Capsaicin: Friend or Foe in Skin Cancer and Other Related Malignancies?

Georgescu, Simona Roxana; Sârbu, Maria Isabela; Matei, Clara; Ilie, Mihaela; Căruntu, Constantin; Constantin, Carolina; Neagu, Monica; Tampa, Mircea

doi:10.3390/nu9121365

Cited by 55 publications

(52 citation statements)

References 115 publications

(162 reference statements)

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“…Carcinogenesis is a complex process and chronic inflammation seems to be a key factor in its development (92)(93)(94)(95)(96). Since OLP is a premalignant disorder, some authors paid attention to the role of HCV in its malignant transformation.…”

Section: Hcv Infection and Oral Cancermentioning

confidence: 99%

Potential pathogenic mechanisms involved in the association between lichen planus and hepatitis C virus infection (Review)

et al. 2018

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Lichen planus (LP) is an immune-mediated inflammatory disease that particularly affects the skin and mucous membranes. Its etiology remains elusive, however some trigger factors, including viral or bacterial antigens, drugs and metals, have been postulated. There is a higher prevalence of hepatitis C virus (HCV) infection among patients with LP, with some geographical variations. HCV is an enveloped RNA virus that belongs to the Flaviviridae family and in most instances causes chronic liver infections. It has been hypothesized that HCV may contribute to LP development, but the link between the two disorders is not fully understood. It is still debatable whether HCV leads to the occurrence of LP lesions directly by replication inside the infected cells or indirectly by activating immunological pathways. Molecular studies have revealed HCV RNA in specimens collected from patients with LP. The autoimmune theory was also suggested given that several studies have revealed viral replication and immune response activation associated with autoantibody synthesis. The aim of this review is to summarize the main potential mechanisms involved in the association between LP and HCV infection. Understanding the link between the two disorders may shed some light on the pathogenesis of LP, which is a challenging issue.

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Section: Hcv Infection and Oral Cancermentioning

confidence: 99%

Potential pathogenic mechanisms involved in the association between lichen planus and hepatitis C virus infection (Review)

et al. 2018

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“…The skin acts as a neuroimmunoendocrine organ with a modulating effect on local blood and lymph flow, sweat glands function, immunoreactivity, and inflammatory response; these effects are facilitated by the integrated nervous system connections that are involved in regulating homeostasis in disruptive conditions such as activation of nociceptors by pain, trauma or inflammation [90][91][92][93][94][95][96]. The concept of dermal neurogenic inflammation was further refined using capsaicin, a molecule that represented the groundstone of inflammation and pain pathogenesis research in the skin, and was subsequently promoted for also having anticarcinogenic and immunomodulatory roles [97,98]. Cannabinoids have proven effective as protective agents in neuroinflammatory disorders, and their anti-inflammatory and immunomodulating effects have also proven beneficial in inflammatory skin disorders [99].…”

Section: Inflammation Traits Of the Skinmentioning

confidence: 99%

Cannabinoids in the Pathophysiology of Skin Inflammation

et al. 2020

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Cannabinoids are increasingly-used substances in the treatment of chronic pain, some neuropsychiatric disorders and more recently, skin disorders with an inflammatory component. However, various studies cite conflicting results concerning the cellular mechanisms involved, while others suggest that cannabinoids may even exert pro-inflammatory behaviors. This paper aims to detail and clarify the complex workings of cannabinoids in the molecular setting of the main dermatological inflammatory diseases, and their interactions with other substances with emerging applications in the treatment of these conditions. Also, the potential role of cannabinoids as antitumoral drugs is explored in relation to the inflammatory component of skin cancer. In vivo and in vitro studies that employed either phyto-, endo-, or synthetic cannabinoids were considered in this paper. Cannabinoids are regarded with growing interest as eligible drugs in the treatment of skin inflammatory conditions, with potential anticancer effects, and the readiness in monitoring of effects and the facility of topical application may contribute to the growing support of the use of these substances. Despite the promising early results, further controlled human studies are required to establish the definitive role of these products in the pathophysiology of skin inflammation and their usefulness in the clinical setting.

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“…Additional nonflavonoid nutraceuticals have been described that have potential, but unconfirmed PPARγ ligand activity and which are also known to have anticancer activity in skin or oral cancer. These compounds include 6‐shogaol, 6‐gingerol, curcumin, lutein/zeaxanthin, and capsaicin . Finally, falcarinol/falcarindiol are polyacetylene phytochemicals that are known to act as partial PPARγ ligands .…”

Section: Evidence That Pparγ Activation Is Protective Against the Devmentioning

confidence: 99%

“…These compounds include 6-shogaol, 66,67 6-gingerol, 66,68 curcumin, 66,69 lutein/zeaxanthin, 70,71 and capsaicin. [72][73][74] Finally, falcarinol/falcarindiol are polyacetylene phytochemicals that are known to act as partial PPARγ ligands. 75 While anticancer activity for these polyacetylenes has been demonstrated, 76 no studies have yet to be performed to address their activity against skin or oral cancer.…”

Section: Pharmacologic Studies Using Pparγ Agonistsmentioning

confidence: 99%

Evidence that peroxisome proliferator‐activated receptor γ suppresses squamous carcinogenesis through anti‐inflammatory signaling and regulation of the immune response

Ren

Konger

2019

Molecular Carcinogenesis

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A variety of evidence suggests that peroxisome proliferator‐activated receptor (PPAR)γ agonists may represent a potential pharmacologic target in the prevention or treatment of skin cancer. In particular, recent reports suggest that PPARγ activation may exert at least some of its anti‐neoplastic effects through the suppression of tumor promoting chronic inflammation as well as by strengthening antitumor immune responses. This activity is thought to occur through a distinct mode of ligand interaction with PPARγ that causes transrepression of transcription factors that are involved in inflammatory and immunomodulatory signaling. However, current thiazolidinedione (TZD)‐type PPARγ agonists have significant safety concerns that limit their usefulness as a preventive or therapeutic option. Due to the relatively large ligand binding pocket of PPARγ, a diverse group of ligands can be seen to interact with distinct modes of binding to PPARγ, leading to the phenomenon of partial agonist activity and selective PPARγ modulators (SPPARγM). This has led to the development of ligands that are tailored to deliver desired pharmacologic activity, but lack some of the negative side effects associated with full agonists, such as the currently utilized TZD‐type PPARγ agonists. In addition, there is evidence that a number of phytochemicals that are currently being touted as antineoplastic nutraceuticals also possess PPARγ activity that may partially explain their pharmacologic activity. We propose that one or more of these partial agonists, SPPARγMs, or putative phytochemical PPARγ ligands could presumably be used as a starting point to design more efficacious anti‐neoplastic PPARγ ligands that lack adverse pharmacological effects.

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Capsaicin: Friend or Foe in Skin Cancer and Other Related Malignancies?

Cited by 55 publications

References 115 publications

Potential pathogenic mechanisms involved in the association between lichen planus and hepatitis C virus infection (Review)

Potential pathogenic mechanisms involved in the association between lichen planus and hepatitis C virus infection (Review)

Cannabinoids in the Pathophysiology of Skin Inflammation

Evidence that peroxisome proliferator‐activated receptor γ suppresses squamous carcinogenesis through anti‐inflammatory signaling and regulation of the immune response

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