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miR-148a-3p 通过靶向 NPTX1 调节特发性牙龈纤维瘤的增殖和凋亡。

miR-148a-3p regulates proliferation and apoptosis of idiopathic gingival fibroma by targeting NPTX1.

机构信息

Kunming Medical University Affiliated Stomatology Hospital, Kunming, China.

Yunnan Key Laboratory of Stomatology, Kunming, China.

出版信息

Oral Dis. 2024 May;30(4):2136-2149. doi: 10.1111/odi.14655. Epub 2023 Jun 25.

Abstract

OBJECTIVE

Idiopathic gingival fibromatosis (IGF) is a rare heterogeneous disease that results in the progressive and diffuse hyperplasia of gingival tissues. MicroRNAs are implicated in the development and progression of various tumors. The present study aimed to explore the potential roles and mechanisms of miR-148a-3p in IGF.

METHODS

Gingival fibroblasts (GFs) were transfected with miR-148a-3p mimics, miR-148a-3p inhibitors, or siNPTX1, and then, the proliferation and apoptosis of GFs and the expression of related genes were evaluated using Cell Counting Kit-8 assays, 5-ethynyl-2'-deoxyuridine assays, flow cytometry, reverse transcription-quantitative polymerase chain reaction, and western blot analysis, respectively.

RESULTS

miR-148a-3p was highly expressed in GFs of IGF (IGF-GFs) as compared with normal GFs (N-GFs). Overexpression of miR-148a-3p promoted the proliferation and inhibited the apoptosis of N-GFs, whereas downregulation of miR-148a-3p had the opposite effect in IGF-GFs. Knockdown of NPTX1 reversed miR-148a-3p-mediated effects in IGF-GFs. Dual-luciferase reporter assay confirmed that NPTX1 is a direct target of miR-148a-3p.

CONCLUSION

These findings identify that miR-148a-3p could regulate cell proliferation and apoptosis by targeting NPTX1, providing new insights for the further study of the molecular mechanism and treatment of IGF.

摘要

目的

特发性牙龈纤维瘤病(IGF)是一种罕见的异质性疾病,导致牙龈组织进行性弥漫性增生。MicroRNAs 与各种肿瘤的发生和发展有关。本研究旨在探讨 miR-148a-3p 在 IGF 中的潜在作用和机制。

方法

用 miR-148a-3p 模拟物、miR-148a-3p 抑制剂或 siNPTX1 转染牙龈成纤维细胞(GFs),然后通过细胞计数试剂盒-8 检测、5-乙炔基-2'-脱氧尿苷检测、流式细胞术、逆转录-定量聚合酶链反应和 Western blot 分析分别评估 GFs 的增殖和凋亡以及相关基因的表达。

结果

与正常 GFs(N-GFs)相比,IGF 中的 miR-148a-3p 在 GFs 中高表达。miR-148a-3p 的过表达促进了 N-GFs 的增殖并抑制了其凋亡,而 IGF-GFs 中 miR-148a-3p 的下调则产生相反的效果。NPTX1 的敲低逆转了 miR-148a-3p 在 IGF-GFs 中的介导作用。双荧光素酶报告基因检测证实 NPTX1 是 miR-148a-3p 的直接靶标。

结论

这些发现表明,miR-148a-3p 可以通过靶向 NPTX1 调节细胞增殖和凋亡,为进一步研究 IGF 的分子机制和治疗提供了新的见解。

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