Endocrinology and Metabolism

Original Articles

Thyroid
Lobeglitazone, A Peroxisome Proliferator-Activated Receptor-Gamma Agonist, Inhibits Papillary Thyroid Cancer Cell Migration and Invasion by Suppressing p38 MAPK Signaling Pathway: Jun-Qing Jin, Jeong-Sun Han, Jeonghoon Ha, Han-Sang Baek, Dong-Jun Lim; Endocrinol Metab. 2021;36(5):1095-1110. Published online October 14, 2021; DOI: https://doi.org/10.3803/EnM.2021.1155

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Background
Peroxisome proliferator-activated receptor-gamma (PPAR-γ) ligands have been widely shown to correlate with epithelial-mesenchymal transition (EMT) and cancer progression. Lobeglitazone (LGZ) is a novel ligand of PPAR-γ; and its role in EMT and metastasis in papillary thyroid carcinoma (PTC) is poorly understood. We aimed to investigate the role of LGZ in metastatic behavior of PTC cells.
Methods
Half maximal inhibitory concentration (IC₅₀) values of LGZ in BRAF-mutated PTC cell lines (BCPAP and K1) were determined using MTT assay. Rosiglitazone (RGZ), the PPAR-γ ligand was used as a positive control. The protein expression of PPAR-γ, cell-surface proteins (E-cadherin, N-cadherin), cytoskeletal protein (Vimentin), transcription factor (Snail), p38 mitogenactivated protein kinase (MAPK), extracellular signal-regulated kinase (ERK) 1/2 pathway, and matrix metalloproteinase (MMP)-2 expression were measured using Western blotting. Changes in E-cadherin expression were also determined using immunocytochemistry. Cell migration and invasion were analyzed using wound healing and Matrigel invasion assays.
Results
Treatment with LGZ or RGZ significantly inhibited transforming growth factor-beta1 (TGF-β1)-induced EMT-associated processes such as fibroblast-like morphological changes, EMT-related protein expression, and increased cell migration and invasion in BCPAP and K1 cells. LGZ restored TGF-β1-induced loss of E-cadherin, as observed using immunocytochemistry. Furthermore, LGZ and RGZ suppressed TGF-β1-induced MMP-2 expression and phosphorylation of p38 MAPK, but not ERK1/2. Although there was no change in PPAR-γ expression after treatment with LGZ or RGZ, the effect of downstream processes mediated by LGZ was hampered by GW9662, a PPAR-γ antagonist.
Conclusion
LGZ inhibits TGF-β1-induced EMT, migration, and invasion through the p38 MAPK signaling pathway in a PPAR-γ-dependent manner in PTC cells.

Citations

Citations to this article as recorded by

Diabetes Mellitus and Thyroid Cancers: Risky Correlation, Underlying Mechanisms and Clinical Prevention
Rongqian Wu, Junping Zhang, Guilin Zou, Shanshan Li, Jinying Wang, Xiaoxinlei Li, Jixiong Xu
Diabetes, Metabolic Syndrome and Obesity.2024; Volume 17: 809. CrossRef
Clinicopathological Evaluation of Papillary Thyroid Microcarcinoma
Ando Takahito, Kimihito Fujii, Hirona Banno, Masayuki Saito, Yukie Ito, Mirai Ido, Manami Goto, Yukako Mouri, Junko Kousaka, Tsuneo Imai, Shogo Nakano
Cureus.2024;[Epub] CrossRef
Pioglitazone, a peroxisome proliferator‑activated receptor γ agonist, induces cell death and inhibits the proliferation of hypoxic HepG2 cells by promoting excessive production of reactive oxygen species
Guohao Huang, Mengfan Zhang, Manzhou Wang, Wenze Xu, Xuhua Duan, Xinwei Han, Jianzhuang Ren
Oncology Letters.2024;[Epub] CrossRef
The Activation of PPARγ by (2Z,4E,6E)-2-methoxyocta-2,4,6-trienoic Acid Counteracts the Epithelial–Mesenchymal Transition Process in Skin Carcinogenesis
Enrica Flori, Sarah Mosca, Giorgia Cardinali, Stefania Briganti, Monica Ottaviani, Daniela Kovacs, Isabella Manni, Mauro Truglio, Arianna Mastrofrancesco, Marco Zaccarini, Carlo Cota, Giulia Piaggio, Mauro Picardo
Cells.2023; 12(7): 1007. CrossRef
Cumulative exposure to metabolic syndrome increases thyroid cancer risk in young adults: a population-based cohort study
Jinyoung Kim, Kyungdo Han, Mee Kyoung Kim, Ki-Hyun Baek, Ki-Ho Song, Hyuk-Sang Kwon
The Korean Journal of Internal Medicine.2023; 38(4): 526. CrossRef
Drug repositioning in thyroid cancer treatment: the intriguing case of anti-diabetic drugs
Alessia Greco, Francesca Coperchini, Laura Croce, Flavia Magri, Marsida Teliti, Mario Rotondi
Frontiers in Pharmacology.2023;[Epub] CrossRef
Fish and the Thyroid: A Janus Bifrons Relationship Caused by Pollutants and the Omega-3 Polyunsaturated Fatty Acids
Salvatore Benvenga, Fausto Famà, Laura Giovanna Perdichizzi, Alessandro Antonelli, Gabriela Brenta, Francesco Vermiglio, Mariacarla Moleti
Frontiers in Endocrinology.2022;[Epub] CrossRef
Identifying and categorizing compounds that reduce corneal transforming growth factor beta induced protein levels: a scoping review
Gabriella Guo Sciriha, Janet Sultana, Joseph Borg
Expert Review of Clinical Pharmacology.2022; 15(12): 1423. CrossRef

Endocrine Research
Mechanism of Lipid Accumulation through PAR2 Signaling in Diabetic Male Mice: Dae Hyun Kim, Ye Ra Kim, EunJin Bang, Sugyeong Ha, Sang Gyun Noh, Byeong Moo Kim, Seong Ho Jeong, Hee Jin Jung, Ji Young Lee, Hae Young Chung; Endocrinol Metab. 2021;36(1):171-184. Published online February 24, 2021; DOI: https://doi.org/10.3803/EnM.2020.850

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Abstract PDF Supplementary Material PubReader ePub

Background
Protease-activated protein-2 (PAR2) has been reported to regulate hepatic insulin resistance condition in type 2 diabetes mice. However, the mechanism of lipid metabolism through PAR2 in obesity mice have not yet been examined. In liver, Forkhead box O1 (FoxO1) activity induces peroxisome proliferator-activated receptor γ (PPARγ), leading to accumulation of lipids and hyperlipidemia. Hyperlipidemia significantly influence hepatic steatoses, but the mechanisms underlying PAR2 signaling are complex and have not yet been elucidated.
Methods
To examine the modulatory action of FoxO1 and its altered interaction with PPARγ, we utilized db/db mice and PAR2-knockout (KO) mice administered with high-fat diet (HFD).
Results
Here, we demonstrated that PAR2 was overexpressed and regulated downstream gene expressions in db/db but not in db+ mice. The interaction between PAR2/β-arrestin and Akt was also greater in db/db mice. The Akt inhibition increased FoxO1 activity and subsequently PPARγ gene in the livers that led to hepatic lipid accumulation. Our data showed that FoxO1 was negatively controlled by Akt signaling and consequently, the activity of a major lipogenesis-associated transcription factors such as PPARγ increased, leading to hepatic lipid accumulation through the PAR2 pathway under hyperglycemic conditions in mice. Furthermore, the association between PPARγ and FoxO1 was increased in hepatic steatosis condition in db/db mice. However, HFD-fed PAR2-KO mice showed suppressed FoxO1-induced hepatic lipid accumulation compared with HFD-fed control groups.
Conclusion
Collectively, our results provide evidence that the interaction of FoxO1 with PPARγ promotes hepatic steatosis in mice. This might be due to defects in PAR2/β-arrestin-mediated Akt signaling in diabetic and HFD-fed mice.

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Biochanin‐A has antidiabetic, antihyperlipidemic, antioxidant, and protective effects on diabetic nephropathy via suppression of TGF‐β1 and PAR‐2 genes expression in kidney tissues of STZ‐induced diabetic rats
Jamal Amri, Mona Alaee, Rasool Babaei, Zahra Salemi, Reza Meshkani, Ali Ghazavi, Ahmad Akbari, Mehdi Salehi
Biotechnology and Applied Biochemistry.2022; 69(5): 2112. CrossRef
Delineation of the healthy rabbit liver by immunohistochemistry – A technical note
Gabriella Meier Bürgisser, Olivera Evrova, Dorothea M. Heuberger, Julia Rieber, Pietro Giovanoli, Maurizio Calcagni, Johanna Buschmann
Acta Histochemica.2021; 123(7): 151795. CrossRef

Review Article

Thyroid
Mutation Profile of Well-Differentiated Thyroid Cancer in Asians: Young Shin Song, Jung Ah Lim, Young Joo Park; Endocrinol Metab. 2015;30(3):252-262. Published online September 22, 2015; DOI: https://doi.org/10.3803/EnM.2015.30.3.252

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Abstract PDF PubReader

Recent advances in molecular diagnostics have led to significant insights into the genetic basis of thyroid tumorigenesis. Among the mutations commonly seen in thyroid cancers, the vast majority are associated with the mitogen-activated protein kinase pathway. B-Raf proto-oncogene (BRAF) mutations are the most common mutations observed in papillary thyroid cancers (PTCs), followed by RET/PTC rearrangements and RAS mutations, while follicular thyroid cancers are more likely to harbor RAS mutations or PAX8/peroxisome proliferator-activated receptor γ (PPARγ) rearrangements. Beyond these more common mutations, alterations in the telomerase reverse transcriptase (TERT) promoter have recently been associated with clinicopathologic features, disease prognosis, and tumorigenesis in thyroid cancer. While the mutations underlying thyroid tumorigenesis are well known, the frequency of these mutations is strongly associated with geography, with clear differences reported between Asian and Western countries. Of particular interest is the prevalence of BRAF mutations, with Korean patients exhibiting the highest rate of BRAF-associated thyroid cancers in the world. Here, we review the prevalence of each of the most common mutations in Asian and Western countries, and identify the characteristics of well-differentiated thyroid cancer in Asians.

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Reply:
Y. Che
American Journal of Neuroradiology.2016; 37(1): E9. CrossRef
Prognostic effects of TERT promoter mutations are enhanced by coexistence with BRAF or RAS mutations and strengthen the risk prediction by the ATA or TNM staging system in differentiated thyroid cancer patients
Young Shin Song, Jung Ah Lim, Hoonsung Choi, Jae‐Kyung Won, Jae Hoon Moon, Sun Wook Cho, Kyu Eun Lee, Young Joo Park, Ka Hee Yi, Do Joon Park, Jeong‐Sun Seo
Cancer.2016; 122(9): 1370. CrossRef

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