J Cancer 2020; 11(7):1800-1807. doi:10.7150/jca.39562 This issue

Research Paper

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

Xinye Cui1, Han Zhang2, An'na Cao2, Liang Cao1✉, Xiang Hu1✉

1. Department of General Surgery, The First Affiliated Hospital, Dalian Medical University, Dalian 116011,China
2. Department of Pathology, Dalian Medical University, Dalian 116044, People's Republic of China

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Cui X, Zhang H, Cao A, Cao L, Hu X. Cytokine TNF-α promotes invasion and metastasis of gastric cancer by down-regulating Pentraxin3. J Cancer 2020; 11(7):1800-1807. doi:10.7150/jca.39562. Available from https://www.jcancer.org/v11p1800.htm

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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.

Keywords: PTX3, Milky spot, TNF-α, Gastric cancer, EMT