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Open AccessArticle

Tumor Angiogenic Inhibition Triggered Necrosis (TAITN) in Oral Cancer

1
Department of Oral Pathology and Medicine, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan
2
Department of Dental Pharmacology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan
3
Advanced Research Center for Oral and Craniofacial Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama 700-8558, Japan
4
Division of Oral and Maxillofacial Surgery, Kagawa Prefectural Central Hospital, Takamatsu, Kagawa 760-8557, Japan
5
Department of Anatomy, Basic Medicine Science College, Harbin Medical University, Harbin 150076, China
*
Authors to whom correspondence should be addressed.
Cells 2019, 8(7), 761; https://doi.org/10.3390/cells8070761
Received: 27 June 2019 / Revised: 18 July 2019 / Accepted: 20 July 2019 / Published: 22 July 2019
(This article belongs to the Special Issue Angiogenesis in Cancer)
CXCR4 is a chemokine receptor crucial in tumor progression, although the angiogenic role of CXCR4 in oral squamous cell carcinoma (OSCC) has not been investigated. Here we show that CXCR4 is crucial for tumor angiogenesis, thereby supporting tumor survival in OSCC. Immunohistochemistry on human clinical specimens revealed that CXCR4 and a tumor vasculature marker CD34 were co-distributed in tumor vessels in human OSCC specimens. To uncover the effects of CXCR4 inhibition, we treated the OSCC-xenografted mice with AMD3100, so-called plerixafor, an antagonist of CXCR4. Notably, we found a unique pathophysiological structure defined as tumor angiogenic inhibition triggered necrosis (TAITN), which was induced by the CXCR4 antagonism. Treatment with AMD3100 increased necrotic areas with the induction of hypoxia-inducible factor-1α in the xenografted tumors, suggesting that AMD3100-induced TAITN was involved in hypoxia and ischemia. Taken together, we demonstrated that CXCR4 plays a crucial role in tumor angiogenesis required for OSCC progression, whereas TAITN induced by CXCR4 antagonism could be an effective anti-angiogenic therapeutic strategy in OSCC treatment. View Full-Text
Keywords: tumor blood vessel; tumor angiogenic inhibition triggered necrosis (TAITN); CXCR4 antagonist; oral squamous cell carcinoma; hypoxia tumor blood vessel; tumor angiogenic inhibition triggered necrosis (TAITN); CXCR4 antagonist; oral squamous cell carcinoma; hypoxia
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Yoshida, S.; Kawai, H.; Eguchi, T.; Sukegawa, S.; Oo, M.W.; Anqi, C.; Takabatake, K.; Nakano, K.; Okamoto, K.; Nagatsuka, H. Tumor Angiogenic Inhibition Triggered Necrosis (TAITN) in Oral Cancer. Cells 2019, 8, 761.

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