SNHG7 increased DPP4 expression and activated the PI3K/Akt signaling pathway by sponging miR-9-5p. The in vitro results were reproduced in vivo. In summary, the present study provided evidence that the SNHG7/miR-9-5p/DPP4 ceRNA network could promote the growth and I-131 resistance of TC cells via PI3K/Akt activation. The present study may offer novel options for TC treatment.

Automated summary

The study investigated the impact of lncRNA SNHG7 on the growth and I-131 resistance of thyroid carcinoma (TC). Upregulated SNHG7 was found in TC tissues and correlated with I-131 resistance, acting as a ceRNA of miR-9-5p to enhance DPP4 expression and activate the PI3K/Akt pathway. The study may provide new options for TC treatment.