Interleukin-28A triggers wound healing migration of bladder cancer cells via NF-κB-mediated MMP-9 expression inducing the MAPK pathway

Cellular Signalling
Se-Jung LeeSung-Kwon Moon

Abstract

Interleukin (IL)-28A, also called IFN-λ2, is a member of the classIIcytokine family and has demonstrated anti-proliferative and anti-viral signals. The present study demonstrated migration inducement of IL-28A-treated bladder cancer cells - a novel function. RNA microarray analysis showed an enhanced expression of IL-28A and its receptor IL-28AR1 in muscle invasive urothelial carcinoma in a human bladder. Strong expression of IL-28A and IL-28AR1 was detected in bladder cancer tissues and cell lines (5637, T-24, and HT1376 cells), as determined by real-time PCR and immunoblot analysis. IL-28A treatment induced migration of bladder cancer cells, independent of the cell growth. IL-28AR1-specific small interfering RNA (si-IL-28AR1) inhibited the induction of migration in IL-28A-treated cells. IL-28A treatment stimulated the expression of matrix metalloproteinases-9 (MMP-9) via activation of transcription factor NF-κB. Gene knockdown for MMP-9 and the p65 subunit of NF-κB, using siRNA transfection, suppressed wound healing migration in IL-28A-treated bladder cancer cells. Also, treatment with IL-28A induced activation of mitogen-activated protein kinase (MAPK) in bladder cancer cells. MAPK function blockage by a MAPK-specific inhibi...Continue Reading

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Citations

Dec 31, 2015·Tumour Biology : the Journal of the International Society for Oncodevelopmental Biology and Medicine·Yuanjun JiangQiao Qiao
Oct 19, 2016·Cancer Research and Treatment : Official Journal of Korean Cancer Association·Shu-Tao TanBin Wu
Aug 25, 2020·Integrative Cancer Therapies·Nursyamirah Abd RazakKamariah Long
Oct 29, 2014·Experimental Biology and Medicine·Cheng TanHui-Xin Yu
May 13, 2021·Nature Communications·Constance McElrathSergei V Kotenko
Jun 8, 2021·Frontiers in Oncology·Yi LiChong Li
Dec 15, 2018·ACS Applied Materials & Interfaces·Ningqiang GongXing-Jie Liang

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