BACKGROUND/AIM: Despite the excellent prognosis post thyroidectomy and radioiodine therapy, papillary thyroid cancer (PTC) patients still undergo dismal outcomes, especially when tumors undergo de-differentiation and thus progress to radioiodine refractory status. Our knowledge on the pathogenesis mechanisms of PTC and NIS protein (responsible for iodine uptake) activity is still behind satisfaction. To increase our knowledge on these issues, we conducted this study.

MATERIALS AND METHODS

We analyzed microarray data to identify the genes differentially expressed between normal and tumor thyroid tissues. Next, pathway enrichment analysis was conducted to derive candidate genes and pathways involved in PTC oncogenesis and NIS activity. The expression of candidate genes was confirmed by an independent TCGA dataset. Then, we used siRNA to knockdown the gene to examine the potential pathogenesis mechanisms of and -P53-NIS axis in cells. Also, we examined whether oncogenic activities, including cell proliferation, colony formation, cell migration and cell invasion, were altered with knockdown. Moreover, NIS protein intensity in cell membrane was also investigated.

RESULTS

Through analyzing microarray data, pathway enrichment and correlation analyses, we focused on since it could be involved in the -P53-NIS axis. Knockdown of significantly reduced the mRNA levels and protein abundance of . In addition, P53 protein was also elevated with knockdown. With knockdown, cell proliferation and colony formation were repressed. And, both cell migration and invasion abilities were interfered. Moreover, knockdown also enhanced the intensity of membrane NIS protein.

CONCLUSION

knockdown not only reduced the oncogenic activities of thyroid cancer but also enhanced the intensity of NIS protein responsible for iodine intake in thyroid gland. Therefore, could serve as a prognosis indicator in thyroid cancer.