TrkB Cancer Research Results

TrkB, Tropomyosin receptor kinase B: Click to Expand ⟱

Source:

Type:

Tropomyosin receptor kinase B (TrkB, encoded by the NTRK2 gene)

• TrkB is a high‐affinity receptor for brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4).

• It has been implicated in promoting cell survival, proliferation, migration, and resistance to apoptosis.

• In several cancer types, increased TrkB expression has been associated with enhanced tumor aggressiveness and metastasis.

Scientific Papers found: Click to Expand⟱

4281-

Api,

The neurotrophic activities of brain‐derived neurotrophic factor are potentiated by binding with apigenin, a common flavone in vegetables, in stimulating the receptor signaling

in-vitro,

AD,

SH-SY5Y

*BDNF↑, Apigenin potentiates the neurotrophic activities of BDNF through direct binding, which may serve as a possible treatment for its curative efficiency in neurodegenerative diseases and depression.
*TrkB↑, activating the signaling cascade of high‐affinity BDNF receptor, Trk B.

4280-

Api,

Protective effects of apigenin in neurodegeneration: An update on the potential mechanisms

Review,

AD,

Review,

Park,

*neuroP↑, Apigenin, a flavonoid found in various herbs and plants, has garnered significant attention for its neuroprotective properties
*antiOx↑, shown to possess potent antioxidant activity, which is thought to play a crucial role in its neuroprotective effects
*ROS↓, Apigenin has been demonstrated to scavenge ROS, thereby reducing oxidative stress and mitigating the damage to neurons
*Inflam↓, apigenin has been found to possess anti-inflammatory properties.
*TNF-α↓, inhibit the production of pro-inflammatory cytokines, such as TNF-α and IL-1β, which are elevated in neurodegenerative diseases
*IL1β↓,
*PI3K↑, apigenin has been shown to activate the PI3K/Akt signaling pathway, which is involved in promoting neuronal survival and preventing apoptosis.
*Akt↑,
*BBB↑, Apigenin has additional neuroprotective properties due to its ability to cross the BBB and enter the brain
*NRF2↑, figure 1
*SOD↑, pigenin has also been shown to activate various antioxidant enzymes, such as superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx)
*GPx↑,
*MAPK↓, Apigenin inhibits the MAPK signalling system, which significantly reduces oxidative stress-induced damage in the brain
*Catalase↑, , including SOD, catalase, GPx and heme oxygenase-1 (HO-1) [37].
*HO-1↑,
*COX2↓, apigenin has the ability to inhibit the expression and function of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE-2), enzymes that produce inflammatory mediators
*PGE2↓,
*PPARγ↑, apigenin has the ability to inhibit the expression and function of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE-2), enzymes that produce inflammatory mediators
*TLR4↓,
*GSK‐3β↓, Apigenin can inhibit the activity of GSK-3β,
*Aβ↓, Inhibiting GSK-3 can reduce Aβ production and prevent neurofibrillary disorders.
*NLRP3↓, Apigenin suppresses nucleotide-binding domain, leucine-rich–containing family, pyrin domain–containing-3 (NLRP3) inflammasome activation by upregulating PPAR-γ
*BDNF↑, Apigenin causes upregulation of BDNF and TrkB expression in several animal models
*TrkB↑,
*GABA↑, Apigenin enhances GABAergic signaling by increasing the frequency of chloride channel opening, leading to increased inhibitory neurotransmission
*AChE↓, It blocks acetylcholinesterase and increases acetylcholine availability.
*Ach↑,
*5HT↑, Apigenin has been shown to increase 5-HT levels, decrease 5-HT turnover, and prevent dopamine changes.
*cognitive↑, Apigenin increases the availability of acetylcholine in the synapse after inhibiting AChE, thereby enhancing cholinergic neurotransmission and improving cognitive function and memory
*MAOA↓, apigenin acts as a monoamine oxidase (MAO) inhibitor and MAO inhibitors increase the levels of monoamines in the brain

3887-

Api,

The flavonoid apigenin protects brain neurovascular coupling against amyloid-β₂₅₋₃₅-induced toxicity in mice

in-vivo,

AD,

mice

*Inflam↓, anti-inflammatory, anticarcinogenic, and free radical-scavenging activities.
*ROS↓,
*Aβ↓, Recent studies revealed its protective effects against amyloid-β (Aβ)-induced neurotoxicity, but the mechanism was unclear. I
*memory↑, involving improvement of the learning and memory capabilities,
*AChE↓, improvement of cholinergic system involving the inhibition of AChE activity and elevation of ACh level, and modification of BNDF, TrkB, and phospho-CREB levels.
*Ach↑,
*Dose↑, Apigenin, at doses of 10 mg/kg and 20 mg/kg, promoted learning and memory
*BDNF↑, apigenin also increased BDNF level and up-regulated its receptor TrkB and pCREB in A25-35 -induced amnesic mice.
*TrkB↑,
*p‑CREB↑,
*BBB↑, Additionally, we found that treatment with apigenin was effective in preserving anatomical and functional integrity of the BBB per- meability.
*Ca+2?, A relevant effect of apigenin by suppressing the Ca 2+ influx through both voltage- and receptor-operated calcium channels might be attributed to the changes of rCBF

4276-

BA,

Baicalin Attenuates Oxygen–Glucose Deprivation/Reoxygenation–Induced Injury by Modulating the BDNF-TrkB/PI3K/Akt and MAPK/Erk1/2 Signaling Axes in Neuron–Astrocyte Cocultures

in-vivo,

Stroke,

Newborn Sprague–Dawley (SD) rats

*BDNF↑, has been indicated to protect neurons by promoting brain-derived neurotrophic factor (BDNF).
*neuroP↑, neuroprotective mechanisms of baicalin against oxygen–glucose deprivation/reoxygenation
*TrkB↑, baicalin significantly increased the expressions of TrkB, PI3K/AKT, and MAPK/ERK.
*PI3K↑,
*Akt↑,
*MAPK↑,
*ERK↑,
*NO↓, elevation of NO and MDA was significantly attenuated by BCL treatment.
*MDA↓,
*SOD↑, BCL treatment increased the expression level of SOD
*TNF-α↓, OGD/R treatment significantly increased the expression levels of TNF-α, IL-1β, and IL-6 (p < 0.01). Compared with that in the OGD/R group, BCL robustly reduced the release of inflammatory cytokines
*IL1β↓,
*IL6?,

4267-

Caff,

Caffeine‐mediated BDNF release regulates long‐term synaptic plasticity through activation of IRS2 signaling

in-vivo,

NA,

Irs2−/− mice

*cognitive↑, Caffeine has cognitive‐enhancing properties with effects on learning and memory, concentration, arousal and mood
*memory↑,
*Mood↑,
*BDNF↑, caffeine induces massive secretion of BDNF in cultured hippocampal neurons
*TrkB↑, These observations strongly suggest that TrkB activation is involved in CAFLTP.

4262-

Chol,

Choline up-regulates BDNF and down-regulates TrkB neurotrophin receptor in rat cortical cell culture

in-vitro,

NA,

rat cortical cell culture

*TrkB↑, Further analysis of choline-exposed cell cultures showed an increased protein level of the TrkB ligand brain-derived neurotrophic factor (BDNF).
*BDNF↑,

4260-

CHr,

Chrysin modulates the BDNF/TrkB/AKT/Creb neuroplasticity signaling pathway: Acting in the improvement of cognitive flexibility and declarative, working and aversive memory deficits caused by hypothyroidism in C57BL/6 female mice

in-vivo,

NA,

 C57BL/6 female mice

*BDNF↑, Chrysin modulates the BDNF/TrkB/AKT/CREB signaling pathway in the brain.
*TrkB↑,
*Akt↑,
*CREB↑,
*memory↑, Chrysin treatment effectively reversed these memory deficits, restored cognitive flexibility, and improved protein levels
*cognitive↑,

4171-

CUR,

Curcumin produces neuroprotective effects via activating brain-derived neurotrophic factor/TrkB-dependent MAPK and PI-3K cascades in rodent cortical neurons

in-vivo,

NA,

rodent

*BDNF↑, treatment of curcumin increased BDNF and phosphor-TrkB
*TrkB↑,
*CREB↑, curcumin-induced increase in phosphorylated cyclic AMP response element binding protein (CREB), which has been implicated as a possible mediator of antidepressant actions
*Mood↑,
*neuroP↑, Therefore, we hypothesize the neuroprotection of curcumin might be mediated via BDNF/TrkB-MAPK/PI-3K-CREB signaling pathway.

4139-

Ex,

Impact of physical exercise on the regulation of brain-derived neurotrophic factor in people with neurodegenerative diseases

Review,

AD,

*BDNF↑, recent studies are analyzed that indicate an increase in BDNF levels following physical activity, particularly in young adults.
*eff↑, with the most significant effects seen in aerobic and high-intensity exercises.
*eff↑, Both acute and prolonged exercise increase BDNF, but the effect is more sustained with regular, long-term regimens.
*cognitive↑, Prolonged aerobic exercise increases BDNF and improves vascular and cognitive functions, with positive effects observed in older adults.
*memory↑, In animal models, forced and voluntary exercise increased hippocampal BDNF, improving spatial memory and synaptic function.
*BrainVol↑,
*TrkB↑, The interaction of BDNF with its receptor TrkB is involved in the processes that lead to enhancements in learning and memory associated with exercise
*GABA↑, BDNF increases the expression of markers associated with GABAergic neurotransmission, such as GABA, GAD65, and GAD67

4247-

GI,

6-Shogaol from Dried Ginger Protects against Intestinal Ischemia/Reperfusion by Inhibiting Cell Apoptosis via the BDNF/TrkB/PI3K/AKT Pathway

vitro+vivo,

NA,

*BDNF↑, activating BDNF/TrkB/PI3K/AKT signaling pathway and inhibiting II/R-induced cell apoptosis. The outcome is further validated both in vivo and in vitro.
*TrkB↑,
*PI3K↑,
*Akt↑,
*Apoptosis↓,
*Inflam↓, dried ginger, behaviors multiple biological activities, including anti-inflammation, antioxidation, and anti-apoptosis.
*antiOx↑,

4243-

Gins,

Effects of Ginseng on Neurological Disorders

Review,

Stroke,

Review,

AD,

Review,

Park,

*BDNF↑, These results suggest that the active ingredient of ginseng may exert antidepressant effects through enhanced BDNF-TrkB signaling pathways
*TrkB↑,
*neuroP↑, Korean Red Ginseng attenuated long-term brain damage and protected neuro in a permanent cerebral ischemia model
*VEGF↑, but also can increase the expression of VEGF and BDNF in PC12 cells subjected OGD/reperfusion
*p‑tau↓, Ginsenoside Rb1 markedly decreased tau protein hyperphosphorylation through JNK/p38 MAPK pathway
*memory↑, ginseng extracts inhibited memory impairment of AD rats.

4241-

HNK,

Effects of Honokiol on Neurological Injury and Cognitive Function in Mice with Intracerebral Hemorrhage by Regulating BDNF-TrkB-CREB Signaling Pathway

in-vivo,

Stroke,

mice

*Apoptosis↓, Honokiol may alleviate hippocampal neuronal apoptosis and damage, and improve cognitive dysfunction in ICH mice by activating the BDNF-TrkB-CREB signaling pathway.
*cognitive↑,
*BDNF↑,
*TrkB↑,
*CREB↑,

4292-

LT,

Luteolin for neurodegenerative diseases: a review

Review,

AD,

Review,

Park,

Review,

MS,

Review,

Stroke,

*Inflam↓, luteolin, showing significant anti-inflammatory, antioxidant, and neuroprotective activity.
*antiOx↑,
*neuroP↑,
*BioAv↝, To increase the bioavailability of luteolin, several delivery methods have been developed; the most thoroughly studied include lipid carriers like liposomes and nanoformulations
*BBB↑, luteolin given intraperitoneally (ip) to mice can readily cross the blood-brain barrier (BBB) and enter the brain
*TNF-α↓, nhibiting pro-inflammatory mediators such as cyclooxygenase-2 (COX-2), nitric oxide (NO), TNF-α, IL-β, IL-6, IL-8, IL-31, and IL-33 in several in vitro models of AD
*IL1β↓,
*IL6↓,
*IL8↓,
*IL33↓,
*NF-kB↓, inhibition of the NF-кB pathway
*BACE↓, leads to the inhibition of a downstream target– β-site amyloid precursor protein cleaving enzyme (BACE1), which is a key mediator in forming Aβ fibrils in AD pathology
*ROS↓, anti-oxidant activity mainly by reducing ROS levels and increasing SOD activity in in vitro models of AD
*SOD↑,
*HO-1↑, increase the expression of antioxidant enzymes such as heme oxygenase-1 (HO-1) via the nuclear factor erythroid 2–related factor 2/ antioxidant responsive element (Nrf-2/ARE) complex activation
*NRF2↑,
*Casp3↓, reducing the levels of caspase-3 and − 9 and improving the B-cell lymphoma protein 2/Bcl-2-associated X protein (Bcl-2/Bax) ratio, as it was reported in in vitro models of AD
*Casp9↑,
*Bax:Bcl2↓,
*UPR↑, enhancing the unfolded protein response (UPR) pathway, leading to an increase in endoplasmic reticulum (ER) chaperone GRP78 and a decrease in the expression of UPR-targeted pro-apoptotic genes via the MAPK pathway.
*GRP78/BiP↑,
*Aβ↓, evidence that suggests that luteolin can directly influence the formation of Aβ plaques by selectively inhibiting the activity of N-acetyl-α-galactosaminyltransferase (ppGalNAc-T) isoforms
*GSK‐3β↓, inactivating the glycogen synthase kinase-3 alpha (GSK-3α) isoform, suppressing Aβ and promoting tau disaggregation
*tau↓,
*CREB↑, luteolin promoted phosphorylation and activation of cAMP response element-binding protein (CREB) leading to the increased miR-132 expression, and eventually neurite outgrowth in PC12 cells
*ATP↑, ROS production was decreased by 40%, MMP levels were restored close to control N2a levels (202%), and ATP levels were improved by 444%).
*cognitive↑, protective effect of luteolin against cognitive dysfunction was also reported in the streptozotocin
*BloodF↑, Luteolin increased regional cerebral blood flow values, alleviated the leakage of the lumen of vessels, and protected the integrity of BBB
*BDNF↑, increasing the level of brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor (TrkB) expression in the cerebral cortex
*TrkB↑,
*memory↑, luteolin supplementation significantly ameliorated memory and cognitive deficits in 3 × Tg-AD mice.
*PPARγ↑, attenuated mitochondrial dysfunction via peroxisome proliferator-activated receptor gamma (PPARγ) activation.
*eff↑, combination of luteolin with another compound– l-theanine (an amino acid found in tea) also improved AD-like symptoms in the Aβ25–35-treated rats

4232-

Lut,

Luteolin Treatment Ameliorates Brain Development and Behavioral Performance in a Mouse Model of CDKL5 Deficiency Disorder

in-vivo,

NA,

three-month-old heterozygous female (+/−) Cdkl5 KO mice

*BDNF↑, provide novel evidence that luteolin treatment, by restoring microglia alterations and transiently boosting BDNF/TrkB signaling
*Mood↑, Treatment with Luteolin Ameliorates Behavioral Deficits in Cdkl5 +/− Mice
*neuroG↑, Treatment with Luteolin Promotes Neurogenesis in the Hippocampus of Cdkl5 +/− Mice
*TrkB↑, Treatment with Luteolin Transiently Boosts BDNF/TrkB Signaling Pathways in the Cortex of Cdkl5 +/− Mice

4227-

Lyco,

Lycopene Alleviates Depression-Like Behavior in Chronic Social Defeat Stress-Induced Mice by Promoting Synaptic Plasticity via the BDNF-TrkB Pathway

in-vivo,

NA,

Chronic Social Defeat Stress-Induced Mice

*BDNF↑, suggesting that lycopene may enhance synaptic plasticity via the BDNF–TrkB/pTrkB signaling pathway.
*TrkB↑,
*PSD95↑, mRNA expression levels of PSD‐95 and Syn in the hippocampus of the CSDS + LYC group mice were substantially upregulated compared to the model group

4160-

NAD,

The biochemical pathways of central nervous system neural degeneration in niacin deficiency

Review,

NA,

*BDNF↑, Recent evidences suggest that niacin administration may up-regulate the expression of BDNF-TrkB.
*TrkB↑,

4162-

QC,

Quercetin attenuates cell apoptosis in focal cerebral ischemia rat brain via activation of BDNF-TrkB-PI3K/Akt signaling pathway

in-vivo,

Stroke,

Rats

*neuroP↑, Quercetin significantly improved neurological function, while it decreased the infarct volume and the number of TdT mediated dUTP nick end labeling positive cells in MCAO rats.
*BDNF↑, The protein expression of BDNF, TrkB and p-Akt also increased in the quercetin treated rats.
*TrkB↑,
*p‑Akt↑,

4214-

Se,

Selenium ameliorates cognitive impairment through activating BDNF/TrkB pathway

in-vivo,

NA,

APP/PS1/tau 3 × Tg-AD mouse model

*memory↑, selenium supplementation can improve spatial learning and memory deficiencies in 3 × Tg-AD mice.
*other↑, Selenium supplementation increased selenium and GSH-Px levels in the brain tissue of 3 × Tg-AD mice and significantly enhanced neuronal conditions
*BDNF↑, the expression levels of proteins related to the BDNF/TrkB pathway significantly increased following selenium supplementation.
*TrkB↑,

4198-

SFN,

Sulforaphane epigenetically enhances neuronal BDNF expression and TrkB signaling pathways

vitro+vivo,

AD,

Mouse primary cortical neurons and a triple-transgenic mouse model of Alzheimers disease  3 × Tg-AD

*TrkB↑, Sulforaphane elevated levels of synaptic TrkB signaling pathway components, including CREB, CaMKII, ERK, and Akt in both primary cortical neurons and 3 × Tg-AD mice.
*CREB↑,
CaMKII ↑,
*ERK↑,
*ac‑H3↑, Sulforaphane increased global acetylation of histone 3 (H3) and H4, inhibited HDAC activity, and decreased the level of HDAC2 in primary cortical neurons
*ac‑H4↑,
*HDAC↓,
*HDAC2↓,
*BDNF↑, sulforaphane increased acetylated H3 and H4 at BDNF promoters, suggesting that sulforaphane regulates BDNF expression via HDAC inhibition.

4215-

SY,

Safflower yellow alleviates cognitive impairment in mice by modulating cholinergic system function, oxidative stress, and CREB/BDNF/TrkB signaling pathway

in-vivo,

NA,

memory dysfunction caused by SCOP, NaNO2 and ethanol in mice

*memory↑, SY could shorten the escape latency and the time of the first crossing platform in the mice with memory acquisition and memory consolidation impairments, and increase the platform crossing times.
*AChE↓, SY decreased the AChE activities, increased the ChAT activities, and modulated oxidative stress markers (SOD, MDA, and GSH-PX) in scopolamine-induced mice
*ChAT↑,
*SOD↓,
*MDA↓,
*GPx↑,
*BDNF↑, SY could activated BDNF/TrkB/CREB signaling pathway and reduced neuronal damage.
*TrkB↑,
*CREB↑,
*ROS↓, SY can restore the function of the cholinergic system, inhibit oxidative stress

2138-

TQ,

Thymoquinone has a synergistic effect with PHD inhibitors to ameliorate ischemic brain damage in mice

in-vivo,

Nor,

TQ (5 mg/kg

Male C57 mice were used to establish an ischemic stroke model by using endothelin-1

*Hif1a↑, TQ can activate the HIF-1α pathway and its downstream genes such as VEGF, TrkB, and PI3K, which in turn enhance angiogenesis and neurogenesis.
*VEGF↑,
*TrkB↑,
*PI3K↑,
*angioG↑, which in turn enhance angiogenesis and neurogenesis.
*neuroG↑,
*motorD↑, TQ has the same effect as DMOG to activate HIF-1 α and can improve motor dysfunction after ischemic stroke

Showing Research Papers: 1 to 21 of 21

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 21

Pathway results for Effect on Cancer / Diseased Cells:

Kinase & Signal Transduction ⓘ

CaMKII ↑, 1,
Total Targets: 1

Pathway results for Effect on Normal Cells:

Functional Outcomes ⓘ

cognitive↑, 6, memory↑, 8, Mood↑, 3, motorD↑, 1, neuroP↑, 6,
Total Targets: 75

Scientific Paper Hit Count for: TrkB, Tropomyosin receptor kinase B

3 Apigenin (mainly Parsley)
1 Baicalin
1 Caffeine
1 Choline
1 Chrysin
1 Curcumin
1 Exercise
1 Ginger/6-Shogaol/Gingerol
1 Ginseng
1 Honokiol
1 Luteolin
1 Lutein
1 Lycopene
1 nicotinamide adenine dinucleotide
1 Quercetin
1 Selenium
1 Sulforaphane (mainly Broccoli)
1 Safflower yellow
1 Thymoquinone

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#:1254  State#:%  Dir#:2
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TrkB Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Kinase & Signal Transduction ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

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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