Influences of S100A8 and S100A9 on Proliferation of Nasopharyngeal Carcinoma Cells through PI3K/Akt Signaling Pathway.

Liting Wen,Danfeng Li,Yu Ding,Bo Yue,Keyong Tian,Kun Liang,Xiaodong Chen,Junyan Liu

doi:10.1155/2021/9917365

Liting Wen, Danfeng Li + Show 6 more

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https://doi.org/10.1155/2021/9917365

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Journal: BioMed research international	Publication Date: Sep 24, 2021
Citations: 7	License type: CC BY 4.0

Affiliation: Air Force Medical University

Abstract

Objective To investigate the effects of S100A8 and S100A9 on proliferation in nasopharyngeal carcinoma cells and the regulatory effects of PI3K/Akt signaling pathway. Methods Nasopharyngeal carcinoma cells (CNE1) were cultured and randomly divided into three groups: control group, S100A8/S100A9 overexpression group, and siRNA S100A8/S100A9 group. CCK-8 method was used to detect the effect of S100A8 and S100A9 on the viability of nasopharyngeal carcinoma cells. The effects of S100A8 and S100A9 on the colony forming ability of nasopharyngeal carcinoma cells were detected by colony forming assay. The effects of S100A8 and S100A9 on the proliferation of nasopharyngeal carcinoma cells were detected by EdU staining. The mRNA levels of PI3K and Akt were detected by RT-PCR. The expression levels of PI3K and Akt in NPC cells were detected by Western blot. Wortmannin, an inhibitor of PI3K/Akt pathway, was used to inhibit the activation of PI3K/Akt pathway. Results Compared with the control group, the cell viability, the number of plate clones, the positive rate of EdU staining, and the mRNA and protein levels of PI3K and Akt were increased in the overexpression group. Compared with the control group, the cell viability, the number of plate clones, the positive rate of EdU staining, and the mRNA and protein levels of PI3K and Akt were decreased in the siRNA group. After inhibiting the activation of PI3K/Akt pathway, the viability of NPC cells in the overexpression group decreased significantly at 48 h and 72 h, while that in the siRNA group increased significantly. Conclusion SiRNA S100A8 and S100A9 could inhibit the proliferation of nasopharyngeal carcinoma cells, and the underlying mechanism may be related to the inhibition of PI3K/Akt signaling pathway.

Highlights

Nasopharyngeal carcinoma (NPC) is a malignant tumor originating from the nasopharyngeal epithelial tissues, with such biological characteristics as direct infiltration and lymphatic metastasis, but its pathogenesis is still not very clear
The results of plate colony formation assay (Figure 2(a)) showed that at 14 d, the overexpression group exhibited a larger number of NPC cell clones (∗p < 0:05), while the small interfering ribonucleic acid (siRNA) group displayed a remarkably smaller number of NPC cell clones (#p < 0:05) compared with the control group (Figure 2(b)), implying that siRNA S100A8/S100A9 can repress the plate colony formation of NPC cells
SiRNA S100A8/S100A9 Could Suppress the Proliferation of NPC Cells. It was manifested in the results of EdU staining (Figure 3(a)) at 14 d; the NPC cell proliferation rate was raised in the overexpression group (∗p < 0:05), but it was reduced in the siRNA group (#p < 0:05) in comparison with that in the control group (Figure 3(b)), indicating that siRNA S100A8/S100A9 can suppress the proliferation of NPC cells

Summary

Introduction

Nasopharyngeal carcinoma (NPC) is a malignant tumor originating from the nasopharyngeal epithelial tissues, with such biological characteristics as direct infiltration and lymphatic metastasis, but its pathogenesis is still not very clear. The treatment for early NPC is dominated by radiotherapy, while radiotherapy, chemotherapy, or molecular targeted therapy is usually employed for patients with advanced NPC. Searching for efficacious molecular targets of clinical treatment is of important significance for improving the quality of life and extending the survival time of the patients, and it is a scientific problem needs to be solved. Recent studies have manifested that the abnormal proliferation of NPC cells plays crucial roles in the occurrence and development of NPC, while the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway has vital regulatory effects on the cell proliferation, differentiation, BioMed Research International and apoptosis [5, 6]. Large quantities of studies have demonstrated that the activation of the PI3K/Akt signaling pathway has a close correlation with tumorigenesis. The activity of PI3K and Akt is increased in NPC tissues, and the high expression levels of PI3K and Akt are related to the prognosis [8]

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Conclusion