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Viral IL‐10 promotes cell proliferation and cell cycle progression via JAK2/STAT3 signaling pathway in nasopharyngeal carcinoma cells
Author(s) -
Ren Yanxin,
Yang Jie,
Li Mei,
Huang Ning,
Chen Yun,
Wu Xifang,
Wang Xiaoli,
Qiu Shun,
Wang Hu,
Li Xiaojiang
Publication year - 2020
Publication title -
biotechnology and applied biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.468
H-Index - 70
eISSN - 1470-8744
pISSN - 0885-4513
DOI - 10.1002/bab.1856
Subject(s) - nasopharyngeal carcinoma , cell cycle , cell growth , cytotoxic t cell , signal transduction , cancer research , cell , biology , flow cytometry , microbiology and biotechnology , chemistry , medicine , in vitro , biochemistry , radiation therapy
Epstein–Barr virus (EBV) is positively related to the morbidity of nasopharyngeal carcinoma (NPC) in Asia. After infection, EBV can produce several proteins, including viral interleukin‐10 (vIL‐10). But the mechanism by which vIL‐10 contributes to NPC cell proliferation and cell cycle progression is not well understood. In this study, EBV negative and positive cell lines, and the JAK2/STAT3 signal pathway inhibitor AG490 were used to illustrate the role of vIL‐10 in NPC. Cell proliferation and cell cycle were measured by CCK‐8 and flow cytometry. The expression levels of related protein were measured by Western blotting. High concentrations of vIL‐10 and IL‐6 were found in the EBV positive patients. The expression level of IL‐6 was positively related to the presence of concentration of vIL‐10. vIL‐10 can promote cancer cell proliferation and G1 to S phase transmission via upregulating the IL‐6 protein level by activating the JAK2/STAT3 signal pathway. Furthermore, EBV can induce the formation of cytotoxic T cells, whereas vIL‐10 can block the function of cytotoxic T cells. Taken together, these results suggest that vIL‐10 promotes cell proliferation and cell cycle progression via JAK2/STAT3 signaling pathway in NPC.