Runt‐Related Transcription Factor 2 (Runx2) Is Responsible for Galectin‐3 Overexpression in Human Thyroid Carcinoma

Kaptan, Engin; Baş, Serap; Sancakli, Aylin; Aktaş, Hatice; Bayrak, Bertan Boran; Yanardağ, Refiye; Bolkent, Şehnaz

doi:10.1002/jcb.26043

Cited by 11 publications

(2 citation statements)

References 53 publications

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“…Gal-3 is a member of the lectin family and plays an important role in cell–cell adhesion and cell–matrix interactions. Kaptan et al [ 102 ] revealed that regulation of Gal-3 expression was strongly correlated with Runx2 TF in human thyroid carcinoma; increase in Gal-3 gene expression was detected in patients with calcification [ 103 ].…”

Section: Cellular and Molecular Mechanisms For Calcification In Thmentioning

confidence: 99%

Molecular Aspects of Thyroid Calcification

Ferreira

Gimba

Vinagre

et al. 2020

IJMS

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In thyroid cancer, calcification is mainly present in classical papillary thyroid carcinoma (PTC) and in medullary thyroid carcinoma (MTC), despite being described in benign lesions and in other subtypes of thyroid carcinomas. Thyroid calcifications are classified according to their diameter and location. At ultrasonography, microcalcifications appear as hyperechoic spots ≤ 1 mm in diameter and can be named as stromal calcification, bone formation, or psammoma bodies (PBs), whereas calcifications > 1 mm are macrocalcifications. The mechanism of their formation is still poorly understood. Microcalcifications are generally accepted as a reliable indicator of malignancy as they mostly represent PBs. In order to progress in terms of the understanding of the mechanisms behind calcification occurring in thyroid tumors in general, and in PTC in particular, we decided to use histopathology as the basis of the possible cellular and molecular mechanisms of calcification formation in thyroid cancer. We explored the involvement of molecules such as runt-related transcription factor-2 (Runx-2), osteonectin/secreted protein acidic and rich in cysteine (SPARC), alkaline phosphatase (ALP), bone sialoprotein (BSP), and osteopontin (OPN) in the formation of calcification. The present review offers a novel insight into the mechanisms underlying the development of calcification in thyroid cancer.

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Section: Cellular and Molecular Mechanisms For Calcification In Thmentioning

confidence: 99%

Molecular Aspects of Thyroid Calcification

Ferreira

Gimba

Vinagre

et al. 2020

IJMS

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“…RUNX2, also known as core binding factor α1 (CBFα1), is the most specific marker gene in the early stages of bone formation, and plays a key role in the regulation of cell proliferation in osteoblasts and endothelial cells [ 27 ]. Similarly, several studies have shown that RUNX2 is also closely associated with the occurrence and development of tumors, such as breast cancer [ 28 ], colorectal cancer [ 29 ], thyroid cancer [ 30 ], and pancreatic cancer [ 31 ]. RUNX3 has been defined as both a tumor suppressor and a tumor promoter, and it can play such contradictory roles even in the same tumor, which may reflect the complex role of RUNX3 in tumorigenesis [ 32 ].…”

Section: Introductionmentioning

confidence: 99%

RUNX transcription factors: biological functions and implications in cancer

Chen,

Wang,

Yang

et al. 2024

Clin Exp Med

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Runt-related transcription factors (RUNX) are a family of transcription factors that are essential for normal and malignant hematopoietic processes. Their most widely recognized role in malignancy is to promote the occurrence and development of acute myeloid leukemia. However, it is worth noting that during the last decade, studies of RUNX proteins in solid tumors have made considerable progress, suggesting that these proteins are directly involved in different stages of tumor development, including tumor initiation, progression, and invasion. RUNX proteins also play a role in tumor angiogenesis, the maintenance of tumor cell stemness, and resistance to antitumor drugs. These findings have led to the consideration of RUNX as a tumor biomarker. All RUNX proteins are involved in the occurrence and development of solid tumors, but the role of each RUNX protein in different tumors and the major signaling pathways involved are complicated by tumor heterogeneity and the interacting tumor microenvironment. Understanding how the dysregulation of RUNX in tumors affects normal biological processes is important to elucidate the molecular mechanisms by which RUNX affects malignant tumors.

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