5HT Cancer Research Results

5HT, Serotonin: Click to Expand ⟱
Source:
Type:
Serotonin (5-hydroxytryptamine or 5-HT) is best known as a neurotransmitter; however, it also plays diverse roles in peripheral tissues, including modulation of cell proliferation, angiogenesis, and immune responses.

Several studies have identified the expression of multiple 5-HT receptors (e.g., 5-HT1A, 5-HT2A, and 5-HT7) in breast cancer cells.
Serotonin may promote tumor cell proliferation and can influence breast cancer progression through receptor-mediated signaling pathways.

Expression of 5-HT and its receptors is documented in various cancers including breast, colorectal, pancreatic, prostate, and hepatocellular carcinoma.
Overexpression of particular 5-HT receptors often correlates with increased cell proliferation, angiogenesis, and metastatic potential.
High levels of 5-HT receptor expression generally serve as a marker for poor prognosis, although the exact prognostic implications vary depending on the specific receptor subtype and tumor type.

-Vomiting caused by chemotherapy was thought to result from the fact that the chemotherapeutics stimulated the secretion of 5-HT in intestinal chromaffin cells, and then 5-HT acted on 5-HT receptor which caused excitation of nerves and vomiting reflex.
Scientific Papers found: Click to Expand⟱
5296- 5-HTP,    Serotonergic Regulation in Alzheimer’s Disease
- Review, AD, NA
*Risk↓, There is evidence that damage or dysfunction of the 5-HT system contributes to the development of AD, and different subtypes of 5-HT receptors are a potential target for the treatment of AD
*5HT↓, Serotonin is an antioxidant that inhibits the generation of ROS, malondialdehyde and carbonyls, prevents thiol oxidation, reduces the degradation of 2-deoxy-D-ribose, and prevents apoptosis
*ROS↓,
*MDA↓,
*Apoptosis↓,
*Mood↑, Serotonin deficiency may be responsible for the increase in aggressive behavior and depression often observed in patients with AD.
*other↑, Exercise and a Mediterranean diet increase 5-HT and BDNF levels, thereby improving mood and cognition.
*other↑, In particular, the evidence suggests that sulforaphane’s beneficial effects can be mainly ascribed to its peculiar ability to activate the Nrf2/ARE pathway [271].

2767- Bos,    The potential role of boswellic acids in cancer prevention and treatment
- Review, Var, NA
*Inflam↓, profound application as a traditional remedy for various ailments, especially inflammatory diseases including asthma, arthritis, cerebral edema, chronic pain syndrome, chronic bowel diseases, cancer
AntiCan↑,
*MAPK↑, 11-keto-BAs can stimulate Mitogen-activated protein kinases (MAPK) and mobilize the intracellular Ca(2+) that are important for the activation of human polymorphonuclear leucocytes (PMNL)
*Ca+2↝,
p‑ERK↓, AKBA prohibited the phosphorylation of extracellular signal-regulated kinase-1 and -2 (Erk-1/2) and impaired the motility of meningioma cells stimulated with platelet-derived growth factor BB
TumCI↓,
cycD1/CCND1↓, In the case of colon cancer, BA treatment on HCT-116 cells led to a decrease in cyclin D, cyclin E, and Cyclin-dependent kinases such as CDK2 and CDK4, along with significant reduction in phosphorylated Rb (pRb)
cycE/CCNE↓,
CDK2↓,
CDK4↓,
p‑RB1↓,
*NF-kB↓, convey inhibition of NF-kappaB and subsequent down-regulation of TNF-alpha expression in activated human monocytes
*TNF-α↓,
NF-kB↓, PC-3 prostate cancer cells in vitro and in vivo by inhibiting constitutively activated NF-kappaB signaling by intercepting the activity of IkappaB kinase (IKK
IKKα↓,
MCP1↓, LPS-challenged ApoE-/- mice via inhibition of NF-κB and down regulation of MCP-1, MCP-3, IL-1alpha, MIP-2, VEGF, and TF
IL1α↓,
MIP2↓,
VEGF↓,
Tf↓,
COX2↓, pancreatic cancer cell lines, AKBA inhibited the constitutive expression of NF-kB and caused suppression of NF-kB regulated genes such as COX-2, MMP-9, CXCR4, and VEGF
MMP9↓,
CXCR4↓,
VEGF↓,
eff↑, AKBA and aspirin revealed that AKBA has higher potential via modulation of the Wnt/β-catenin pathway, and NF-kB/COX-2 pathway in adenomatous polyps
PPARα↓, AKBA is also responsible for down-regulation of PPAR-alpha and C/EBP-alpha in a dose and temporal dependent manner in mature adipocytes, ultimately leading to pparlipolysis
lipid-P?,
STAT3↓, activation of STAT-3 in human MM cells could be inhibited by AKBA
TOP1↓, (PKBA; a semisynthetic analogue of 11-keto-β-boswellic acid), had been reported to influence the activity of topoisomerase I & II,
TOP2↑,
5HT↓, (5-LO), responsible for catalyzing the synthesis of leukotrienes from arachidonic acid and human leucocyte elastase (HLE), and serine proteases involved in several inflammatory processes, is considered to be a potent molecular target of BA derivative
p‑PDGFR-BB↓, BA up-regulates SHP-1 with subsequent dephosphorylation of PDGFR-β and downregulation of PDGF-dependent signaling after PDGF stimulation, thereby exerting an anti-proliferative effect on HSCs hepatic stellate cells
PDGF↓,
AR↓, AKBA targets different receptors that include androgen receptor (AR), death receptor 5 (DR5), and vascular endothelial growth factor receptor 2 (VEGFR2), and leads to the inhibition of proliferation of prostate cancer cells
DR5↑, induced expression of DR4 and DR5.
angioG↓, via apoptosis induction and suppression of angiogenesis
DR4↑,
Casp3↑, AKBA resulted in activation of caspase-3 and caspase-8, and initiation of poly (ADP) ribose polymerase (PARP) cleavage.
Casp8↑,
cl‑PARP↑,
eff↑, AKBA was preincubated with LY294002 or wortmannin (inhibitors of PI3K), it caused a significant enhancement of apoptosis in HT-29 cells
chemoPv↑, chemopreventive response of AKBA was estimated against intestinal adenomatous polyposis through the inhibition of the Wnt/β-catenin and NF-κB/cyclooxygenase-2 signaling pathway
Wnt↓,
β-catenin/ZEB1↓,
ascitic↓, AKBA by the suppression of ascites,
Let-7↑, AKBA could up-regulate the expression of let-7 and miR-200
miR-200b↑,
eff↑, anti-tumorigenic effects of curcumin and AKBA on the regulation of specific cancer-related miRNAs in colorectal cancer cells, and confirmed their protective action
MMP1↓, . It can inhibit the expression of MMP-1, MMP-2, and MMP-9 mRNAs along with secretions of TNF-α and IL-1β in THP-1 cells.
MMP2↓,
eff↑, combined administration of metformin, an anti-diabetic drug, and boswellic acid nanoparticles exhibited significant synergism through the inhibition of MiaPaCa-2 pancreatic cancer cell proliferation
BioAv↓, BA as a therapeutic drug is its poor bioavailability
BioAv↑, administration of BSE-018 concomitantly with a high-fat meal led to several-fold increased areas under the plasma concentration-time curves as well as peak concentrations of beta-boswellic acid (betaBA)
Half-Life↓, drug needs to be given orally at the interval of six hours due to its calculated half- life, which was around 6 hrs.
toxicity↓, BSE has been found to be a safe drug without any adverse side reactions, and is well tolerated on oral administration.
Dose↑, Boswellia serrata extract to the maximum amount of 4200 mg/day is not toxic and it is safe to use though it shows poor bioavailability
BioAv↑, Approaches like lecithin delivery form (Phytosome®), nanoparticle delivery systems like liposomes, emulsions, solid lipid nanoparticles, nanostructured lipid carriers, micelles and poly (lactic-co-glycolic acid) nanoparticles
ChemoSen↑, Like any other natural products BA can also be effective as chemosensitizer

229- MFrot,  MF,    Molecular mechanism of effect of rotating constant magnetic field on organisms
- in-vivo, Nor, NA
*NO↑, lasted 3hrs
*5HT↓, 5-HT content in mice brain decreased significantly after the treatment of RCMF
*eff↝, 5-HT content reached the lowest point after magnetic field treatment for 90 min and 60 min in decortex brain and small intestine respectively, but it returned to the normal level after two hours
*eff↝, inhibition of magnetic field on vomiting reaction was parallel to the decreasing level of 5-HT content in brain and small intestine tissue
*β-Endo↑, After animals and voluntary patients were treated by magnetic field, their plasma β-endorphin increased 23 times higher than before.
*other↓, Under the action of magnetic field, the synthesis and secretion of melatonin are weakened in pineal gland, and the melatonin content decreases in plasma

198- MFrot,  MF,    Biological effects of rotating magnetic field: A review from 1969 to 2021
- Review, Var, NA
AntiCan↑, RMF can inhibit the growth of various types of cancer cells in vitro and in vivo and improve clinical symptoms of patients with advanced cancer.
breath↑, 0.4T, 7Hz RMF was applied to treat 13 advanced non-small cell lung cancer patients (2 h/day, 5 days per week, for 6–10 weeks)
Pain↓, Decreased pleural effusion (2 patients, 15.4%), remission of shortness of breath (5 patients, 38.5%), relief of cancer pain (5 patients, 38.5%), increased appetite (6 patients, 46.2%), improved physical strength (9 patients, 69.2%), regular bowel mov
Appetite↑,
Strength↑,
BowelM↑,
TumMeta↓, The same RMF (2 h/day, for 43 days) can also suppress the growth and metastasis of B16-F10 cells in vivo
TumCCA↑, The up-regulated transcription of miR-34a induced cell proliferation inhibition, cell cycle arrest, and cell senescence by targeting E2F1/E2F3, two members of E2F family which are major regulators of the cell cycle,
ETC↓, 2h exposure) effectively inhibited the growth of two types of cultured brain cancer cells, glioblastoma cells and diffuse intrinsic pontine glioma cells. They found that the mitochondrial electron transport chain was significantly disturbed by RMF,
MMP↓, which caused loss of mitochondrial integrity, decreased mitochondrial carbon flux in cancer cells, and eventual cancer cell death (Sharpe et al., 2021).
TumCD↑,
selectivity↑, same group further reported that the same RMF can also selectively kill cultured human glioblastoma and non-small cell lung cancer cells, and leave normal cells unharmed
ROS↑, Mechanistic studies revealed that RMF can increase the mitochondrial ROS level, which further activated the caspase-3 and disturbed the electron fflow in the respiratory chain pathway in cancer cells. (Helekar et al., 2021).
Casp3↑,
TumCG↓, 0.4T, 7.5Hz RMF (2 h/day, for 5 days) inhibited the growth of mouse melanoma cell line B16–F10 in vitro,
TumCCA↑, and its mechanism involved cell cycle arrest and decomposition of chromatins.
ChrMod↑,
TumMeta↓, (2 h/day, for 43 days) can also suppress the growth and metastasis of B16–F10 cells in vivo,
Imm↑, benefiting from improved immune function, including decreased regulatory T cells, increased T cells, and dendritic cells
DCells↑,
Akt↓, inhibiting the activation of the AKT pathway (Tang et al., 2016). T
OS⇅, 51 women with advanced breast cancer underwent RMF treatment. The results showed that 27 patients among them achieved signicant therapeutic effects, and there were no side-effects
toxicity↓,
QoL↑, 13 advanced non-small cell lung cancer patients the quality of life was improved in different degrees. Median survival and 1-year survival rate was 50% and 100% longer
hepatoP↑, In addition, it seems that the RMF can also attenuate liver damage in mice bearing MCF7 and GIST-T1 cells (Zha et al., 2018)
Pain↓, The results showed that the RMF treatment reduced abdominal pain by 42.9% (9/21), nausea/vomiting by 19.0% (4/21), weight loss by 52.4% (11/21), ongoing blood loss by 9.5% (2/21), improved physical strength by 23.8% (5/21) and sleep quality by 19.0%
Weight↑,
Strength↑,
Sleep↑,
IL6↓, Furthermore, decreased levels of interleukin-6 (IL-6), granulocyte colony-stimulating factor (G-CSF) and keratinocyte-derived chemokine (KC) were observed
CD4+↑, it was discovered that macrophages and dendritic cells were activated, CD4+ T and CD8+ T lymphocytes increased, and the ratio of Th17/Treg was balanced.
CD8+↑,
Ca+2↑, effects of RMF were strongly associated with increased calcium tunnel activity and intracellular Ca2+ level in CNS
radioP↑, These results suggest that RMF may be helpful to alleviate the damage of hematopoietic function caused by radiotherapy and chemotherapy
chemoP↑,
*BMD↑, 0.4T, 8Hz RMF treatment (30min/day, for 30 days) along with calcium supplement, synergistically improved bone density
*AntiAge↑, In 2019, Xu et al. reported that a 4h exposure to a 0.2T, 4Hz RMF delayed the aging of human umbilical vein endothelial cells (HUVEC)
*AMPK↑, Mechanistic research revealed that RMF treatment increased the expression of AMPK while reducing the expression of p21, p53 and mTOR.
*P21↓,
*P53↓,
*mTOR↓,
*OS↑, They also discovered that the RMF (2 h/day, for 6, 10 or 14days) can prolong the health status lifespan of Caenorhabditis elegans.
*β-Endo↑, 0.1–0.8T, 0.33Hz RMF treatment signicantly increased the β-endorphin level in the blood of rabbits and humans (23 times higher than before). Moreover, it decreased serotonin (5-HT) in brains, small intestine tissue and serum of mice.
*5HT↓,

1509- SFN,    Combination therapy in combating cancer
- Review, NA, NA
NRF2↑, chemopreventive properties that are thought to be due to potent upregulation of Nrf2
ChemoSideEff↓, chemopreventive properties
eff↑, combined SFN with taxol in treatment of prostate cancer cell line DU145, and observed that SFN potentiated the effects of low doses of taxol
TumCP↓,
Apoptosis↑,
TumCCA↑, induce G2/M cell cycle arrest in vitro and in vivo
eff↑, SFN positively enhanced bortezomib, lenalidomide, and conventional drugs, such as dexamethasone, doxorubicin, and melphalan in a synergistic manner
PSA↓, SFN has shown to significantly reduce levels of prostate-specific antigen (PSA) (44.4% SFN group vs. 71.8% in placebo)
P53↑, SFN activates various anti-cancer responses such as p53, ARE, IRF-1, Pax-6 and XRE while suppressing proteins involved in tumorigenesis and progression, such as HIF1α, AP-1 and CA IX
Hif1a↓, while suppressing proteins involved in tumorigenesis and progression, such as HIF1α, AP-1 and CA IX
CAIX↓,
chemoR↓, SFN has thus shown to reduce chemoresistance and may be a potential agent to be used in conjunction with chemotherapeutics
5HT↓, SFN downregulates 5-HT receptor expression in Caco-2 cells

1513- SFN,  acetaz,    Next-generation multimodality of nutrigenomic cancer therapy: sulforaphane in combination with acetazolamide actively target bronchial carcinoid cancer in disabling the PI3K/Akt/mTOR survival pathway and inducing apoptosis
- in-vitro, BrCC, H720 - in-vivo, BrCC, NA - in-vitro, BrCC, H727
eff↑, Combining AZ+SFN reduced tumor cell survival compared to each agent alone, both in vitro and in vivo xenograft tissues.
tumCV↓,
Apoptosis↑,
P21↑,
PI3K↓,
Akt↓,
mTOR↓,
5HT↓, significantly reducing 5-HT secretion in carcinoid syndrome.
NRF2↑, AZ and SFN increased the expression of Nrf2 by 61% and 104%, respectively. Combination treatment further increased expression by 127%


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

lipid-P?, 1,   NRF2↑, 2,   ROS↑, 1,  

Metal & Cofactor Biology ⓘ

Tf↓, 1,  

Mitochondria & Bioenergetics ⓘ

ETC↓, 1,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

CAIX↓, 1,   PPARα↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 2,   Casp3↑, 2,   Casp8↑, 1,   DR4↑, 1,   DR5↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

BowelM↑, 1,   ChrMod↑, 1,   tumCV↓, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   cycE/CCNE↓, 1,   P21↑, 1,   p‑RB1↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↓, 1,   Let-7↑, 1,   mTOR↓, 1,   PI3K↓, 1,   STAT3↓, 1,   TOP1↓, 1,   TOP2↑, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration ⓘ

Ca+2↑, 1,   miR-200b↑, 1,   MMP1↓, 1,   MMP2↓, 1,   MMP9↓, 1,   PDGF↓, 1,   TumCI↓, 1,   TumCP↓, 1,   TumMeta↓, 2,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,   p‑PDGFR-BB↓, 1,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   COX2↓, 1,   CXCR4↓, 1,   DCells↑, 1,   IKKα↓, 1,   IL1α↓, 1,   IL6↓, 1,   Imm↑, 1,   MCP1↓, 1,   MIP2↓, 1,   NF-kB↓, 1,   PSA↓, 1,  

Synaptic & Neurotransmission ⓘ

5HT↓, 3,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   chemoR↓, 1,   ChemoSen↑, 1,   Dose↑, 1,   eff↑, 7,   Half-Life↓, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   ascitic↓, 1,   IL6↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   Appetite↑, 1,   breath↑, 1,   chemoP↑, 1,   chemoPv↑, 1,   ChemoSideEff↓, 1,   hepatoP↑, 1,   OS⇅, 1,   Pain↓, 2,   QoL↑, 1,   radioP↑, 1,   Sleep↑, 1,   Strength↑, 2,   toxicity↓, 2,   Weight↑, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 92

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

MDA↓, 1,   ROS↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,  

Cell Death ⓘ

Apoptosis↓, 1,   MAPK↑, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,   other↑, 2,  

DNA Damage & Repair ⓘ

P53↓, 1,  

Cell Cycle & Senescence ⓘ

P21↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,  

Migration ⓘ

Ca+2↝, 1,   β-Endo↑, 2,  

Angiogenesis & Vasculature ⓘ

NO↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

5HT↓, 3,  

Drug Metabolism & Resistance ⓘ

eff↝, 2,  

Clinical Biomarkers ⓘ

BMD↑, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   Mood↑, 1,   OS↑, 1,   Risk↓, 1,  
Total Targets: 23

Scientific Paper Hit Count for: 5HT, Serotonin
2 Magnetic Field Rotating
2 Magnetic Fields
2 Sulforaphane (mainly Broccoli)
1 5-Hydroxytryptophan
1 Boswellia (frankincense)
1 acetazolamide
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#:1119  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

Home Page