The pathogenesis of cystitis glandular (CG) is unclear, but it is generally considered to be a neoplastic lesion of urothelial hyperplasia formed by long-term chronic stimulation. There is growing evidence that circRNAs play important roles in a variety of cellular processes. However, there are few reports on the role and molecular mechanism of circRNA in CG. In this study, we first isolated primary cells from CG tissues and adjacent normal tissues. Further experiments showed that CircTHBS1 was up-regulated in primary CG cells (pCGs). The results of CCK-8 showed that the overexpression of CircTHBS1 promoted the viability of pCGs, while the deletion of CircTHBS1 reduced the cell viability. Knocking out CircTHBS1 also inhibited the migration of pCGs. In addition, we demonstrated that CircTHBS1 played a role in the adsorption of miR-211 by "sponge" in pCG. In turn, miR-211 can directly target CYCLIN D2 (CCND2) 3'UTR to perform its function. Finally, we confirmed the role and mechanism of CircTHBS1/miR-211/CCND2 regulation axis in pCGs. In summary, our study is the first to reveal the role and underlying mechanism of CircTHBS1 in CG, providing a potential biomarker and therapeutic target for human CG.

中文翻译：

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CircTHBS1靶向miR-211/CCND2通路促进原发性腺性膀胱炎细胞增殖和迁移潜能。

腺性膀胱炎（CG）的发病机制尚不清楚，但一般认为是长期慢性刺激形成的尿路上皮增生的肿瘤性病变。越来越多的证据表明 circRNA 在多种细胞过程中发挥着重要作用。然而，关于circRNA在CG中的作用和分子机制的报道很少。在这项研究中，我们首先从 CG 组织和邻近的正常组织中分离出原代细胞。进一步的实验表明，CircTHBS1 在原代 CG 细胞 (pCG) 中上调。CCK-8 的结果表明，CircTHBS1 的过表达促进了 pCGs 的活力，而 CircTHBS1 的缺失降低了细胞活力。敲除 CircTHBS1 也抑制了 pCGs 的迁移。此外，我们证明了 CircTHBS1 通过“