Abstract | BACKGROUND: METHODS:
Lipid extracts were made from conditioned media of three human oral squamous cell carcinoma (OSCC) cell lines as well as one normal human oral keratinocytes cell line. These were then injected intraplantarly into rat hindpaws to measure spontaneous nocifensive behavior, as well as thermal and mechanical allodynia. For interventional experiments, the animals were pretreated with AMG517 (TRPV1 antagonist) or HC030031 (TRPA1 antagonist) prior to extract injection. RESULTS: These studies demonstrate that lipids released from the three OSCC cell lines, but not the normal cell line, were capable of producing significant spontaneous nocifensive behaviors, as well as thermal and mechanical allodynia. Notably each of the cell lines produced a different magnitude of response for each of three behavioral assays. Importantly, pre-treatment with a TRPVI antagonist blocked lipid-mediated nocifensive and thermal hypersensitivity, but not mechanical hypersensitivity. In addition, pre-treatment with a TRPA1 antagonist only reversed thermal hypersensitivity without affecting lipid-induced nocifensive behavior or mechanical allodynia. CONCLUSIONS: These data reveal a novel mechanism for cancer pain and provide strong direction for future studies evaluating the cellular mechanism regulating the TRP-active lipids by OSCC tumors.
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Authors | Shivani Ruparel, Michelle Bendele, Ashley Wallace, Dustin Green |
Journal | Molecular pain
(Mol Pain)
Vol. 11
Pg. 30
(May 26 2015)
ISSN: 1744-8069 [Electronic] United States |
PMID | 26007300
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Lipids
- TRPV Cation Channels
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Topics |
- Animals
- Humans
- Hyperalgesia
(metabolism)
- Lipid Metabolism
- Lipids
- Male
- Mouth Neoplasms
(metabolism)
- Nociceptors
(metabolism)
- Pain
(metabolism)
- Pain Measurement
(methods)
- Rats
- Rats, Sprague-Dawley
- Sensory Receptor Cells
(metabolism)
- TRPV Cation Channels
(antagonists & inhibitors, metabolism)
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