Involvement of ERK and JNK pathways in IFN-[gamma]-induced B7-DC expression on tumor cells

• Published in: Journal of cancer research and clinical oncology Vol. 137; no. 2; p. 243
• Main Authors: Deng, Junfang, Qian, Yigang, Geng, Lei, Xie, Haiyang, Wang, Yan, Jiang, Guoping, Zhou, Lin, Zhang, Ming, Zheng, Shusen
• Format: Journal Article
• Language: English
• Published: Heidelberg Springer Nature B.V 01.02.2011
• Subjects: Cellular biology; Gene expression; Immune system; Interferon; Signal transduction
• ISSN: 0171-5216; 1432-1335
• DOI: 10.1007/s00432-010-0876-x

B7-DC on tumor cells was demonstrated to promote tumor immunity; however, the precise mechanism responsible for the aberrant B7-DC expression remains unknown. Interferon gamma (IFN-γ) can induce B7-DC expression on macrophages and has been shown to regulate anti-tumor immunity by various mechanisms. This study was designed to investigate the relationship of IFN-γ and B7-DC on tumor cells and further explored the signal transduction pathways involved. RT-PCR and flow cytometry were used for the analysis of B7-DC expression on various tumor cells. The phosphorylation of p38, ERK1/2, JNK, Akt, and JAK2 was determined by Western blot. IFN-γ markedly up-regulated B7-DC expression on various tumor cells and resulted in the phosphorylation of JAK2, JNK, ERK, p38, and Akt. Inhibition of ERK or JNK pathway significantly decreased IFN-γ-induced B7-DC expression, whereas inhibition of phosphorylation of Akt, p38, and JAK2 had very little effect on IFN-γ-induced B7-DC expression. Our findings demonstrate that the pretreatment of tumor cells with IFN-γ enhances B7-DC expression through ERK and JNK pathways.[PUBLICATION ABSTRACT]