Authors

Li Jia1, #, Min Yin2, *, Hongkun Bao2, #, Qingyuan Tao1, Yijun Yan1, Bin Zheng1, Wendi Jin1

Departments

1Affiliated Hospital of Yunnan University (Yunnan Second People's Hospital) Nuclear Medicine, Kunming 650021, Yunnan, China - 2School of Medicine,Yunnan University, Kunming 650091, Yunnan, China

Abstract

Objective: For exploring the influence of PD-L1 inhibitors on Thyroid carcinoma(TC) and the related mechanism of action. 

Methods: Nude mice models bearing subcutaneous TC were established with 20 BALB/c-Nu nude mice, and randomized into two groups. One group was injected with PD-L1 inhibitors (treatment group), and the other group was injected with the same amount of normal saline (model group). During the intervention period, the subcutaneous tumour volume and inflammatory factors of the two groups were measured. After the fourth injection, all rats were killed, and their tumours were weighed. In addition, TC cells were purchased, followed by quantification of their PD-1 and PD-L1 proteins. The growing ability and apoptosis of the TC cells intervened with PD-L1 inhibitor were evaluated. 

Results: After injection of PD-L1 inhibitors, TC-bearing nude mice showed notable decreases in tumour volume and weight and an increase in tumour inhibition rate (all P<0.05). The treatment group presented lower levels of inflammatory factors and higher levels of survival rate and survival time than the model group (all P<0.05). In in vitro experiment, TC cells showed higher PD-1 and PD-L1 proteins than normal thyroid epithelial cells (P<0.05), and intervention with PD-L1 inhibitors inhibited cell growing ability and accelerated cell apoptosis (both P<0.05). 

Conclusion: PD-L1 inhibitors can improve the development of subcutaneous tumour in tumour-bearing nude mice through accelerating the apoptosis of TC cells and suppressing their growth, which lays a foundation for the future clinical application of PD-L1 inhibitors in the therapy of TC.

Keywords

PD-L1 inhibitors, thyroid carcinoma, tumor-bearing nude mice, inflammatory factor, apoptosis.

DOI:

10.19193/0393-6384_2022_1_83