Upregulation of CCL2 via ATF3/c-Jun interaction mediated the Bortezomib-induced peripheral neuropathy

Highlights • Painful peripheral neuropathy induced by chemotherapy drugs often serves as the common reason for treatment discontinuation or dose reduction rather than tumor progression, the underlying mechanism in the Bortezomib-induced painful peripheral neuropathy remains unclear. • Here we found...

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Published inBrain, behavior, and immunity Vol. 53; pp. 96 - 104
Main Authors Liu, Cuicui, Luan, Shuo, OuYang, Handong, Huang, Zhenzhen, Wu, Shaoling, Ma, Chao, Wei, Jiayou, Xin, Wenjun
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Inc 01.03.2016
Subjects
Activating Transcription Factor 3 - metabolism
Allergy and Immunology
Allodynia
Animals
Antineoplastic Agents - administration & dosage
Antineoplastic Agents - pharmacology
ATF3
Bortezomib
Bortezomib - adverse effects
Bortezomib - pharmacology
c-Jun
CCL2
Chemokine CCL2 - biosynthesis
Chemokine CCL2 - metabolism
Ganglia, Spinal - drug effects
Ganglia, Spinal - metabolism
Hyperalgesia - chemically induced
Hyperalgesia - metabolism
JNK Mitogen-Activated Protein Kinases - metabolism
Male
Multiple Myeloma - drug therapy
Neurons - drug effects
Neurons - metabolism
Peripheral Nervous System Diseases - chemically induced
Peripheral Nervous System Diseases - metabolism
Psychiatry
Rats
Rats, Sprague-Dawley
Signal Transduction
Transcriptional Activation
Up-Regulation
Allodynia
c-Jun
CCL2
Bortezomib
ATF3
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Summary:Highlights • Painful peripheral neuropathy induced by chemotherapy drugs often serves as the common reason for treatment discontinuation or dose reduction rather than tumor progression, the underlying mechanism in the Bortezomib-induced painful peripheral neuropathy remains unclear. • Here we found that upregulated CCL2 expression in DRGs was critical to the development of BTZ-induced mechanical allodynia. • Furthermore, c-Jun might be essential for BTZ-induced CCL2 upregulation via binding directly to the specific position of the ccl2 promoter. • Finally, c-Jun and ATF3 interaction might contribute to the enhanced transcription of ccl2 after BTZ treatment. • Our findings revealed a novel mechanism underlying Bortezomib-induced painful peripheral neuropathy.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:0889-1591
1090-2139
DOI:10.1016/j.bbi.2015.11.004