Bone cancer pain is refractory to currently available clinical treatment owing to
its complicated underlying mechanisms. Studies found that extracellular matrix
molecules can participate in the regulation of chronic pain. Decorin is one of
the most abundant extracellular matrix molecules, and the present study
evaluated the effect of decorin on the development of bone cancer pain. We found
that decorin was upregulated in the L4–L6 spinal dorsal horn of the bone cancer
pain rats. Spinal microinjection of a decorin-targeting RNAi lentivirus
alleviated bone cancer pain-induced mechanical allodynia and reduced the
expression of pGluR1-Ser831 in the bone cancer pain rats. Meanwhile, decorin
knockdown impaired the excitatory synaptogenesis in cultured neurons and
prevented the clustering and insertion of pGluR1-Ser831 into postsynaptic
membranes. Taken together, the results of our study suggested that decorin
contributes to the development of bone cancer pain possibly by regulating the
activity of excitatory synaptic molecules in the spinal cord. Our findings
provide a better understanding of the function of decorin as a possible
therapeutic target for alleviating bone cancer pain.
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