Abstract
As important modulators in various physiological processes, circular RNAs (circRNAs) have been increasingly demonstrated in tumors, including papillary thyroid cancer (PTC). Hsa_circRNA_102002 (circ_102002) is a circRNA derived from alternative splicing of ubiquitin-specific peptidase 22 (USP22) transcript, the role of which needs further investigation. Our results suggested the upregulation of circ_102002 in PTC tissues and cells, and its promoting effects on epithelial–mesenchymal transition (EMT) and cell migration. Mechanism studies showed that circ_102002 could sponge microRNA-488-3p (miR-488-3p) and downregulate its expression. The target relationship between miR-488-3p and hyaluronic acid synthetase 2 (HAS2) in PTC was systematically studied. In addition, our results showed that HAS2 overexpression could restore the inhibited cell EMT and migration. Moreover, the inhibitory effect of downregulation of circ_102002 on PTC growth was evaluated in a mouse xenograft model, which involved miR-488-3p and HAS2 regulation. These findings about the signal axis of circ_102002/miR-488-3p/HAS2 may further elucidate the PTC pathogenesis and improve clinical treatment.
Highlights
Papillary thyroid cancer (PTC) is the most common endocrine malignant tumor, representing ~90% of all thyroid cancers [1]
Hsa_circ_102002 was found to be the most significant differentially expressed circRNA in papillary thyroid cancer (PTC) samples compared to normal samples (Fig. 1a)
Increasing number of circRNAs are identified and becoming a research hotspot, some of which have been investigated in PTC
Summary
Papillary thyroid cancer (PTC) is the most common endocrine malignant tumor, representing ~90% of all thyroid cancers [1]. The detection and treatment methods have made some progress and improved the prognosis, metastases commonly involve cervical lymph nodes and lung [2]. Lung metastasis occurs in 7–30% in children and adolescents (≤20 years), only ~4% in adult population [3, 4]. These PTC patients still suffered from poor outcomes. Exploration of the molecular mechanism related to the pathogenesis of PTC metastasis may offer
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