ArticleOncology letters2025
hsa_circ_0004846 enhances the malignant phenotype of papillary thyroid carcinoma cells via the miR‑142‑3p/PELI1 axis.
Article in Oncology letters, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Circular RNAs (circRNAs) are closely associated with human tumorigenesis; however, whether hsa_circ_0004846 serves a role in the progression of papillary thyroid carcinoma (PTC) remains unclear. Therefore, the present study aimed to investigate the effect of hsa_circ_0004846 on PTC. The results demonstrated that circ_0004846 was abnormally upregulated in PTC tissues and thyroid cancer cell lines (BCPAP, TPC-1 and IHH-4). Furthermore, hsa_circ_0004846-overexpressing or -depleted PTC cell lines (TPC-1 and IHH-4) were constructed using a lentiviral vector system. Notably, hsa_circ_0004846 overexpression markedly promoted cell proliferation, migration and invasion, as evidenced by activation of the PI3K/AKT pathway and the upregulation of vimentin, a class-III intermediate filament, which acts by regulating cell attachment and migration. However, hsa_circ_0004846 knockdown displayed the opposite effects. Mechanistically, the regulatory association among hsa_circ_0004846, microRNA (miR)-142-3p and Pellino E3 ubiquitin protein ligase 1 (PELI1) was validated using a dual-luciferase reporter assay. Specifically, the results demonstrated that hsa_circ_0004846 could sponge miR-142-3p, and the expression levels of miR-142-3p were negatively associated with those of hsa_circ_0004846. In addition, PELI1, a cancer-related E3 ubiquitin ligase, was identified as a downstream target of the hsa_circ_0004846/miR-142-3p axis in PTC. Therefore, PELI1 silencing could reverse the hsa_circ_0004846-induced malignant phenotype of PTC cells. Taken together, the results of the current study highlighted the effect of the hsa_circ_0004846/miR-142-3p/PELI1 regulatory network on PTC progression, thus providing a promising target for PTC treatment.
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