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Home  > Press Release  > Interleukin-13 receptor α2 is a novel marker and potential therapeutic target for human melanoma

Interleukin-13 receptor α2 is a novel marker and potential therapeutic target for human melanoma

Abstract

Malignant melanoma is one of the untreatable cancers in which conventional therapeutic strategies, including chemotherapy, are hardly effective. Therefore, identification of novel therapeutic targets involved in melanoma progression is urgently needed for developing effective therapeutic methods. Overexpression of interleukin-13 receptor α2 (IL13Rα2) is observed in several cancer types including glioma and pancreatic cancer. Although IL13Rα2 is implicated in the progression of various types of cancer, its expression and roles in the malignant melanoma have not yet been elucidated. In the present study, we showed that IL13Rα2 was expressed in approximately 7.5% melanoma patients. While IL13Rα2 expression in human melanoma cells decreased their proliferation in vitro, it promoted in vivo tumour growth and angiogenesis in melanoma xenograft mouse model. We also found that the expression of amphiregulin, a member of the epidermal growth factor (EGF) family, was correlated with IL13Rα2 expression in cultured melanoma cells, xenograft tumour tissues and melanoma clinical samples. Furthermore, expression of amphiregulin promoted tumour growth, implicating causal relationship between the expression of IL13Rα2 and amphiregulin. These results suggest that IL13Rα2 enhances tumorigenicity by inducing angiogenesis in malignant melanoma, and serves as a potential therapeutic target of malignant melanoma.

Journal Article

JOURNAL:
Scientific Reports
TITLE:
Interleukin-13 receptor α2 is a novel marker and potential therapeutic target for human melanoma
DOI:
https://doi.org/10.1038/s41598-019-39018-3

Correspondence to

WATABE TETSURO PhD, Professor
Department of Biochemistry,
Graduate School of Medical and Dental Sciences,
Tokyo Medical and Dental University (TMDU)
Phone:+81-3-5803-5449 Fax:+81-3-5803-0187
E-mail: t-watabe.bch (at) tmd.ac.jp


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