Significance of IL28RA in diagnosis of early pancreatic cancer and its regulation to pancreatic cancer cells by JAK/STAT signaling pathway – effects of IL28RA on pancreatic cancer

L. Yang, W.-C. Wei, X.-N. Meng, J. Gao, N. Guo, F.-T. Wu, W.-W. Zeng

Department of Gastroenterology, People’s Hospital of Dongying City, Dongying, Shandong Province, P.R., China. zengweiwei1978@163.com

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• Oncology

OBJECTIVE: To explore the significance of IL28RA in diagnosis of early pancreatic cancer and its regulation to pancreatic cancer cells by the Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling pathway.
PATIENTS AND METHODS: A total of 81 patients with early pancreatic cancer were enrolled as a pancreatic cancer group, and 81 patients with benign pancreatic diseases were enrolled as a benign disease group. Western blot was adopted to analyze the serum IL28RA expression of the two groups and its diagnostic value in early pancreatic cancer. A pancreatic cancer cell model was constructed, and the IL28RA expression in pancreatic cancer cells, PANC-1 and BXPC-3, was up-regulated to explore the biological function of pancreatic cancer cells after up-regulation of IL28RA and the effects on JAK-STAT signaling pathway.
RESULTS: Lowly expressed in serum of patients with pancreatic cancer, IL28RA showed a sensitivity of 80.25%, specificity of 75.31%, and area under the curve (AUC) of 0.846 in diagnosis of early pancreatic cancer. It was found that up-regulation of IL28RA expression in pancreatic cancer cells inhibited proliferation and invasion abilities of pancreatic cancer cells, increased apoptosis rate and expression of pro-apoptotic protein bax, decreased expression of anti-apoptosis protein bcl-2, and significantly inhibited phosphorylation level of JAK2 and STAT3 proteins.
CONCLUSIONS: IL28RA is lowly expressed in pancreatic cancer patients, and has certain diagnostic value for early pancreatic cancer. Its up-regulated expression can inhibit the proliferation and invasion of pancreatic cancer cells, and promote their apoptosis by inhibiting the activation of JAK-STAT signaling pathway.

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