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Background: The spread of tumors through neural routes is common in severaltypes of cancer in which patients suffer from a moderate-to-severe neuropathy,neural damage and a distorted quality of life. Here we aim to examine theexpression profiles of transient receptor potential vanilloid 1 (TRPV1) and oftransient receptor potential vanilloid 4 (TRPV4), toll-like receptor 4 (TLR4)and extracellular signal-regulated kinase (ERK1/2), and to assess the possibletherapeutic strategies through blockade of transient receptor potential (TRP)channels. Methods: Cancer was induced within the sciatic nerves of maleCopenhagen rats, and tissues from dorsal root ganglia (DRG) were collected andused for measurements of immunofluorescence and Western blotting. The TRPV1antagonist capsazepine, the selective TRPV4 antagonist HC-067047 and thecalcium ions inhibitor ruthenium red were used to treat thermal and/ormechanical hyperalgesia. Results: Transient receptor potential vanilloid 1showed a lower expression in DRGs on days 7 and 14. The expression of TRPV4,TLR4 and ERK1/2 showed an increase on day 3 then a decrease on days 7 and 14.TRPV1 and TLR4 as well as TRPV4 and ERK1/2 co-existed on the same neuronalcells. The neuropathic pain was reversed in dose-dependent manners by using theTRP antagonists and the calcium ions inhibitor. Conclusion: The decreasedexpression of TRPV1 and TRPV4 is associated with high activation. The increasedexpression of TLR4 and ERK1/2 reveals earlier immune response and tumorprogression, respectively, and their ultimate decrease is an indicator of nervedamage. We studied the possible role of TRPV1 and TRPV4 in transducingcancer-induced hyperalgesia. The possible treatment strategies ofcancer-induced thermal and/or mechanical hyperalgesia using capsazepine,HC-067047 and ruthenium red are examined.

Expression profiles of TRPV1, TRPV4, TLR4 and ERK1/2 in the dorsal root ganglionic neurons of a cancer-induced neuropathy rat model