New Mechanism of Bone Cancer Pain: Tumor Tissue-Derived Endogenous Formaldehyde Induced Bone Cancer Pain via TRPV1 Activation

被引：14
|
作者：
Wan, You [1 ]
机构：
[1] Peking Univ, Neurosci Res Inst, Beijing 100191, Peoples R China
来源：
TRANSLATIONAL RESEARCH IN PAIN AND ITCH | 2016年 / 904卷
关键词：
Bone cancer pain; Formaldehyde; Transient receptor potential vanilloid subfamily member 1 (TRPV1); Insulin-like growth factor I (IGF-I); DORSAL-ROOT GANGLION; PRIMARY SENSORY NEURONS; GROWTH-FACTOR-I; PHOSPHATIDYLINOSITOL; 3-KINASE; DIFFERENT INTENSITIES; INFLAMMATORY PAIN; RECEPTOR TRPV1; FORMALIN PAIN; DEMETHYLASE; UP-REGULATION;
D O I：
10.1007/978-94-017-7537-3_4
中图分类号：
Q [生物科学];
学科分类号：
07 ; 0710 ; 09 ;
摘要：
In recent years, our serial investigations focused on the role of cancer cells-derived endogenous formaldehyde in bone cancer pain. We found that cancer cells produced formaldehyde through demethylation process by serine hydroxymethyltransferase (SHMT1 and SHMT2) and lysine-specific histone demethylase 1 (LSD1). When the cancer cells metastasized into bone marrow, the elevated endogenous formaldehyde induced bone cancer pain through activation on the transient receptor potential vanilloid subfamily member 1 (TRPV1) in the peripheral nerve fibers. More interestingly, TRPV1 expressions in the peripheral fibers were upregulated by the local insulin-like growth factor I (IGF-I) produced by the activated osteoblasts. In conclusion, tumor tissue-derived endogenous formaldehyde induced bone cancer pain via TRPV1 activation.
引用
收藏
页码：41 / 58
页数：18
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