558P - IL-1beta mediates anti-progression activities in renal cell carcinoma by inducing MCP-1

Date 17 December 2016
Event ESMO Asia 2016 Congress
Session Poster lunch
Topics Renal Cell Cancer
Translational Research
Presenter Ji-Rui Yang
Citation Annals of Oncology (2016) 27 (suppl_9): ix181-ix183. 10.1093/annonc/mdw602
Authors J. Yang1, C. Sun2, S. Lu3, W. Hsieh4, Y. Wen5, C. Lee4
  • 1National Institute Of Cancer Research, National Health Research Institutes, 35053 - Zhunan/TW
  • 2Department Of Nephrology, Chang Gung Memorial Hospital, 201 - Keelung/TW
  • 3Department Of Nephrology, Chang Gung Memorial Hospital, Keelung/TW
  • 4National Institute Of Cancer Research, National Health Research Institutes, 350553 - Zhunan/TW
  • 5Department Of Biological Science And Technology, Chung Hwa University of Medical Technology, Tainan/TW



Inflammation has a pivotal role in the carcinogenesis of renal cell carcinoma (RCC). Interleukin-1beta (IL-1ß) is a major mediator of inflammatory responses, thus its roles in RCC attract attention. A pro-metastasis role of IL-1ß has been proposed by a previous in vitro study. We aimed to assess the connection between IL-1ß and clinical consequences of RCC patients.


Blood samples, tumor and the adjacent non-tumor tissues were collected from 26 RCC patients with pathological information. Intratumoral expressions of pro-IL-1ß and IL-1ß, or MCP-1 were examined by western blotting or immunohistochemical staining. Levels of IL-1ß and MCP-1 in serum or culture media of RCC cells were analyzed by ELISA and cytometric beads array. In vitro malignancies of RCC cells were examined by soft-agar clonogenicity and Matrigel-coated trans-well invasiveness.


Neither intratumoral expression nor serum level of IL1ß was associated with RCC progression in our patient cohort, implying that IL-1ß may elicit multiple activities in RCC. Here, we showed that IL-1ß treatment inhibits in vitro cancerous properties of RCC cell lines. IL1ß induced the secretion of MCP-1 by RCC cells. Exogenous MCP-1 negatively regulated the proliferation and BrdU incorporation of RCC cells. Blockage of IL-1ß or MCP-1 activities with neutralizing antibodies significantly increased the invasiveness of IL-1ß-highly secreting RCC cells. Furthermore, neutralizing antibodies against MCP-1 attenuated the invasion inhibitory effect of exogenous IL-1ß. Immunohistochemical staining showed that aggressive RCC expressed downregulated intratumoral MCP-1 whereas the tumors with MCP-1 overexpression were less malignant. A public array database showed that lower MCP-1 expression (n = 152) is associated with more aggressive tumor stages (T≧III, M1, N1) compared to those with earlier stages (n = 132, P = 0.015).


IL-1ß-induced intratumoral MCP-1 expression is a novel mechanism by which IL-1ß exerts anti-tumor activities in RCC. Our data add another layer of complexity to IL-1ß effect on cancer and suggest more clinical applicability of MCP-1 than IL-1ß in RCC.

Clinical trial indentification

Legal entity responsible for the study



Chang Gung Memorial Hospital, National Health Research Institute, and Chung Hwa University of Medical Technology


All authors have declared no conflicts of interest.