Knockdown of Programmed Death 1 Inhibited Progression of Papillary Thyroid Carcinoma in Mice.

[BACKGROUND] PD-L1 and PD1 mainly focused on melanoma, lung cancer and other tumors, while the related studies on early lymph node metastasis of papillary thyroid carcinoma were rarely reported.

[OBJECTIVE] For elucidating the role of programmed death 1 (PD1)/programmed death ligand 1 (PD-L1) pathway in tumor growth of papillary thyroid carcinoma (PTC).

[METHODS] Human thyroid cancer cell line and human normal thyroid cell line were obtained and transfected with si-PD1 or pCMV3-PD1 for the construction of PD1 knockdown or overexpression models. BALB/c mice were purchased for studies. Nivolumab was implemented for inhibition of PD1. Western blotting was performed for determining protein expression, while RTqPCR was used to measure relative mRNA levels.

[RESULTS] The PD1 and PD-L1 levels were both significantly upregulated in PTC mice, while the knockdown of PD1 downregulated both PD1 and PD-L1 levels. Protein expression of VEGF and FGF2 was increased in PTC mice, while si-PD1 decreased their expression. Silencing of PD1 using si-PD1 and nivolumab both inhibited tumor growth in PTC mice.

[CONCLUSION] Suppressing PD1/PD-L1 pathway significantly contributed to the tumor regression of PTC in mice.