Abstract
Simple SummaryDespite the considerable development of diagnostic tools, distinguishing between benign and malignant parathyroid tumors poses a significant diagnostic challenge. Epigenetic regulations, including noncoding microRNAs (miRNAs), have recently emerged as a new and promising source of biomarkers. MiRNAs are post-transcriptional regulators of gene expression. These tissue-specific molecules are known to be deregulated between cancer and normal cells. This review delineates changes in miRNA expression in parathyroid carcinoma (PC), advancing our understanding of PC tumorigenesis and emphasizing, at the same time, that miRNAs can be further exploited for diagnostic and therapeutic purposes.Parathyroid tumors are a genetically heterogenous group with a significant variability in clinical features. Due to a lack of specific signs and symptoms and uncertain histopathological criteria, parathyroid carcinomas (PCs) are challenging to diagnose, both before and after surgery. There is a great interest in searching for accurate molecular biomarkers for early detection, disease monitoring, and clinical management. Due to improvements in molecular pathology, the latest studies have reported that PC tumorigenesis is strongly linked to the epigenetic regulation of gene expression. MicroRNA (miRNA) profiling may serve as a helpful adjunct in distinguishing parathyroid adenoma (PAd) from PC and provide further insight into regulatory pathways involved in PTH release and parathyroid tumorigenesis. So far, only a few studies have attempted to show the miRNA signature for PC, and very few overlaps could be found between these relatively similar studies. A global miRNA downregulation was detected in PC compared with normal glands among differentially expressed miRNAs. This review summarizes changes in miRNA expression in PC and discusses the future research directions in this area.
Highlights
Parathyroid glands are endocrine organs that regulate calcium homeostasis by releasing parathormone (PTH) [1]
Primary hyperparathyroidism (PHPT) is caused by parathyroid adenoma (PAd) (80–85%), parathyroid gland hyperplasia (PHyp) (10–15%) and parathyroid carcinoma (PC), which occurs in about 1–5% of cases of PHPT [8,9]
PCs might be caused by anomalies in genes, such as cell division cycle 73 (CDC73), MEN-1, retinoblastoma 1 (RB), tumor protein p53 (TP53), cyclin D1 (CCND1), the enhancer of zeste 2 polycomb repressive complex 2 subunits (EZH2), adenomatous polyposis coli (APC), glycogen synthase kinase 3 beta (GSK3B), and prune homolog 2 (PRUNE2) [17]
Summary
Parathyroid glands are endocrine organs that regulate calcium homeostasis by releasing parathormone (PTH) [1]. Patients with PC usually present a long clinical history complicated by tumor recurrences and progressive end organ damage [13,14,15] Clinical symptoms such as renal failure, bone disease, cardiac arrhythmia, or neurocognitive dysfunction are mainly related to excess PTH secretion and intractable hypercalcemia [12,16,17,18,19]. The same observation was presented by Kong et al in their study, in which they emphasized the value of preoperative suspicion of the disease [8] In this regard, the search for accurate biomarkers for early detection, disease monitoring, and risk assessment is a priority for a correct diagnosis. It remains one of the clinical challenges in precisely distinguishing PC and PAd
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