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. 2021 Oct 14;36(5):1095–1110. doi: 10.3803/EnM.2021.1155

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Copyright © 2021 Korean Endocrine Society

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. 7 — Schematic representation of transforming growth factor-beta1 (TGF-β1)-induced epithelial-mesenchymal transition (EMT) and role of lobeglitazone (LGZ), a peroxisome proliferator-activated receptor gamma (PPAR-γ) agonist in BRAF^V600E-mutated papillary thyroid carcinoma cells. LGZ suppresses the p38 mitogen-activated protein kinase (MAPK) signaling pathway and finally reduces migration and invasion of papillary thyroid carcinoma (PTC) cells induced by TGF-β1. “→” indicates promotion; “⊥” indicates inhibition. ERK, extracellular signal-regulated kinase.