S100A7 promotes the migration, invasion and metastasis of human cervical cancer cells through epithelial-mesenchymal transition

Abstract

S100A7 is an EF-hand calcium-binding protein that has been suggested to be implicated in cell proliferation, migration, invasion and tumor metastasis. However, its role in cervical cancer has not yet been fully clarified. The present study used immunohistochemistry analysis of S100A7 in clinical specimens of cervical cancer to show that S100A7 expression was significantly upregulated in cervical cancer tissues compared with normal cervical tissues and S100A7 expression in high grade cervical intraepithelial neoplasm (CIN) was significantly higher than cervical cancer. Statistical analysis showed that S100A7 expression was associated with tumor grade (P <0.01) and lymph node metastasis (P <0.05). Functional studies showed that overexpression of S100A7 in cervical cancer cells promoted migration, invasion and metastasis of cervical cancer cells without influencing cell proliferation. Furthermore, S100A7 was found to be secreted into the conditioned media and extracellular S100A7 enhanced cell migration and invasion. Mechanistically, S100A7 bound to RAGE and activated ERK signaling pathway. And S100A7 enhanced cell mesenchymal properties and induced epithelial–mesenchymal transition. In summary, these data reveal a crucial role for S100A7 in regulating cell migration, invasion, metastasis and EMT of cervical cancer and suggest that targeting S100A7 may offer a new targeted strategy for cervical cancer.

Galectin-1 Promotes Metastasis in Gastric Cancer Through a Sphingosine-1-Phosphate Receptor 1-Dependent Mechanism

“…The phenomenon known as epithelial-mesenchymal transition (EMT) promotes invasion and metastasis in many cancers [29][30][31], and we hypothesized that S1PR1 might be involved in EMT of GC cells. We treated MGC-803 cells with 10 ng/ml TGF-β1 for 24 hours.…”

Adipose Stem Cells and Cancer: Concise Review

“…Limited studies have been done to evaluate the effect of ASCs on cervical cancer. However, one study by Tian et al found that S100A7, described above for its role in breast cancer proliferation and metastasis, has also been shown to enhance cell migration, invasion, metastasis and the epithelial to mesenchymal transition of cervical cancer . ASC secretion of two pro‐inflammatory cytokines IL‐8 and IL‐6, described below, was increased when cocultured with bladder cancer cells .…”

Psoriasin overexpression confers drug resistance to cisplatin by activating ERK in gastric cancer

“…by regulating cell proliferation, metastasis, migration, invasion, apoptosis and angiogenesis (17)(18)(19). Mechanistically, several signaling pathways have been demonstrated to have a correlation with psoriasin, including Hippo, receptor for advanced glycation endproducts (RAGE), extracellular signal-regulated kinase (ERK), β-catenin and nuclear factor (NF)-κB pathways.…”

“…Similarly, psoriasin promotes cell survival by binding to c-Jun activation domain-binding protein1 and enhancing the phosphorylation of NF-κB and protein kinase B in breast cancer (20). Another study demonstrated that psoriasin binds to RAGE and activates ERK signaling to increase migration and invasion in cervical cancer (18). However, the role of psoriasin in GC and its underlying mechanisms remain unclear.…”

“…Psoriasin, a low molecular weight protein (11.4 kDa), is localized in the cytoplasm, cell nucleus or secreted outside of the cell in certain cases (9,10). Dysregulated expression of psoriasin has been observed in various types of cancer, including oral squamous cell carcinoma (11), breast cancer (10,12), lung cancer (13), bladder cancer (14), skin cancer (15), head and neck cancer (16), prostate cancer (17) and cervical cancer (18). Functionally, psoriasin usually has malignant functions in cancer; however, it can also exhibit tumor suppressive effects in certain types of oral carcinoma and breast cancer by decreasing β-catenin activity (11,12).…”