Upregulation of interleukin-8 and activin A induces osteoclastogenesis in ameloblastoma
- Xin Liu
- Zhifeng Chen
- Tianjun Lan
- Peisheng Liang
- Qian Tao
Affiliations: Department of Oral and Maxillofacial Surgery, Guanghua School of Stomatology, Hospital of Stomatology, Sun Yat‑sen University, Guangzhou, Guangdong 510055, P.R. China, Department of Oral and Maxillofacial Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China
- Published online on: April 23, 2019 https://doi.org/10.3892/ijmm.2019.4171
Copyright: © Liu
et al. This is an open access article distributed under the
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Ameloblastoma is a common odontogenic benign tumor located in the jaws and is characterized by severe local bone destruction. The current study aimed to investigate the effect of interactions between tumor cells and bone marrow stromal cells (BMSCs) on osteoclast formation in ameloblastoma. The impact of ameloblastoma/BMSC interactions on cytokine production, gene expression and osteoclastogenesis was examined using an immortalized ameloblastoma cell line that the authors' previously established. The results demonstrated that interactions between ameloblastoma cells and BMSCs increased interleukin (IL)‑8 and activin A secretion by BMSCs. IL‑8 expression in BMSCs was modulated by tumor‑derived tumor necrosis factor‑α and IL‑8 contributed to osteoclast formation not only directly but also by stimulating receptor activator of NF‑κB ligand (RANKL) expression in BMSCs. Activin A secretion in BMSCs was stimulated by ameloblastoma cells via cell‑to‑cell‑mediated activation of c‑Jun N‑terminal kinase activation, acting as a cofactor of RANKL to induce osteoclast formation and function. The present study highlights the critical role of communication between BMSCs and ameloblastoma cells in bone resorption in ameloblastoma.