mTOR Cancer Research Results

mTOR, mammalian target of rapamycin: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
mTOR (mechanistic target of rapamycin) is a central regulator of cell growth, proliferation, metabolism, and survival. It is a serine/threonine kinase that integrates signals from nutrients, growth factors, and cellular energy status.
mTOR promotes protein synthesis and cell growth by activating downstream targets such as S6 kinase and 4E-BP1. In cancer, this pathway can become hyperactivated, leading to uncontrolled cell proliferation.

mTor Inhibitors:
-rapamycin (Sirolimus): classic natural product mTOR inhibitor
-Curcumin
-Resveratrol
-Epigallocatechin Gallate (EGCG)
-Honokiol
Scientific Papers found: Click to Expand⟱
6461- 1,8-Cin,    1,8-cineole (eucalyptol): A versatile phytochemical with therapeutic applications across multiple diseases
- Review, AD, NA - Review, Var, NA
*Inflam↓, long history of use in traditional medicine and exhibits an array of biological properties, including anti-inflammatory, antioxidant, antimicrobial, bronchodilatory, analgesic, and pro-apoptotic effects.
*antiOx↑,
*neuroP↑, recent studies have highlighted the neuroprotective, analgesic, and pro-apoptotic properties of 1,8-cineole, underscoring its potential beneficial role in a broad spectrum of conditions such as Alzheimer’s disease, neuropathic pain, and cancer
*BioAv↑, Marked by a logP value of 2.74, 1,8-cineole strikes an optimal equilibrium between solubility and permeability, hinting at its favorable potential for oral bioavailability
*Half-Life↝, In rabbits, oral administration of 200 mg/kg has led to rapid attainment of peak plasma concentration within 1 h, indicating efficient absorption
*toxicity↓, compound’s toxicity profile, the oral acute LD50 value in rats is documented at 2480 mg/kg body weight
*PGE2↓, 1,8-cineole decreased the release of prostaglandin E2 and leukotriene B4 (LTB4) from peripheral blood mononuclear cells in asthmatic patients, and reduced TNF-α, IL-1β, LTB4, and thromboxane B2 in lipopolysaccharide (LPS)-stimulated peripheral blood
*TNF-α↓,
*IL1β↓,
*NO↓, 1,8-cineole hindered LPS-induced nitric oxide (NO) production in mouse macrophage cell lines
*NF-kB↓, inhibition of nuclear translocation of NF-κB p65 and PPARγ, leading to the suppression of immune response genes.
*PPARγ↓,
COX2↓, ,8-cineole has been found to impede UVB-induced COX-2 protein and mRNA production in HaCaT cells
*ROS↓, 1,8-cineole’s antioxidant properties play a crucial role in its therapeutic potential, as it is effective in neutralizing reactive oxygen species (ROS)
*SOD↑, 1,8-cineole treatment enhanced antioxidant enzymes activities, such as superoxide dismutase (SOD) and catalase (CAT), increased total antioxidant capacity, and decreased ROS and malondialdehyde (MDA)
*Catalase↑,
*TAC↑,
*MDA↓,
*lipid-P↓, 1,8-cineole has demonstrated the ability to inhibit LP
*NRF2↑, The antioxidant activity of 1,8-cineole is mediated, in part, by activating the Nrf2/Keap1 system
*HO-1↑, increased expression of phase II detoxifying enzymes and antioxidant proteins, such as heme oxygenase-1 and NAD(P)H: quinone oxidoreductase 1 (NOQ1)
*NADPH↑,
*GPx↑, 1,8-cineole treatment has been shown to enhance the activities of antioxidant enzymes, such as SOD, GPx, and CAT,
*AntiBio↑, Antibacterial properties: activity, synergy with antibiotics, and impact on biofilm formation and cell morphology
*eff↑, Although 1,8-cineole exhibited weaker bactericidal activity than commonly used antibiotics such as gentamicin and amoxicillin (AMX)/clavulanic acid, it significantly reduced the minimum inhibitory concentration of antibiotics when used in combination
*AntiFungal↑, Antifungal properties: inhibition of fungal growth and disruption of biofilm formation
*AntiViral↑, Antiviral properties: inhibition of viral replication and enhancement of antiviral responses
*TRPA1↑, 1,8-cineole could activate TRPA1 channels in the dorsal root ganglia (DRG),
eff↑, when combined with simvastatin, increased G0/G1 cell cycle arrest and sensitized cells to apoptosis
TumCCA↑, 1,8-cineole induced G0/G1 arrest and senescence in HepG2 cells through oxidative stress and various signaling pathways such as MAPK, AMPK, and Akt/mTOR
ROS↑,
MAPK↝,
mTOR↝,
Apoptosis↑, HCT116 and RKO human colon cancer cell lines, 1,8-cineole selectively promoted apoptosis rather than necrosis
survivin↓, This process was linked to survivin and Akt inactivation, along with p38 activation.
Akt↓,
p38↑,
cl‑PARP↑, triggered subsequent cleavage of PARP and caspase-3, resulting in apoptosis.
cl‑Casp3⇅,
P53↑, increasing p53 expression, as well as the expression of apoptotic proteins (Bax/Bcl-2, Cyt-c, caspase-9, and caspase-3)
BAX↑,
Cyt‑c↑,
Casp9↑,
Dose↝, efficacious concentrations of 1,8-cineole reported for inhibiting in vitro cancer cell proliferation range from micromolar [135], [136] to millimolar (mM)
*Aβ↓, 1,8-cineole in rat PC12 cells (pheochromocytoma cells) demonstrated effective mitigation of the Aβ induced cytotoxicity and oxidative stress
*tau↓, 1,8-cineole has shown the ability to modulate tau phosphorylation by suppressing GSK-3β activity and to reduce Aβ production by inhibiting beta-site amyloid precursor protein cleaving enzyme-1 (BACE-1), both in vitro and in vivo
*GSK‐3β↓,
*BACE↓,
*cardioP↑, 1,8-cineole enhanced cell viability, inhibited cardiac hypertrophy, attenuated cardiac remodeling, improved cardiac function, and decreased the concentrations of atrial natriuretic peptide and brain natriuretic peptide in rat hearts
MFN2↑, 1,8-cineole was also found to inhibit the activation of dynamin-related protein 1 and promote mitochondrial fusion by increasing MFN2.

2678- BBR,    Berberine as a Potential Agent for the Treatment of Colorectal Cancer
- Review, CRC, NA
*Inflam↓, BBR exerts remarkable anti-inflammatory (94–96), antiviral (97), antioxidant (98), antidiabetic (99), immunosuppressive (100), cardiovascular (101, 102), and neuroprotective (103) activities.
*antiOx↑,
*cardioP↑,
*neuroP↑,
TumCCA↑, BBR could induce G1 cycle arrest in A549 lung cancer cells by decreasing the levels of cyclin D1 and cyclin E1
cycD1/CCND1↓,
cycE/CCNE↓,
CDC2↓, BBR also induced G1 cycle arrest by inhibiting cyclin B1 expression and CDC2 kinase in some cancer cells
AMPK↝, BBR has been suggested to induce autophagy in glioblastoma by targeting the AMP-activated protein kinase (AMPK)/mechanistic target of rapamycin (mTOR)/ULK1 pathway
mTOR↝,
Casp8↑, BBR has been revealed to stimulate apoptosis in leukemia by upregulation of caspase-8 and caspase-9
Casp9↑,
Cyt‑c↑, in skin squamous cell carcinoma A431 cells by increasing cytochrome C levels
TumCMig↓, BBR has been confirmed to inhibit cell migration and invasion by inhibiting the expression of epithelial–mesenchymal transition (EMT)
TumCI↓,
EMT↓,
MMPs↓, metastasis-related proteins, such as matrix metalloproteinases (MMPs) and E-cadherin,
E-cadherin↓,
Telomerase↓, BBR has shown antitumor effects by interacting with microRNAs (125) and inhibiting telomerase activity
*toxicity↓, Numerous studies have revealed that BBR is a safe and effective treatment for CRC
GRP78/BiP↓, Downregulates GRP78
EGFR↓, Downregulates EGFR
CDK4↓, downregulates CDK4, TERT, and TERC
COX2↓, Reduces levels of COX-2/PGE2, phosphorylation of JAK2 and STAT3, and expression of MMP-2/-9.
PGE2↓,
p‑JAK2↓,
p‑STAT3↓,
MMP2↓,
MMP9↓,
GutMicro↑, BBR can inhibit tumor growth through meditation of the intestinal flora and mucosal barrier, and generally and ultimately improve weight loss. BBR has been reported to modulate the composition of intestinal flora and significantly reduce flora divers
eff↝, BBR can regulate the activity of P-glycoprotein (P-gp), and potential drug-drug interactions (DDIs) are observed when BBR is coadministered with P-gp substrates
*BioAv↓, the efficiency of BBR is limited by its low bioavailability due to its poor absorption rate in the gut, low solubility in water, and fast metabolism. Studies have shown that the oral bioavailability of BBR is 0.68% in rats
BioAv↑, combining it with p-gp inhibitors (such as tariquidar and tetrandrine) (196, 198), and modification to berberine organic acid salts (BOAs)

15- CUR,  UA,    Effects of curcumin and ursolic acid in prostate cancer: A systematic review
- Review, Pca, NA
NF-kB↝, involve NF-κB, Akt, androgen receptors, and apoptosis pathways.
Akt↝, see figure 5
AR↝,
Apoptosis↝,
Bcl-2↝,
Casp3↝,
BAX↝,
P21↝,
ROS↝,
Bcl-xL↝,
JNK↝,
MMP2↝,
P53↝,
PSA↝,
VEGF↝,
COX2↝,
cycD1/CCND1↝,
EGFR↝,
IL6↝,
β-catenin/ZEB1↝,
mTOR↝,
NRF2↝,
AP-1↝,
Cyt‑c↝,
PI3K↝,
PTEN↝,
Cyc↝,
TNF-α↝,

4800- Lyco,    Recent insights on pharmacological potential of lycopene and its nanoformulations: an emerging paradigm towards improvement of human health
- Review, Var, NA
*antiOx↑, It is a potent antioxidant and free radical scavenger owing to the presence of 13 carbon–carbon double bonds, out of which 11 are conjugated and the remaining 2 are non-conjugated.
Keap1↝, many biological effects on different types of cancers like prostate, breast, skin, and oral cancer by targeting the Keap1-NF-kB, Keap1-Nrf 2 and PI3K/AKT/m-TOR signalling pathway.
NF-kB↝,
NRF2↝,
PI3K↝,
Akt↝,
mTOR↝,
*GutMicro↑, lycopene also has the ability to modify the gut microbiome

3741- MF,    Promising application of Pulsed Electromagnetic Fields (PEMFs) in musculoskeletal disorders
- Review, NA, NA
*eff↑, effectively treat numerous musculoskeletal disorders, such as delayed union or nonunion fractures, osteoarthritis (OA), osteoporosis (OP), osteonecrosis (ON), tendon disorders, etc.
*BMD↑, n 1964, Bassett et al. [8] demonstrated the effects of electric currents on new bone growth in vivo
*Inflam↓, arani et al. also demonstrated the PEMFs exerted a strong anti-inflammatory effect on the joint environment via acting as agonist of A2A and A3 adenosine receptors [
*PGE2↓, The receptor activation can reduce the release of prostaglandin E2 (PGE2) and pro-inflammatory cytokines IL-6 and IL-8, as well as inhibit the activation of the transcription factor NF-KB
*IL6↓,
*IL8↓,
*NF-kB↓,
*mTOR↝, mTOR) pathway has also been demonstrated to be the underlying signaling pathway of PEMFs involved in bone formation

4203- SIL,    Unlocking the Neuroprotective Potential of Silymarin: A Promising Ally in Safeguarding the Brain from Alzheimer’s Disease and Other Neurological Disorders
- Review, NA, NA
*MAPK↝, Silymarin utilizes a range of molecular mechanisms, including modulation of MAPK, AMPK, NF-κB, mTOR, and PI3K/Akt pathways
*AMPK↝,
*NF-kB↓,
*mTOR↝,
*PI3K↝,
*Akt↝,
*BioAv↝, silymarin faces challenges related to bioavailability and aqueous solubility, hindering its development as a clinical drug
*memory↑, silymarin dose-dependently improves the memory and expression of BDNF in TBI-induced mice along with a significant reduction in the level of glutamate and TNF-α, affirming that silymarin could be a potential therapeutic agent for addressing cognitiv
*BDNF↑,
*TNF-α↓,


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(tgid=1) ⓘ

Keap1↝, 1,   MFN2↑, 1,   NRF2↝, 2,   ROS↑, 1,   ROS↝, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC2↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↝, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Akt↝, 2,   Apoptosis↑, 1,   Apoptosis↝, 1,   BAX↑, 1,   BAX↝, 1,   Bcl-2↝, 1,   Bcl-xL↝, 1,   Casp3↝, 1,   cl‑Casp3⇅, 1,   Casp8↑, 1,   Casp9↑, 2,   Cyt‑c↑, 2,   Cyt‑c↝, 1,   JNK↝, 1,   MAPK↝, 1,   p38↑, 1,   survivin↓, 1,   Telomerase↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

GRP78/BiP↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↑, 1,   P53↝, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK4↓, 1,   Cyc↝, 1,   cycD1/CCND1↓, 1,   cycD1/CCND1↝, 1,   cycE/CCNE↓, 1,   P21↝, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

EMT↓, 1,   mTOR↝, 4,   PI3K↝, 2,   PTEN↝, 1,   p‑STAT3↓, 1,  

Migration(tgid=13) ⓘ

AP-1↝, 1,   E-cadherin↓, 1,   MMP2↓, 1,   MMP2↝, 1,   MMP9↓, 1,   MMPs↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   β-catenin/ZEB1↝, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,   EGFR↝, 1,   VEGF↝, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 2,   COX2↝, 1,   IL6↝, 1,   p‑JAK2↓, 1,   NF-kB↝, 2,   PGE2↓, 1,   PSA↝, 1,   TNF-α↝, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↝, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   Dose↝, 1,   eff↑, 1,   eff↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

AR↝, 1,   EGFR↓, 1,   EGFR↝, 1,   GutMicro↑, 1,   IL6↝, 1,   PSA↝, 1,  
Total Targets: 73

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1,   TRPA1↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   Catalase↑, 1,   GPx↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,   TAC↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↝, 1,   NADPH↑, 1,   PPARγ↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↝, 1,   MAPK↝, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

GSK‐3β↓, 1,   mTOR↝, 2,   PI3K↝, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   IL6↓, 1,   IL8↓, 1,   Inflam↓, 3,   NF-kB↓, 3,   PGE2↓, 2,   TNF-α↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

BDNF↑, 1,   tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,   BACE↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Clinical Biomarkers(tgid=22) ⓘ

BMD↑, 1,   GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 2,   memory↑, 1,   neuroP↑, 2,   toxicity↓, 2,  

Infection & Microbiome(tgid=24) ⓘ

AntiFungal↑, 1,   AntiViral↑, 1,  
Total Targets: 46

Scientific Paper Hit Count for: mTOR, mammalian target of rapamycin
1 1,8-Cineole
1 Berberine
1 Curcumin
1 Ursolic acid
1 Lycopene
1 Magnetic Fields
1 Silymarin (Milk Thistle) silibinin
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

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