Background Thyroid cancer is an endocrine malignancy that is growing in incidence worldwide. Despite progress in diagnostics and treatment of thyroid cancer, prognosis remains poor. Emerging research has shown that circular RNAs (circRNAs) have crucial regulatory roles in cancers. However, the possible functions and mechanisms of hsa_circ_0011385 remain undetermined. Materials and methods Expression levels of hsa_circ_0011385 and miR-361-3p were evaluated by qRT-PCR assay. The interaction between hsa_circ_0011385 and miR-361-3p was verified by dual-luciferase reporter assay. Effects of hsa_circ_0011385 or miR-361-3p on cell viability, proliferation, cell cycle, apoptosis, migration and invasion were confirmed by cell counting kit-8 (CCK-8), carboxyfluoresceinsuccinimidyl ester (CFSE), flow cytometry, and Transwell assays in vitro. The effect of hsa_circ_0011385 on thyroid cancer progression was also determined by in vivo tumor formation assay. Target genes of miR-361-3p were predicted by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and the expression of apoptosis- and metastasis-related proteins were assessed by Western blot assay. Results Hsa_circ_0011385 upregulated in thyroid cancer; hsa_circ_0011385 knockdown inhibited thyroid cancer cell proliferation, migration and invasion, and promoted cell cycle arrest and apoptosis. In addition, hsa_circ_0011385 could negatively regulate miR-361-3p by functioning as a sponge. Hsa_circ_0011385 promoted thyroid cancer cell proliferation, migration and invasion and suppressed cell cycle arrest and apoptosis by targeting miR-361-3p in vitro. We also found that hsa_circ_0011385 knockdown dramatically inhibited thyroid cancer growth in vivo. Furthermore, hsa_circ_0011385 regulated expression of apoptosis and metastasis-related proteins in thyroid cancer. Conclusions Hsa_circ_0011385facilitated thyroid cancer cell proliferation, invasion and migration, and inhibited thyroid cancer cell cycle arrest and apoptosis by targeting miR-361-3p, suggesting that the hsa_circ_0011385/miR-361-3p axis might be a promising therapeutic target for thyroid cancer.

中文翻译：

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Hsa_circ_0011385 通过靶向 miR-361-3p 加速甲状腺癌的进展。

背景甲状腺癌是一种内分泌恶性肿瘤，其发病率在全球范围内呈上升趋势。尽管甲状腺癌的诊断和治疗取得了进展，但预后仍然很差。新兴研究表明，环状 RNA (circRNA) 在癌症中具有至关重要的调节作用。然而，hsa_circ_0011385 的可能功能和机制仍未确定。材料和方法 hsa_circ_0011385 和 miR-361-3p 的表达水平通过 qRT-PCR 测定进行评估。hsa_circ_0011385 和 miR-361-3p 之间的相互作用通过双荧光素酶报告基因分析得到验证。hsa_circ_0011385 或 miR-361-3p 对细胞活力、增殖、细胞周期、细胞凋亡、迁移和侵袭的影响通过细胞计数试剂盒 8 (CCK-8)、羧基荧光琥珀酰亚胺酯 (CFSE)、流式细胞术和 Transwell 分析证实体外。hsa_circ_0011385 对甲状腺癌进展的影响也通过体内肿瘤形成试验确定。通过基因本体论（GO）和京都基因与基因组百科全书（KEGG）分析预测miR-361-3p的靶基因，并通过Western印迹法评估细胞凋亡和转移相关蛋白的表达。结果 Hsa_circ_0011385 在甲状腺癌中上调；hsa_circ_0011385 敲低抑制甲状腺癌细胞增殖、迁移和侵袭，并促进细胞周期停滞和凋亡。此外，hsa_circ_0011385 可以通过充当海绵来负调节 miR-361-3p。Hsa_circ_0011385通过体外靶向miR-361-3p促进甲状腺癌细胞增殖、迁移和侵袭，抑制细胞周期停滞和凋亡。我们还发现 hsa_circ_0011385 敲低显着抑制了体内甲状腺癌的生长。此外，hsa_circ_0011385 调节甲状腺癌中凋亡和转移相关蛋白的表达。结论 Hsa_circ_0011385通过靶向miR-361-3p促进甲状腺癌细胞增殖、侵袭和迁移，抑制甲状腺癌细胞周期停滞和凋亡，提示hsa_circ_0011385/miR-361-3p轴可能是甲状腺癌的一个有希望的治疗靶点。