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Updated: Oct 4, 2025

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
FoxP3 promotes lymph node metastasis in patients with papillary thyroid carcinoma complicated with Hashimoto's
Rong Zeng1, Yi Lyu2, Heng Niu3
1Department of Medical Oncology, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, Kunming 650032, China.
Background:
To investigate the effect of Treg cells on patients with PTC complicated with HT.
Methods:
We collected thyroid fresh tissue of human after surgery, paraffin tissue and serum samples (cancer tissue which was diagnosed by pathology). Analysed the expression of nuclear specific marker gene FoxP3 in Treg cells by Envision immunohistochemical staining. Transwell cell chamber was used to simulate the co-action environment of umbilical cord blood initial T lymphocytes and thyroid papillary carcinoma cells (TPC-1and K1). Compared with human normal thyroid follicular epithelial cell line Nthy-ori 3-1. Flow cytometry was used to detect the proportion of Treg cells (CD4+CD25+CD127-/CD4+CD25+%) at 0, 24, 36, 48, 60 h after co-administration of thyroid papillary carcinoma cell lines (TPC-1 and K1) and umbilical cord blood initial T lymphocytes. The expression of FoxP3 protein in co-acting T lymphocytes was detected by Western blot.
Results:
The results showed that the positive expression of FoxP3 in the tumor microenvironment of PTC patients with or without HT promoted lymph node metastasis of tumors and played a role in inhibiting tumor immunity. PTC cancer cells could induce initial T lymphocyte differentiating into Treg cells. At 36 h, the ratio of Th17 cells and Treg cells which were differentiated was the highest. The balance of Th17/Treg was significantly biased toward Th17. The proportion of FoxP3 induced by K1 cell line with lymph node metastasis was higher than that of TPC-1 cell line without lymph node metastasis.
Conclusions:
FoxP3 could promote lymph node metastasis to inhibit tumor immunity by dysregulation of Th17/Treg balance in PTC patients complicated with HT.
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