Title:Knockdown of Programmed Death 1 Inhibited Progression of Papillary
Thyroid Carcinoma in Mice
Volume: 30
Issue: 5
Author(s): Hui Wang, Qianqian Chu, Shihong Ma*Ying Tao
Affiliation:
- Department of General Surgery, Shanghai Xuhui Center Hospital, Shanghai, 200031, China
Keywords:
Papillary thyroid carcinoma, PD1, PD-L1, VEGF, tumor growth, si-PD1.
Abstract:
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 in vivo studies. Nivolumab was implemented for in vivo
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.
