Novel midkine inhibitor iMDK inhibits tumor growth and angiogenesis in oral squamous cell carcinoma

Masanori Masui; Tatsuo Okui; Tsuyoshi Shimo; Kiyofumi Takabatake; Takuya Fukazawa; Kenichi Matsumoto; Naito Kurio; Soichiro Ibaragi; Yoshio Naomoto; Hitoshi Nagatsuka; Akira Sasaki

Novel midkine inhibitor iMDK inhibits tumor growth and angiogenesis in oral squamous cell carcinoma

Masanori Masui, Tatsuo Okui, Tsuyoshi Shimo, Kiyofumi Takabatake, Takuya Fukazawa, Kenichi Matsumoto, Naito Kurio, Soichiro Ibaragi, Yoshio Naomoto, Hitoshi Nagatsuka, Akira Sasaki

Research output: Contribution to journal › Article

13 Citations (Scopus)

Abstract

Midkine is a heparin-binding growth factor highly expressed in various human malignant tumors. However, its role in the growth of oral squamous cell carcinoma is not well understood. In this study, we analyzed the antitumor effect of a novel midkine inhibitor (iMDK) against oral squamous cell carcinoma. Administration of iMDK induced a robust antitumor response and suppressed cluster of differentiation 31 (CD31) expression in oral squamous cell carcinoma HSC-2 cells and SAS cells xenograft models. iMDK inhibited the proliferation of these cells dose-dependently, as well as the expression of midkine and phospho-extracellular signal-regulated kinase in HSC-2 and SAS cells. Moreover, iMDK significantly inhibited vascular endothelial growth factor and induced tube growth of human umbilical vein endothelial cells in a dose-dependent fashion. These findings suggest that midkine is critically involved in oral squamous cell carcinoma and iMDK can be effectively used for the treatment of oral squamous cell carcinoma.

Original language	English
Pages (from-to)	2775-2781
Number of pages	7
Journal	Anticancer research
Volume	36
Issue number	6
Publication status	Published - Jun 2016

Keywords

Angiogenesis
IMDK
Midkine
Oral squamous cell carcinoma

ASJC Scopus subject areas

Oncology
Cancer Research

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Masui, M., Okui, T., Shimo, T., Takabatake, K., Fukazawa, T., Matsumoto, K., Kurio, N., Ibaragi, S., Naomoto, Y., Nagatsuka, H., & Sasaki, A. (2016). Novel midkine inhibitor iMDK inhibits tumor growth and angiogenesis in oral squamous cell carcinoma. Anticancer research, 36(6), 2775-2781.

Novel midkine inhibitor iMDK inhibits tumor growth and angiogenesis in oral squamous cell carcinoma. / Masui, Masanori; Okui, Tatsuo; Shimo, Tsuyoshi; Takabatake, Kiyofumi; Fukazawa, Takuya; Matsumoto, Kenichi; Kurio, Naito; Ibaragi, Soichiro; Naomoto, Yoshio; Nagatsuka, Hitoshi ; Sasaki, Akira.

In: Anticancer research, Vol. 36, No. 6, 06.2016, p. 2775-2781.

Research output: Contribution to journal › Article

Masui, Masanori ; Okui, Tatsuo ; Shimo, Tsuyoshi ; Takabatake, Kiyofumi ; Fukazawa, Takuya ; Matsumoto, Kenichi ; Kurio, Naito ; Ibaragi, Soichiro ; Naomoto, Yoshio ; Nagatsuka, Hitoshi ; Sasaki, Akira. / Novel midkine inhibitor iMDK inhibits tumor growth and angiogenesis in oral squamous cell carcinoma. In: Anticancer research. 2016 ; Vol. 36, No. 6. pp. 2775-2781.

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abstract = "Midkine is a heparin-binding growth factor highly expressed in various human malignant tumors. However, its role in the growth of oral squamous cell carcinoma is not well understood. In this study, we analyzed the antitumor effect of a novel midkine inhibitor (iMDK) against oral squamous cell carcinoma. Administration of iMDK induced a robust antitumor response and suppressed cluster of differentiation 31 (CD31) expression in oral squamous cell carcinoma HSC-2 cells and SAS cells xenograft models. iMDK inhibited the proliferation of these cells dose-dependently, as well as the expression of midkine and phospho-extracellular signal-regulated kinase in HSC-2 and SAS cells. Moreover, iMDK significantly inhibited vascular endothelial growth factor and induced tube growth of human umbilical vein endothelial cells in a dose-dependent fashion. These findings suggest that midkine is critically involved in oral squamous cell carcinoma and iMDK can be effectively used for the treatment of oral squamous cell carcinoma.",

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AB - Midkine is a heparin-binding growth factor highly expressed in various human malignant tumors. However, its role in the growth of oral squamous cell carcinoma is not well understood. In this study, we analyzed the antitumor effect of a novel midkine inhibitor (iMDK) against oral squamous cell carcinoma. Administration of iMDK induced a robust antitumor response and suppressed cluster of differentiation 31 (CD31) expression in oral squamous cell carcinoma HSC-2 cells and SAS cells xenograft models. iMDK inhibited the proliferation of these cells dose-dependently, as well as the expression of midkine and phospho-extracellular signal-regulated kinase in HSC-2 and SAS cells. Moreover, iMDK significantly inhibited vascular endothelial growth factor and induced tube growth of human umbilical vein endothelial cells in a dose-dependent fashion. These findings suggest that midkine is critically involved in oral squamous cell carcinoma and iMDK can be effectively used for the treatment of oral squamous cell carcinoma.

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