Diagnostic performance of HMGA2 gene expression for differentiation of malignant thyroid nodules: A systematic review and meta‐analysis

Kim, Bo Hyun; Kim, Seong Jang; Kim, Mijin; Lee, Sang‐Woo; Jeong, Shin Young; Pak, Kyoungjune; Kim, Keun‐Young; Kim, In Joo

doi:10.1111/cen.13853

Cited by 1 publication

(1 citation statement)

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“…HMGA2 is expressed during embryogenesis and is generally not or rarely expressed in adult tissues, which makes it an interesting therapeutic target since it is re-expressed in various types of human cancer, including prostate cancer [ 42 ], breast cancer [ 39 ], oesophageal cancer [ 49 ] and thyroid cancer [ 50 ]. In addition, HMGA2 has several times been identified as a molecular marker to distinguish between benign and malignant follicular thyroid neoplasia [ 22 , 51 , 52 ]. In our study, we validated that HMGA2 is a direct downstream target of miR-204-5p by luciferase assay, in accordance with other studies [ 11 , 53 ].…”

Section: Discussionmentioning

confidence: 99%

Unraveling the Roles of miR-204-5p and HMGA2 in Papillary Thyroid Cancer Tumorigenesis

Branteghem

Augenlicht

Demetter

et al. 2023

IJMS

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Thyroid cancer is the most common endocrine malignant tumor with an increasing incidence rate. Although differentiated types of thyroid cancer generally present good clinical outcomes, some dedifferentiate into aggressive and lethal forms. However, the molecular mechanisms governing aggressiveness and dedifferentiation are still poorly understood. Aberrant expression of miRNAs is often correlated to tumor development, and miR-204-5p has previously been identified in papillary thyroid carcinoma as downregulated and associated with aggressiveness. This study aimed to explore its role in thyroid tumorigenesis. To address this, gain-of-function experiments were performed by transiently transfecting miR-204-5p in thyroid cancer cell lines. Then, the clinical relevance of our data was evaluated in vivo. We prove that this miRNA inhibits cell invasion by regulating several targets associated with an epithelial-mesenchymal transition, such as SNAI2, TGFBR2, SOX4 and HMGA2. HMGA2 expression is regulated by the MAPK pathway but not by the PI3K, IGF1R or TGFβ pathways, and the inhibition of cell invasion by miR-204-5p involves direct binding and repression of HMGA2. Finally, we confirmed in vivo the relationship between miR-204-5p and HMGA2 in human PTC and a corresponding mouse model. Our data suggest that HMGA2 inhibition offers promising perspectives for thyroid cancer treatment.

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