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Related Experiment Video

Updated: Mar 12, 2026

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model

Published on: March 17, 2023

Exploring the molecular mechanisms underlying the inflammation-cancer transformation in Hashimoto thyroiditis using

Mengsha Zou¹, Shang Shi¹, Huihui Li¹

¹Thyroid Department, The Affiliated Lihuili Hospital of Ningbo University, Ningbo City, Zhejiang Province, P. R. China.

|March 11, 2026

Summary

Hashimoto thyroiditis (HT) inflammation drives papillary thyroid carcinoma (PTC) via IL1B-negative follicular epithelial cells recruiting mast cells. Mast cell IL-8 then activates the PI3K/AKT pathway, promoting cancer development.

Keywords:

Hashimoto thyroiditis Papillary thyroid carcinoma follicular epithelial cells immunity mast cells

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Last Updated: Mar 12, 2026

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In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

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Published on: August 23, 2019

Area of Science:

Oncology
Immunology
Cell Biology

Background:

Hashimoto thyroiditis (HT) is linked to papillary thyroid carcinoma (PTC) development.
The tumor immune microenvironment and inflammation-to-cancer mechanisms in HT-PTC are not well understood.

Purpose of the Study:

To investigate the molecular mechanisms driving the inflammation-to-cancer transition in HT-PTC coexistence.
To identify key cell-cell interactions and signaling pathways involved.

Main Methods:

Single-cell RNA sequencing (scRNA-seq) of HT and PTC tissues.
Copy number variation (CNV) analysis to identify malignant cells.
Cell-cell communication analysis and in vitro validation using Transwell co-culture models.

Main Results:

Identified 11 cell subtypes, with IL1B upregulated in malignant follicular epithelial cells (FECs).
IL1B-negative FECs communicate with mast cells via the FN1/CD44 axis.
Mast cells secrete IL-8, activating the PI3K/AKT pathway and promoting malignant phenotypes under inflammation.

Conclusions:

IL1B-negative FECs recruit mast cells through the FN1/CD44 axis.
Mast cell-derived IL-8 activates the PI3K/AKT pathway, driving the HT to PTC transition.
Provides novel insights into the inflammation-to-cancer mechanism in HT-PTC.