Background

MiR-1271-5p and coagulation factor XIII A (F13A1) are reported to be associated with the malignant progression of various types of cancers. The aim of this present research study was to delineate miR-1271-5p and F13A1 functional significance on oral squamous cell carcinoma (OSCC) progression.

Methods

MiR-1271-5p and F13A1 expression levels were determined via RT-qPCR and western blot, their overexpression or knockdown effects on OSCC cells were assessed through various in vitro assays, including colony formation, wound healing, transwell and flow cytometry, and their mutual relationship were investigated using an online software and validated confirmed by additional in vitro experiments. Further, mechanistic assays were performed to determine their influence on the PI3K/AKT pathway.

Results

Our results indicated downregulation of miR-1271-5p and upregulation of F13A1 in the investigated OSCC cell lines. In addition, upon overexpressing miR-1271-5p or knocking down F13A1, the cell proliferation, migration and invasion were suppressed and apoptotic rate was enhanced. Further investigations showed that the growth and invasive capabilities of OSCC cells were limited by miR-1271-5p through the downregulation of F13A1 mediated PI3K/AKT pathway.

Conclusion

MiR-1271-5p could suppress OSCC progression by influencing F13A1 expression to inhibit the PI3K/AKT signaling, indicating the promising potential of targeting miR-1271-5p as a novel approach for treating OSCC.

中文翻译：

---

MicroRNA-1271-5p通过抑制F13A1表达抑制口腔鳞状细胞癌的增殖、侵袭和迁移

背景

据报道，miR-1271-5p 和凝血因子 XIII A (F13A1) 与多种癌症的恶性进展相关。本研究的目的是阐明 miR-1271-5p 和 F13A1 对口腔鳞状细胞癌 (OSCC) 进展的功能意义。

方法

通过 RT-qPCR 和蛋白质印迹测定 MiR-1271-5p 和 F13A1 的表达水平，通过各种体外测定评估它们对 OSCC 细胞的过表达或敲低效应，包括集落形成、伤口愈合、Transwell 和流式细胞术，以及它们的相互关系。使用在线软件研究了关系，并通过额外的体外实验进行了验证。此外，还进行了机械分析以确定它们对 PI3K/AKT 通路的影响。

结果

我们的结果表明，在所研究的 OSCC 细胞系中，miR-1271-5p 下调，F13A1 上调。此外，过表达miR-1271-5p或敲低F13A1后，细胞增殖、迁移和侵袭受到抑制，细胞凋亡率增加。进一步研究表明，miR-1271-5p通过下调F13A1介导的PI3K/AKT通路来限制OSCC细胞的生长和侵袭能力。

结论

miR-1271-5p 可以通过影响 F13A1 表达来抑制 PI3K/AKT 信号传导来抑制 OSCC 进展，这表明靶向 miR-1271-5p 作为治疗 OSCC 的新方法具有广阔的前景。