TRPV1

Official Full Name

transient receptor potential cation channel subfamily V member 1

Organism

Homo sapiens

GeneID

7442

Background

Capsaicin, the main pungent ingredient in hot chili peppers, elicits a sensation of burning pain by selectively activating sensory neurons that convey information about noxious stimuli to the central nervous system. The protein encoded by this gene is a receptor for capsaicin and is a non-selective cation channel that is structurally related to members of the TRP family of ion channels. This receptor is also activated by increases in temperature in the noxious range, suggesting that it functions as a transducer of painful thermal stimuli in vivo. Four transcript variants encoding the same protein, but with different 5' UTR sequence, have been described for this gene. [provided by RefSeq, Jul 2008]

Synonyms

VR1;

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Detailed Information

The transient receptor potential (TRP) family is a heterogeneous group of non-selective cation channels that share a common structure of six transmembrane domains with a hydrophobic pore located between the fifth and sixth domains. TRP ion channels are involved in the transmission of sensory inputs such as heat, pain, and taste. TRPV1, also known as Vanilloid-receptor 1 or capsaicin receptor, is one of the most important members of the TRPV family. This channel is expressed on a variety of cells in the skin, including keratinocytes, T-cells, mast cells, and cutaneous sensory neurons. It is a ligand-gated non-selective cation channel activated by low pH, voltage, heat (>43°), but also by several endogenous lipid molecules such as anandamide (AEA), Nacyl-dopamines or the lipoxygenases products 12-and 15-(S)-HPETE (hydroperoxyeicosatetraenoic acid).

Physiological and Pathophysiological Roles of TRPV1

Similarly to most TRP channels, TRPV1 is an outwardly rectifying Ca²⁺ permeable non-selective cation channel. Its activators most often used in experiments are low pH, heat (>43°), and capsaicin. Resiniferatoxin (RTX) is a potent agonist of TRPV1, it activates the channel at lower concentrations than capsaicin, but its effects also develop much more slowly. TRPV1 is one of the most mixed ion channels. It is activated by multiple exogenous and endogenous compounds, including various painful arthropod toxins.

TRPV1 channel is not only involved in the thermal and pain sensation but also in other processes such as T cells activation, urinary bladder functions, insulin sensitivity, or airway hypersensitivity. Chronic capsaicin administration desensitizes TRPV1 and makes the neurons less sensitive to noxious stimuli. This action requires the presence of extracellular Ca²⁺ and activation of Ca²⁺-calmodulin dependent protein kinase that promotes channel phosphorylation. This property of capsaicin has been used to treat pain associated with disease conditions such as arthritis and diabetic peripheral neuropathy. TRPV1 was shown to be implicated in immune cell functioning, neuropathic pain, neurogenic inflammation, autoimmune disorders, and cancer. Until now, TRPV1 agonist, capsaicin or resiniferatoxin, and antagonists have been tested to treat osteoarthritis, migraine, overactive bladder, atopic dermatitis, and neuropathic pain. In addition, in some studies, capsaicin-induced TRPV1 activation was also related to anti-inflammatory and anticancer effects. Therefore, the identification of novel modulators of TRPV1 activity might be helpful to the field of medicine.

TRPV1 and Cancer

It is well known that chronic inflammation is related to tumorigenesis and aberrant calcium signaling promotes proliferation, metastasis, and cancer cell survival. TRPV1 is associated with both calcium signaling and the process of inflammation, thus, its contribution to cancer progression gained more attention. Functional expression of TRPV1 was demonstrated in multiple tumor types including human breast cancer cell lines (MCF-7 and BT-20), human papillary thyroid carcinoma BCPAP cells, prostate cancer (LNCaP and PC-3), glioma, and urothelial cancer cells.

Several studies addressed the TRPV1 activation in anti-cancer therapy through harnessing the Ca²⁺ signaling. Activation of TRPV1 by capsaicin was shown to significantly reduce proliferation and induce apoptosis of aggressive triple-negative breast cancer cell line. Several studies have indicated that the administration of chemotherapy along with TRPV1 activator—capsaicin, can produce synergistic effect, which leads to increased apoptosis and suppression of tumor cell migration. Studies by Deveci et al. showed that activation of TRPV1 is associated with a significantly higher level of apoptosis in the MCF-7 human breast cancer cell line than in the cells treated with anticancer drug 5-Fluorouracil alone. Besides, alteration of TRPV1 activity by capsaicin was shown to significantly reduce the migration and invasion of human papillary thyroid carcinoma BCPAP cells. Different from the antitumor effect of capsaicin, Caprodossi et al. have indicated that capsaicin administration upregulated genes associated with angiogenesis, invasiveness and metastasis processes in the human urothelial cancer cell line that was TRPV1-deficient. The same cell line transfected with TRPV1 and treated with capsaicin showed a significant increase in intracellular Ca²⁺ levels, followed by growth inhibition and apoptosis increased.

References:

Martins D, et al. "Hotheaded": the role OF TRPV1 in brain functions. Neuropharmacology, 2014, 85: 151-157.
Bonchak J G, Swerlick R A. Emerging therapies for atopic dermatitis: TRPV1 antagonists. Journal of the American Academy of Dermatology, 2018, 78(3): S63-S66.
Edwards J G. TRPV1 in the central nervous system: synaptic plasticity, function, and pharmacological implications. Capsaicin as a therapeutic molecule. Springer, Basel, 2014: 77-104.
Carnevale V, Rohacs T. TRPV1: a target for rational drug design. Pharmaceuticals, 2016, 9(3): 52.
Bujak J K, et al. Inflammation, cancer and immunity–implication of TRPV1 channel. Frontiers in oncology, 2019, 9: 1087.
Brito R, et al. TRPV1: a potential drug target for treating various diseases. Cells, 2014, 3(2): 517-545.

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