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整合素-α5 促进口腔鳞状细胞癌的进展并调节 PI3K/AKT 信号通路。

Integrin-α5 promoted the progression of oral squamous cell carcinoma and modulated PI3K/AKT signaling pathway.

机构信息

Oral and Maxillofacial Surgery, Liaocheng People's Hospital, Liaocheng, China.

The Eighth Department of Neurology, Liaocheng Third People's Hospital, Liaocheng, China.

出版信息

Arch Oral Biol. 2019 May;101:85-91. doi: 10.1016/j.archoralbio.2019.03.007. Epub 2019 Mar 11.

Abstract

BACKGROUND

Integrin-α5 (ITGA5) gene has been reported to be critical for the progression of several cancers. However, the effects of ITGA5 in oral squamous cell carcinoma (OSCC) remain unclear.

METHODS

We firstly used bioinformatics methods to analyze the ITGA5 gene expression based on the public dataset. HO1-N-1 and SCC-9 cells with silenced ITGA5 were constructed using siRNA. Then, we determined the biological functions of ITGA5 in OSCC cells using cell counting kit-8 (CCK-8) assay, colony formation assay, wound healing assay and transwell assays. The expression of PI3K, p-PI3K, AKT, p-AKT, ERK and pERK were determined by western blot.

RESULTS

Our results revealed that ITGA5 expression was up-regulated in OSCC. The biological experiments further confirmed that ITGA5 expression was higher in OSCC cell lines. Moreover, we found that knockdown of ITGA5 inhibited the proliferation, migration and invasion of OSCC cells. The expression of phosphorylated-(p) PI3K, p-AKT and p-ERK obviously decreased after knockdown of ITGA5 in OSCC cells.

CONCLUSION

In summary, ITGA5 could promote the progression of OSCC via activating the PI3K/AKT signaling pathway, and it can be regarded as a potential biomarker for OSCC treatment.

摘要

背景

整合素-α5(ITGA5)基因已被报道对几种癌症的进展至关重要。然而,ITGA5 在口腔鳞状细胞癌(OSCC)中的作用尚不清楚。

方法

我们首先使用生物信息学方法基于公共数据集分析 ITGA5 基因表达。使用 siRNA 构建沉默 ITGA5 的 HO1-N-1 和 SCC-9 细胞。然后,我们使用细胞计数试剂盒-8(CCK-8)测定、集落形成测定、划痕愈合测定和 Transwell 测定来确定 ITGA5 在 OSCC 细胞中的生物学功能。通过 Western blot 测定 PI3K、p-PI3K、AKT、p-AKT、ERK 和 pERK 的表达。

结果

我们的结果表明 ITGA5 在 OSCC 中表达上调。生物学实验进一步证实 ITGA5 在 OSCC 细胞系中表达更高。此外,我们发现敲低 ITGA5 抑制了 OSCC 细胞的增殖、迁移和侵袭。敲低 ITGA5 后,OSCC 细胞中磷酸化(p)PI3K、p-AKT 和 p-ERK 的表达明显下降。

结论

总之,ITGA5 可以通过激活 PI3K/AKT 信号通路促进 OSCC 的进展,它可以被视为 OSCC 治疗的潜在生物标志物。

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