Cytokine TNF-α promotes invasion and metastasis of gastric cancer by down-regulating Pentraxin3

Abstract

As a novel multifaceted player in cancer, Pentraxin3(PTX3) was recognized to be a possible factor related with tumor development. Recent researches have indicated that PTX3 is involved in immune response, inflammation, as well as cancer, and is greatly controlled by numerous cytokines. Tumor necrosis factor (TNF-α) is an imperative cytokine that demonstrates an extensive array of biological consequences in gastric cancer advancement. Here, we inspected the expression of PTX3 in gastric carcinoma tissues along with gastric cell lines and established that PTX3 was suggestively inferior in gastric cancer tissue and cells. The treatment of the gastric cell lines BGC-823 as well as SGC-7901 with rhTNF-α caused substantial decrease in the expression of PTX3. Furthermore, PTX3 controlled the capability of cell migration, invasion as well as epithelial-mesenchymal transition (EMT) in gastric cancer cell lines mediated by TNF-α. Additionally, PTX3 upregulation inhibited tumorigenicity in vivo and could be reversed by exogenous TNF-α. Conversely, overexpression of PTX3 inhibited progress both in vitro as well as in vivo in gastric cancer mediated by TNF-α. Further studies are necessary to demonstrate the mechanism of interaction between PTX3 and cytokines.

Pentraxin-3 inhibits milky spots metastasis of gastric cancer by inhibiting M2 macrophage polarization

“…Furthermore, the CSC phenotype can be obtained by inducing the tumor EMT state 20 . In our previous studies, we have confirmed that overexpression of PTX3 can inhibit the EMT process in GCCs (BGC-823 and SGC-7901) 17 . However, we have not yet proved whether PTX3 affects the stemness of GCCs.…”

“…Evidence from clinical and experimental studies has indicated that TAMs promote the invasion and metastasis of solid tumors by releasing a variety of cytokines. We have proven through previous studies that PTX3 can affect chemokine to inhibit the invasion and metastasis of GCCs 17 . Therefore, we speculated whether PTX3 is linked to macrophages.…”

“…In our previous experiments, the high expression of PTX3 in normal gastric mucosal epithelial cells and adjacent cancer tissues was demonstrated via qRT-PCR and western blot 17 . In this research, we used the tissue arrays including 30 cancerous tissues and para-cancerous tissues, and added the IHC analysis for the difference of PTX3 expression as a supplement and found similar results (Fig.…”

“…Since PTX3 may affect many types of tumor cells, it is essential to clarify the biological role of PTX3 in tumor development. In our previous studies, we have demonstrated the differences in the expression of PTX3 between GCCs and normal gastric mucosal epithelial cells and GC tissues and adjacent tissues and proved the role of PTX3 in the epithelial-mesenchymal transition (EMT) process of GCCs 17 . EMT plays an important role in the formation and metastasis of GC because GC stem cells have high invasiveness and EMT properties.…”

The LPS-Treated Human Gastric Cancer Cells (AGS) Show a Significant Higher Tendency to Proliferation, Inflammation and Cannabinoid Receptor 1 Expression

“…Our findings revealed that cell proliferation was increased following LPS stimulation in AGS cells. Earlier researches demonstrated the effects of IL-1β (27), and other inflammatory cytokines (28) in gastric cancer progression and showed that upregulation of CBRs led to the activation of downstream pathways involved in cell progression and survival and cancer cell invasion through some pathways such as PI3K/PKB phosphorylation (29,30), ERK cascade (31), and CXCR4/CXCL12 (32). Taken together, previous results and findings suggest that inflammatory cytokines may exert their function through upregulation of CB1R.…”