期刊
ONCOLOGY REPORTS
卷 44, 期 6, 页码 2547-2558出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2020.7788
关键词
head and neck cancer; bone pain; HMGB1; RAGE; sensory neuron
类别
资金
- Ministry of Education, Culture, Sports, Science, and Technology of Japan [18K17225, 20H03889]
- Grants-in-Aid for Scientific Research [18K17225, 20H03889] Funding Source: KAKEN
Advanced head and neck cancer (HNC) can invade facial bone and cause bone pain, thus posing a significant challenge to the quality of life of patients presenting with advanced HNC. The present study was designed to investigate HNC bone pain (HNC-BP) in an intratibial mouse xenograft model that utilized an HNC cell line (SAS cells). These mice develop HNC-BP that is associated with an expression of phosphorylated ERK1/2 (pERK1/2), which is a molecular indicator of neuron excitation in dorsal root ganglia (DRG) sensory neurons. Our experiments demonstrated that the inhibition of high mobility group box 1 (HMGB1) by short hairpin (shRNA) transduction, HMGB1 neutralizing antibody, and HMGB1 receptor antagonist suppressed the HNC-BP and the pERK1/2 expression in DRG. It was also observed that HNC-derived HMGB1 increased the expression of the acid-sensing nociceptor, transient receptor potential vanilloid 1 (TRPV1), which is a major cause of osteoclastic HNC-BP in DRG. Collectively, our results demonstrated that HMGB1 originating in HNC evokes HNC-BP via direct HMGB1 signaling and hypersensitization for the acid environment in sensory neurons.
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