TRPV1 Cancer Research Results

TRPV1, transient receptor potential vanilloid 1: Click to Expand ⟱

Source:

Type:

TRPV1 is a ligand-gated ion channel classically associated with nociception and heat sensation.
- TRPV1 is a nonselective cation channel that allows the influx of calcium (and other cations) when activated by various stimuli such as capsaicin, heat, or low pH.
- TRPV1 can influence key cellular processes including proliferation, apoptosis, and migration by modulating intracellular calcium levels and downstream signaling cascades.

- In some cases, TRPV1 activation can induce cell death, which might translate into less aggressive tumor behavior; however, this is not a universal finding.
- TRPV1 is a non-selective cation channel, which is frequently overexpressed in highly malignant cancers.
- Capsaicin may be able to induce cell death in urothelial cancer and glioma cells via TRPV1-dependent stimulation of excessive calcium (Ca2+) influx
- Activation of TRPV1 promotsd the generation of ROS.
- Variability in TRPV1 expression and function suggests that it might serve as one component of a broader prognostic panel rather than a standalone marker.

Scientific Papers found: Click to Expand⟱

5312-

acet,

Analgesic Effect of Acetaminophen: A Review of Known and Novel Mechanisms of Action

*COX1↓, believed that acetaminophen induces analgesia by inhibiting cyclooxygenase enzymes
*other?, believed that acetaminophen is metabolized to p-aminophenol, which crosses the blood-brain barrier and gets metabolized by fatty acid amide hydrolase to yield N-acylphenolamine (AM404).
*BBB↑,
TRPV1↑, by activating TRPV1 receptor, AM404 produced outward currents that were measured using whole-cell patch-clamp recordings and acted as a partial agonist in trigeminal neurons

5842-

CAP,

Capsaicin: Current Understanding of Its Mechanisms and Therapy of Pain and Other Pre-Clinical and Clinical Uses

Review,

Nor,

Review,

Diabetic,

*Pain↓, capsaicin promotes pain relief when used in the right dosage and frequency.
*TRPV1↑, capsaicin-induced pain is also used to assess new molecules that target TRPV1 receptor. Capsaicin activates TRPV1
AMPK↑, The inhibitory effect of capsaicin on this process seems to involve the activation of 5’ adenosine monophosphate-activated protein kinase (AMPK) in conjunction with intracellular ROS release
ROS↑,
TumCP↑, AMPK activation is also linked to inhibition of cell proliferation and apoptosis [153,154]
Apoptosis↑,
TumCCA↑, capsaicin targets preadipocyte proliferation by blocking the S-phase of the cell cycle [149].
Casp3↑, capsaicin induces apoptosis in preadipocytes via the activation of caspase-3, Bax, and Bak, cleavage of PARP, and down-regulation of Bcl-2
BAX↑,
Bak↑,
cl‑PARP↑,
Bcl-2↓,
RNS↑, capsaicin induces apoptosis in BMSC via increased production of ROS and reactive nitrogen species (RNS) [
*glucose↓, healthy male volunteers revealed that capsaicin lowers glucose and increases insulin levels shortly after oral administration
*Insulin↑,
*BP↓, Capsaicin stimulates the release of CGRP through the activation of TRPV1 and therefore decreases blood pressure
*AntiAg↑, Capsaicin has been shown to inhibit platelet aggregation [199,200], which may also provide protection against cardiovascular diseases
ER Stress↑, endoplasmic reticulum stress in human nasopharyngeal carcinoma and pancreatic cancer cells,
Hif1a↓, capsaicin increases the degradation of hypoxia inducible factor 1α in non-small cell lung cancer,
chemoPv↑, mounting evidence supporting a chemo-preventive role for capsaicin in cancer cell culture and animal models,

5839-

CAP,

Capsaicin: beyond TRPV1

Review,

Var,

TRPV1↑, Besides its classical effects through activating the Transient Receptor Potential Vanilloid type 1 (TRPV1), growing experimental evidence demonstrates that capsaicin has pleiotropic actions in a TRPV1-independent manner.
eff↑, cancer cell lines co-treated with capsaicin and a well-characterized Hsp90 inhibitor, 17-AAG, showed improved anti-tumor effects (32).
DNMT1↓, Capsaicin generates an inhibitory effect on DNMT1

5834-

CAP,

Capsaicin and TRPV1: A Novel Therapeutic Approach to Mitigate Vascular Aging

Study,

Nor,

*AntiCan↑, capsaicin possesses anti-cancer, anti-inflammatory, and antioxidant properties and is used as a topical analgesic
*Inflam↓,
*antiOx↑,
*TRPV1↑, Studies demonstrate that capsaicin directly activates TRPV1 by binding to intracellular sites within the channel protein
*AMPK↑, Moreover, capsaicin and TRPV1 can activate the AMPK pathway [82, 83]
*SIRT1↑, elevating SIRT1 levels
*NADPH↓, suppressing NADPH oxidase and reducing reactive oxygen species
*ROS↓,
*MAPK↓, inhibiting MAPK pathways
*eNOS↑, activating eNOS
*Wnt/(β-catenin)↓, inhibiting the Wnt/β-catenin signaling pathway
RenoP↑, Furthermore, TRPV1 activation decreases renal perfusion pressure while increasing glomerular filtration rate and the excretion of sodium/water, thereby modulating renal hemodynamics and excretory functions

5831-

CAP,

Unraveling TRPV1’s Role in Cancer: Expression, Modulation, and Therapeutic Opportunities with Capsaicin

TRPV1↑, Activation of TRPV1 triggers calcium influx and affects cell signaling linked to growth and death.
Ca+2↑,
AntiCan↑, Capsaicin has been extensively studied for its anti-cancer effects, such as inhibiting cell proliferation and modulating cancer-related pain.
TumCP↓,
Pain↓,
TumCG↓, reduced tumor growth and enhanced chemosensitivity, positioning it as a promising adjunct in cancer therapy
ChemoSen↑, Capsaicin sensitizes cancer cells to chemotherapy drugs, thereby improving therapeutic outcomes [25]
Apoptosis↑, apsaicin-induced TRPV1 activation triggers apoptosis in colorectal cancer cells through the calcineurin–NFAT2–p53 signaling pathway [39]
ROS↑, Increased intracellular calcium from TRPV1 activation causes mitochondrial overload, leading to disrupted function, elevated ROS, loss of membrane potential, and cytochrome C release [Figure 2].
MMP↓,
Cyt‑c↑,
Casp↑, This triggers caspase activation and cell death.

5830-

CAP,

Inhibition of pyroptosis and apoptosis by capsaicin protects against LPS-induced acute kidney injury through TRPV1/UCP2 axis in vitro

in-vitro,

Nor,

HK-2

*IL1β↓, capsaicin ameliorated LPS-induced cytotoxicity in vitro and attenuated the release of interleukin (IL)-1β and IL-18.
*IL18↓,
*TRPV1↑, Molecularly, capsaicin activated transient receptor potential cation channel subfamily V member 1 –mitochondrial uncoupling protein 2 axis and inhibited caspase-1-mediated pyroptosis
*ROS↓, capsaicin alleviated LPS-induced ROS production and mitochondrial membrane potential disruption and inhibited apoptosis.
*MMP↑,
*Apoptosis↓,
*RenoP↑, These findings suggest that capsaicin shows a protective effect in in vitro acute kidney injury model.
*Inflam↓, Capsaicin ameliorates LPS-induced cytotoxicity and inflammation response in HK-2 cells
*UCPs↑, Capsaicin alleviates LPS-induced pyroptosis in HK-2 cells by activating TRPV1/UCP2 axis

5825-

CAP,

Bioavailability of capsaicin and its implications for drug delivery

Review,

Var,

Review,

Arthritis,

Review,

Obesity,

*AntiCan↑, Emerging studies show that it displays potent anti-tumor activity in several human cancers.
*TRPV1↑, The “heat-sensation” of capsaicin arises due to the binding of capsaicin to transient receptor potential vanilloid (TRPV) ion-channel receptors
*cardioP↑, some of the biological activities of capsaicin, like its anti-neoplastic, cardioprotective effects, have been found to be independent of the TRPV1 receptor.
AntiCan↓, Exposure to high doses of capsaicin (above 100 mg capsaicin per kg body weight) for a prolonged time causes peptic ulcers, accelerates the development of prostate, stomach, duodenal, and liver cancers and enhances breast cancer metastasis [5, 6].
Apoptosis↑, Capsaicin induces robust apoptosis in multiple types of human cancer cells both in vitro and in mice models.
ChemoSen↑, Capsaicin potentiates the apoptotic activity of cisplatin in human stomach cancer and attenuates cisplatin-induced renal toxicity in rodent models
*Inflam↓, oral or local administration of capsaicin reduces inflammation and pain from rheumatoid arthritis, fibromyalgia and chemical hyperalgesia
*Pain↓,
*AntiAg↑, The anti-platelet and anti-coagulant activity of capsaicin was independent of TRPV1
*Weight↓, capsaicinoids show anti-obesity activity by enhancing energy expenditure of the body
*BioAv↑, Capsaicin is robustly absorbed from the skin upon topical administration [4]
BioAv↑, capsaicin is rapidly absorbed from the stomach and the intestine following oral administration.
Half-Life↝, The liver and kidney displayed maximal amounts of capsaicin in 3 hours and 6 hours, respectively.
Half-Life↓, An interesting fact to note is that the bioavailability and half-life of capsaicin is quite low in the plasma, irrespective of the route of administration.

5827-

CAP,

The Effect of Topical Capsaicin 8% on Pain in Chemotherapy-induced Peripheral Neuropathy

Trial,

Var,

17 patients,

Pain↓, For 9 patients (53%), pain became “acceptable” at t2 and t3, with a significant reduction (pain intensity difference
NP/CIPN↓,
Dose↝, Topical capsaicin 8% is a valuable treatment for pain in chemotherapy-induced peripheral neuropathy for many patients.
TRPV1↑, Capsaicin is a selective agonist of the transient receptor potential (cation channel) vanilloid, subfamily member 1 (TRPV1).
Ca+2↑, When TRPV1 is activated, this leads to calcium influx, enhancing nociception.

5826-

CAP,

Capsaicin induces mitochondrial dysfunction and apoptosis in anaplastic thyroid carcinoma cells via TRPV1-mediated mitochondrial calcium overload

in-vitro,

Thyroid,

TRPV1↑, we reported that capsaicin (CAP), a transient receptor potential vanilloid type1 (TRPV1) agonist, inhibited the viability of anaplastic thyroid cancer cells.
tumCV↓,
Ca+2↑, Capsaicin treatment triggered Ca2+ influx by TRPV1 activation, resulting in disequilibrium of intracellular calcium homeostasis.
mtDam↑, In addition, the disruption of mitochondrial calcium homeostasis caused by capsaicin led to mitochondrial dysfunction in ATC cells
ROS↑, as evidenced by the production of mitochondrial reactive oxygen species (ROS), depolarization of mitochondrial membrane potential (ΔΨm), and opening of mitochondrial permeability transition pore (mPTP)
MMP↓,
MPT↑,
Cyt‑c↑, the resulting release of cyt c into the cytosol triggered apoptosome assembly and subsequent caspase activation and apoptosis.
Casp↑,
Apoptosis↑,

5844-

CAP,

Non-pungent long chain capsaicin-analogs arvanil and olvanil display better anti-invasive activity than capsaicin in human small cell lung cancers

in-vitro,

Lung,

DMS114

eff↑, The non-pungent capsaicin analogs arvanil and olvanil display improved anti-invasive activity relative to capsaicin in human SCLC cells.
AMPK↑, Furthermore, the anti-invasive activity of arvanil, olvanil and capsaicin was mediated by the AMPK pathway.
toxicity↝, These adverse side effects of capsaicin have led patients to abandon taking the drug
BioAv↑, Arvanil and olvanil were selected because they are orally available, non-pungent, and have comparable pharmacological activity profile, relative to capsaicin.
TRPV1↑, Arvanil and olvanil bind to TRPV1 with higher affinity than capsaicin.
TumCI↓, Capsaicin displays anti-invasive activity in human SCLC cells

5861-

CAP,

Anticancer Properties of Capsaicin Against Human Cancer

Review,

Var,

*antiOx↑, antioxidant (8), anti-inflammatory (9) and anti-obesity (10) properties.
*Inflam↓,
*Obesity↓,
chemoPv↑, Many laboratories have reported that capsaicin possesses chemopreventive and chemotherapeutic effects
Apoptosis↑, Capsaicin has been shown to induce apoptosis in many different types of cancer cell lines including pancreatic (19) colonic (24), prostatic (25), liver (26), esophagieal (27), bladder (28), skin (29), leukemia (30), lung (31), and endothelial cells (
selectivity↑,
TRPV1↑, Transient receptor potential vanilloids (TRPVs) are receptors of capsaicin which lead to Ca2+-mediated mitochondrial damage and cytochrome c release.
Ca+2↑,
mtDam↑,
Cyt‑c↑,
P53↑, Capsaicin was found to induce p53 phosphorylation at the Ser-15 residue (30) and enhanced p53 acetylation through down-regulation of sirtuin 1 (
SIRT1↓,
TumCCA↑, Capsaicin induced G0/G1 phase arrest in human esophageal carcinoma cells with an increase of p21 and a decrease of CDK4, CDK6 and cyclin E (
P21↑,
CDK4↓,
CDK6↓,
cycE/CCNE↓,
angioG↓, Capsaicin has anti-angiogenic properties both in vitro and in vivo
TumMeta↓, Capsaicin treatment significantly reduced the metastatic burden in transgenic adenocarcinoma of the mouse prostate (TRAMP) mice (57).

5860-

CAP,

Beneficial Effects of Capsaicin in Disorders of the Central Nervous System

Review,

AD,

Review,

Park,

Review,

Stroke,

*neuroP↑, In Alzheimer’s disease, capsaicin reduces neurodegeneration and memory impairment.
*memory↑, dietary capsaicin (0.01% in a chow) improved memory in a mouse model of Alzheimer’s disease
*Pain↓, Additionally, this compound exerts pain-relieving effects in migraine and cluster headaches.
*TRPV1↑, capsaicin stimulates TRPV1 receptors
*Aβ↓, Alzheimer’s disease, that dietary capsaicin (0.01% in a chow) reduced beta-amyloid plaque formation and tau phosphorylation in different brain areas
*tau↓,
*cognitive↑, attenuated neurodegeneration and cognitive impairment
*Risk↓, In western regions of China, chili peppers are more often consumed and there is a smaller number of people with dementia than in other regions where dietary capsaicin intake is lower
*motorD↓, capsaicin reduced neurodegeneration and motor impairment in animal models of Parkinson’s disease
*ROS↓, this compound decreased the production of reactive oxygen species and proinflammatory cytokines (TNF-α and IL-β) by activated microglia
*TNF-α↓,
*IL1β↓,
*eff↑, Capsaicin exerts beneficial effects in stroke models not only by enhancing neuroprotection but also by influencing cerebral vasculature.
*Risk↓, Moreover, it was reported that dietary capsaicin (0.02% in a chow) delays the onset of stroke in stroke-prone rats with hypertension.

5859-

CAP,

Are We Ready to Recommend Capsaicin for Disorders Other Than Neuropathic Pain?

Review,

Var,

*TRPV1↑, the absorbed capsaicin activates its receptor TRPV1, which causes the rapid influx of sodium ions (Na+) and calcium (Ca2+) from the extracellular environment to the cell interior.
*Ca+2↑,
*Na+↑,
*UCPs↑, by increasing thermogenic gene expression such as uncoupling protein 1 (UCP-1), Sirtuin 1 (SIRT-1) [25] and peroxisome proliferator-activated receptor -γ (PPARγ) coactivator 1α (PGC-1α)
*SIRT1↑,
*PPARγ↑,
*Inflam↓, suppressing inflammatory responses, increasing lipid oxidation, inhibiting adipogenesis
*lipid-P↑,
*IL6↓, decreasing the expression of inflammatory biomarkers such as IL-6, TNF, and CCL-2, associated with NF-κB inactivation
*TNF-α↓,
*NF-kB↓,
*p‑Akt↑, Phosphorylation of Akt is also described after capsaicin treatment, which results in disruption of the NRF2/Keap complex and release of activated transcription factor NRF2
*NRF2↑,
*HO-1↑, triggers the transcription of heme-oxygenase1 genes, which are essential for heme degradation and prevention of oxidative damage
*ROS↑,
*GutMicro↑, It is suggested that regular treatment with capsaicin increases diversity in the gut microbiota and abundance of short-chain fatty acid (SCFA)-producing bacteria

5858-

CAP,

Capsaicin as a Microbiome Modulator: Metabolic Interactions and Implications for Host Health

Review,

Nor,

Review,

AD,

*BBB↓, crosses the blood–brain barrier, alters neurotransmitter levels, and accumulates in brain regions involved in cognition.
*GutMicro↑, capsaicin appears to undergo microbial transformation and influences gut microbial composition, favoring short-chain fatty acid producers and suppressing pro-inflammatory taxa. often favoring the growth of beneficial taxa such as Ruminococcaceae, Lac
Obesity↓, These changes contribute to anti-obesity, anti-inflammatory, and potentially anticancer effects
*Inflam↓,
*AntiCan↑,
*TRPV1↑, Capsaicin is a potent agonist perceived by TRPV1, a transmembrane cation channel that functions with Ca2+.
*Ca+2↑, causes an increase in Ca2+ flux,
*antiOx↑, Capsaicin is a bioactive compound of chili peppers responsible for their spicy flavor, which also shows antioxidant, anti-obesity, analgesic, anti-inflammatory, anticarcinogenic, and cardioprotective effects
*cardioP↑,
*BioAv↓, capsaicin exhibits low systemic bioavailability due to its rapid metabolism in the liver and other tissues, resulting in a short plasma half-life of approximately 25 min in humans
*Half-Life↓,
*BioAv↝, Capsaicin’s bioavailability is determined by multiple interrelated factors, including its physicochemical properties, metabolic transformations, route of administration, and the biological context of the host, including gut microbiota composition.
*BioAv↑, For instance, polymeric micelles, liposomes, and hydroxypropyl-β-cyclodextrin complexes have demonstrated the capacity to enhance capsaicin’s oral bioavailability, prolong its plasma half-life, and improve therapeutic consistency
*neuroP↑, capsaicin exposure alters glutamate, GABA, and serotonin levels in distinct brain regions, with potential implications for neuroprotection, mood regulation, and energy metabolism.
Apoptosis↑, apoptosis is the main mechanism by which capsaicin induces cell death in cancer cells.
p38↑, capsaicin triggers a calcium flux within the cell via TRPV1, activating the p38 pathway.
ROS↑, As a result, reactive oxygen species (ROS) are produced, along with depolarization of the mitochondrial membrane potential and opening of the mitochondrial permeability transition pore.
MMP↓,
MPT↑,
Cyt‑c↑, Consequently, cytochrome c is released, the apoptosome is assembled, and caspases are activated, ultimately leading to cell death
Casp↑,
TRIB3↑, capsaicin enhances TRIB3 gene expression, which allowed an increase in the antiproliferative and proapoptotic effects of TRIB3 in cancer cells
NADH↓, Capsaicin has also been seen to downregulate and inhibit tumor-associated NADH oxidase (tNOX) and Sirtuin1 (SIRT1) in multiple cancer cell lines such as bladder cancer, which led to reduced cell growth and migration
SIRT1↓,
TumCG↓,
TumCMig↓,
TOP1↓, pointing out that capsaicin had an inhibitory effect on topoisomerases I and II, causing a reduction in metabolic activity and proliferation of a human colon cancer cell line
TOP2↓,
β-catenin/ZEB1↓, with capsaicin, the β-catenin transcription gets downregulated
*ROS↓, Capsaicin has also been proven to alleviate redox imbalance or oxidative stress, thanks to its antioxidative activity.
*Aβ↓, Alsheimer’s disease, attenuating neurodegeneration in mice by reducing amyloid-beta levels via the promotion of non-amyloidogenic processing of amyloid precursor protein

5855-

CAP,

Unravelling the Mystery of Capsaicin: A Tool to Understand and Treat Pain

in-vivo,

Nor,

NP/CIPN↓, For example, the 8% patch is currently used in the treatment of localized neuropathic conditions, such as postherpetic neuralgia (PHN).
BioAv↑, Because capsaicin is not water-soluble, alcohols and other organic solvents are used to solubilize capsaicin in topical preparations and sprays.
Half-Life↑, Capsaicin levels declined very rapidly, with a mean population elimination half-life of 1.64 h.
TRPV1↑, Rapid desensitization first involves capsaicin binding of TRPV1
Pain↓, hese studies suggest that a high-dose patch of capsaicin has tolerable efficacy in patients with a localized pain as a result of nerve injury
TRPV1↑, agents acting on TRPV1 receptors, as well as capsaicin itself,

5854-

CAP,

Pharmacological activity of capsaicin: Mechanisms and controversies (Review)

Review,

Var,

Review,

AD,

Obesity↓, Capsaicin can also promote weight loss, making it potentially useful for treating obesity.
Half-Life↓, The clinical usefulness of capsaicin is limited by its short half-life.
antiOx↑, Capsaicin exerts analgesic, antioxidant, cardioprotective, anticancer and thermogenic effects, and it can promote weight loss
TRPV1↑, (TRPV1), to which capsaicin binds specifically.
STAT3↓, capsaicin may inhibit signal transducer and activator of transcription 3 (STAT3), but the minimal concentration needed to inhibit STAT3 (50 M) is substantially higher than the concentration required to stimulate TRPV1 (1–5 M)
Ca+2↑, mechanisms appear to involve accumulation of intracellular Ca2+, generation of reactive oxygen species, disruption of mitochondrial membrane potential and upregulation of the transcription factors NF-κB and STATS.
ROS↑,
MMP↓,
*neuroP↑, Capsaicin has demonstrated therapeutic potential in several animal models of Alzheimer's disease (AD).
*tau↓, capsaicin substantially ameliorated synaptic damage and tau hyperphosphorylation induced by cold water stress.
*Inflam↓, capsaicin appeared to activate TRPV1 in M1/M2 dopaminergic neurons, which may alleviate neuro-inflammation and oxidative stress from activated glia
*ROS?,

5850-

CAP,

Anticancer Activity of Natural and Synthetic Capsaicin Analogs

Review,

Var,

TRPV1↑, Capsaicin functions as a classic agonist of the TRPV1 receptor
Ca+2↑, multiple mechanisms such as increase of intracellular calcium, induction of calpain activity, reactive oxygen species (ROS) generation, inhibition of coenzyme Q, suppression of mitochondrial respiration,
ROS↑,
mitResp↓,
ChemoSen↑, capsaicin promotes the apoptotic activity of cancer chemotherapy agents by multiple mechanisms
P-gp↓, capsaicin has been reported to inhibit p-glycoprotein efflux transporters in KB-C2 human endocervical adenocarcinoma cells.

5849-

CAP,

The Impact of TRPV1 on Cancer Pathogenesis and Therapy: A Systematic Review

Review,

Var,

TRPV1↑, TRPV1 belongs to the transient receptor potential channel vanilloid subfamily and is also known as the capsaicin receptor and vanilloid receptor 1 (VR1).
Ca+2↑, The activation of TRPV1 induces the cellular influx of Ca2+ and Na+ ions 17-19, and the excess intracellular Ca2+ and Na+ leads to cell death 20.
TumCD↑,
TumCCA↑, Induced cell cycle arrest in G0/G1 phase and apoptosis by activating p53 to upregulate Fas/CD95 in TRPV1-overexpressing cells
Apoptosis↑,
P53↑,
Fas↑,
PI3K↑, Activated PI3K and p44/42 MAPK pathways to suppress ceramide production and increased androgen receptor expression
AR↑,
STAT3↓, attenuating STAT3 phosphorylation
ROS↑, Induced apoptosis by producing ROS originating from the mitochondria
MMP↓, Disrupted mitochondrial membrane potential and suppressed ATP synthesis to induce apoptosis
ATP↓,
CHOP↑, Stimulated ROS generation, increased CHOP expression level, and promoted apoptosis
TumCMig↓, As TRPV1 serves as the main Ca2+-influx channel, it is reasonable to suggest that TRPV1 could act as an enhancer or inhibitor of migration and invasion in a tissue- or cell-specific manner.
Twist↓, Capsaicin downregulated Tiwst1, Snail1, MMP2, and MMP9 and upregulated E-cadherin
Snail↓,
MMP2↓,
MMP9↓,
E-cadherin↑,

5845-

CAP,

Unveiling the Molecular Mechanisms Driving the Capsaicin-Induced Immunomodulatory Effects on PD-L1 Expression in Bladder and Renal Cancer Cell Lines

in-vivo,

RCC,

A498

in-vitro,

RCC,

T24/HTB-9

NA,

Bladder,

5637

TRPV1↑, CPS has been found to induce both carcinogenic and anti-carcinogenic effects in a transient receptor potential vanilloid subtype 1 (TRPV1)-dependent and -independent manner [7,8,9,10,11].
TumCP↓, CPS at high doses reduces proliferation of RCCs in a TRPV1-dependent manner, induces caspase-dependent apoptosis and growth of 786-O RC xenografts in vivo
Casp↑,
Apoptosis↑,
SIRT1↓, Moreover, by downregulating SIRT1, CPS enhances the acetylation of cortactin and β-catenin to decrease MMP-2 and MMP-9 activation and impair cell migration in BC cells [15,16].
MMP2↓,
MMP9↓,
TumCMig↓,
TumCCA↑, CPS suppresses cell proliferation, and induces cell cycle arrest and reactive oxygen species (ROS) production in BC cells, through FOXO3a-mediated pathways [17,18].
ROS↑,
DNAdam↑, CPS Induces DNA Damage in Living 5637, T24 and A498 Cancer Cell Lines
PD-L1↑, We found that CPS increased the PD-L1 expression, both at mRNA and protein levels, in T24 and 5637 cells
eff↓, ROS generation was completely reverted by NAC in CPS-treated A498 cells at 3–6 h treatment

5202-

CAP,

Capsaicin Suppresses Cell Proliferation, Induces Cell Cycle Arrest and ROS Production in Bladder Cancer Cells through FOXO3a-Mediated Pathways

vitro+vivo,

Bladder,

5637

0, 50, 100, 150, 200 and 300 µM

and NOD/SCID mice.

in-vitro,

Bladder,

T24/HTB-9

antiOx↑, Capsaicin (CAP), a highly selective agonist for transient receptor potential vanilloid type 1 (TRPV1), has been widely reported to exhibit anti-oxidant, anti-inflammation and anticancer activities.
Inflam↓,
AntiCan↓,
TRPV1↑, CAP could specifically activate TRPV1 [12,13] and interfere with the calcium signaling pathway
TumCP↓, CAP could suppress BCa tumorigenesis by inhibiting its proliferation both in vitro and in vivo.
TumCCA↑, CAP induced cell cycle arrest at G0/G1 phase and ROS production.
ROS↑,
FOXO3↑, strong increase of FOXO3a after treatment with CAP.
TumCMig↓, CAP Inhibited BCa Cell Proliferation and Migration

2349-

CAP,

The TRPV1-PKM2-SREBP1 axis maintains microglial lipid homeostasis in Alzheimer’s disease

in-vivo,

AD,

mouse brain

*TRPV1↑, capsaicin-mediated pharmacological activation of TRPV1 via inhibition of PKM2 dimerization and reduction of SREBP1 activation
*PKM2↓,
*SREBP2↑,
*memory↑, Capsaicin also rescued neuronal loss, tau pathology, and memory impairment in 3xTg mice.

2012-

CAP,

Capsaicin induces cytotoxicity in human osteosarcoma MG63 cells through TRPV1-dependent and -independent pathways

NA,

OS,

MG63

0-40 μM

20 μM

AntiTum↑, capsaicin induces apoptosis in various tumor cells as a mechanism of its anti-tumor activity
Apoptosis↑, capsaicin-induced apoptosis and the activation of transient receptor potential receptor vanilloid 1 (TRPV1) in a dose- and time-dependent manner in human osteosarcoma MG63 cells in vitro
TRPV1↑, TRPV1 activation is required for the capsaicin-induced overproduction of ROS and decrease in SOD activity
ROS↑, overproduction of reactive oxygen species (ROS)
SOD↓, decrease in superoxide dismutase (SOD) activity
AMPK↑, capsaicin induced the activation of adenosine 5ʹ-monophosphate-activated protein kinase (AMPK), p53 and C-jun N-terminal kinase (JNK)
P53↑,
JNK↑,
Bcl-2↓, decrease in the level of B-cell lymphoma 2 (Bcl-2)
Cyt‑c↑, increase in the levels of Cytochrome C
cl‑Casp3↑, cleaved-caspase-3
cl‑PARP↑, cleaved polyadenosine diphosphate-ribose polymerase (PARP) in a time-dependent manner following capsaicin treatment in MG63 cells
Ca+2↑, Once the channel is activated, it can enable the rapid increase of intracellular calcium (Ca2+) levels and initiate cell death
MMP↓, several independent studies have demonstrated that capsaicin disrupted MMP (Δψm)

2018-

CAP,

MF,

Capsaicin: Effects on the Pathogenesis of Hepatocellular Carcinoma

Review,

HCC,

TRPV1↑, Capsaicin is an agonist for transient receptor potential cation channel subfamily V member 1 (TRPV1)
eff↑, It is noteworthy that capsaicin binding to the TRPV1 receptor may be increased using a static magnetic field (SMF), thus enhancing the anti-cancer effect of capsaicin on HepG2 (human hepatoblastoma cell line) cells through caspase-3 apoptosis
Akt↓, capsaicin can regulate autophagy by inhibiting the Akt/mTOR
mTOR↓,
p‑STAT3↑, Capsaicin can upregulate the activity of the signal transducer and activator of transcription 3 (p-STAT3)
MMP2↑, increase of the expression of MMP-2
ER Stress↑, capsaicin may induce apoptosis through endoplasmic reticulum (ER) stress
Ca+2↑, and the subsequent ER release of Ca2+
ROS↑, Capsaicin-induced ROS generation
selectivity↑, On the other hand, an excess of capsaicin is cytotoxic on HepG2 cells, and normal hepatocytes to a smaller extent, by collapse of the mitochondrial membrane potential with ROS formation
MMP↓,
eff↑, combination of capsaicin and sorafenib demonstrated significant anticarcinogenic properties on LM3 HCC cells, restricting tumor cell growth

2019-

CAP,

Capsaicin: A Two-Decade Systematic Review of Global Research Output and Recent Advances Against Human Cancer

Review,

Var,

chemoPv↑, Capsaicin has shown significant prospects as an effective chemopreventive agent
Ca+2↑, Capsaicin was shown to cause upstream activation of Ca2+
antiOx↑, Another plausible mechanism implicated in the chemopreventive action of capsaicin is its anti-oxidative effects.
*ROS↓, capsaicin inhibits ROS release and the subsequent mitochondrial membrane potential collapse, cytochrome c expression, chromosome condensation, and caspase-3 activation induced by oxidized low-density lipoprotein in normal human HUVEC cells
*MMP∅,
*Cyt‑c∅,
*Casp3∅,
*eff↑, dietary curcumin and capsaicin concurrent administration in high-fat diet-fed rats were shown to mitigate the testicular and hepatic antioxidant status by increasing GSH levels, glutathione transferase activity, and Cu-ZnSOD expression
*Inflam↓, Anti-inflammation is another mechanism implicated in the chemopreventive action of capsaicin.
*NF-kB↓, inhibition of NF-kB by capsaicin
*COX2↓, compound elicits COX-2 enzyme activity inhibition and downregulation of iNOS
iNOS↓,
TRPV1↑, major pro-apoptotic mechanisms of capsaicin is via the vanilloid receptors, primarily TRPV1
i-Ca+2?, causing a concomitant influx of Ca2+: severe condition of mitochondria calcium overload. at high concentration (> 10 µM), capsaicin induces a slow but persistent increase in intracellular Ca2+
MMP↓, depolarization of mitochondria membrane potential
Cyt‑c↑, release of cytochrome C
Bax:Bcl2↑, activation of Bax and p53 through C-jun N-terminal kinase (JNK) activation
P53↑,
JNK↑,
PI3K↓, blocking the Pi3/Akt/mTOR signalling pathway, capsaicin increases levels of autophagic markers (LC3-II and Atg5)
Akt↓,
mTOR↓,
LC3II↑,
ATG5↑,
p62↑, enhances p62 and Fap-1 degradation and increases caspase-3 activity to induce apoptosis in human nasopharyngeal carcinoma cells
Fap1↓,
Casp3↑,
Apoptosis↑,
ROS↑, generation of ROS in human hepatoma (HepG2 cells)
MMP9↓, inhibition of MMP9 by capsaicin occurs via the suppression of AMPK-NF-κB, EGFR-mediated FAK/Akt, PKC/Raf/ERK, p38 MAPK, and AP-1 signaling pathway
eff↑, capsaicin 8% patch could promote the regeneration and restoration of skin nerve fibres in chemotherapy-induced peripheral neuropathy in addition to pain relief
eff↓, capsaicin has shown several unpleasant side effects, including stomach cramps, skin and gastric irritation, and burning sensation
eff↑, liposomes and micro-emulsion-based drugs have been known to significantly improve oral bioavailability and reduce the irritation of drugs
selectivity↑, In addition, these delivery systems can be surfaced-modified to perform site-directed/cell-specific drug delivery, thereby ensuring increased cell death of cancer cells while sparing non-selective normal cells
eff↑, Furthermore, owing to its antioxidant potential, capsaicin has been applied as a bioreduction and capping agent to synthesize biocompatible silver nanoparticles
ChemoSen↑, capsaicin has been combined with other anticancer therapies for more pronounced anticancer effects

2020-

CAP,

Capsaicinoids and Their Effects on Cancer: The “Double-Edged Sword” Postulate from the Molecular Scale

Review,

Var,

AntiTum↑, highlighting its antitumor properties mediated by cytotoxicity and immunological adjuvancy against at least 74 varieties of cancer,
selectivity↑, while non-cancer cells tend to have greater tolerance
TRPV1↑, activation or phosphorylation of TRPV1
MMP↓, leads to cell membrane depolarization through the influx of Na2+ and Ca2+,
Ca+2↑,
ER Stress↑, endoplasmic reticulum stress [73], and the inhibition of angiogenesis
angioG↓,
Casp3?, increase in caspase-3 activation, PARP-1 cleavage
cl‑PARP↑,
selectivity↑, oxidative stress threshold reached by these could be potentially higher than that caused in normal cells (tNOX−) when exposed to CAP, possibly also contributing to the selectivity of its effects
ROS↑, increase in the production of reactive oxygen species (ROS),
*ROS∅, Remarkably, in this same work, cells derived from the normal epithelium of human pancreatic ducts (HPDE6-E6E7) showed high tolerance to the same treatment by keeping their ROS levels stable
selectivity↑, In this sense, non-transformed human astrocytes from a primary culture showed greater tolerance to CAP, as they did not experience any of the mentioned effects when exposed to the same treatment

Showing Research Papers: 1 to 25 of 25

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 25

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 3, HO-1↑, 1, lipid-P↑, 1, NRF2↑, 1, ROS?, 1, ROS↓, 5, ROS↑, 1, ROS∅, 1, UCPs↑, 2,

Mitochondria & Bioenergetics ⓘ

Insulin↑, 1, MMP↑, 1, MMP∅, 1,

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1, glucose↓, 1, NADPH↓, 1, PKM2↓, 1, PPARγ↑, 1, SIRT1↑, 2, SREBP2↑, 1,

Cell Death ⓘ

p‑Akt↑, 1, Apoptosis↓, 1, Casp3∅, 1, Cyt‑c∅, 1, MAPK↓, 1, TRPV1↑, 8,

Transcription & Epigenetics ⓘ

other?, 1,

Proliferation, Differentiation & Cell State ⓘ

Wnt/(β-catenin)↓, 1,

Migration ⓘ

AntiAg↑, 2, Ca+2↑, 2, Na+↑, 1,

Angiogenesis & Vasculature ⓘ

eNOS↑, 1,

Barriers & Transport ⓘ

BBB↓, 1, BBB↑, 1, Na+↑, 1,

Immune & Inflammatory Signaling ⓘ

COX1↓, 1, COX2↓, 1, IL18↓, 1, IL1β↓, 2, IL6↓, 1, Inflam↓, 8, NF-kB↓, 2, TNF-α↓, 2,

Synaptic & Neurotransmission ⓘ

tau↓, 2,

Protein Aggregation ⓘ

Aβ↓, 2,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↑, 2, BioAv↝, 1, eff↑, 2, Half-Life↓, 1,

Clinical Biomarkers ⓘ

BP↓, 1, GutMicro↑, 2, IL6↓, 1,

Functional Outcomes ⓘ

AntiCan↑, 3, cardioP↑, 2, cognitive↑, 1, memory↑, 2, motorD↓, 1, neuroP↑, 3, Obesity↓, 1, Pain↓, 3, RenoP↑, 1, Risk↓, 2, Weight↓, 1,
Total Targets: 63

Scientific Paper Hit Count for: TRPV1, transient receptor potential vanilloid 1

24 Capsaicin
1 acetaminophen
1 Magnetic Fields

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1227  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

TRPV1 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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