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⟱

318-

AgNPs,

Silver nanoparticles regulate autophagy through lysosome injury and cell hypoxia in prostate cancer cells

in-vitro,

Pca,

PC3

lysoM↓, decline of lysosomal membrane integrity
lysosome↓, decrease of lysosomal quantity
AMPKα↑,
TumAuto↑, autophagy activation
mTOR↑,

280-

ALA,

Alpha‐lipoic acid inhibits lung cancer growth via mTOR‐mediated autophagy inhibition

in-vivo,

Lung,

A549

 orally administrated with LA (50 mg·kg−1·day−1) in drinking water

 mice

p‑mTOR↑, significantly increased mTOR phosphorylation level by 76.9%
TumCG↓, LA suppressed lung cancer growth in mice.
TumAuto↓, (note this research paper takes the approach of wanting to reduce autophagy)
p‑P70S6K↑, phosphorylation level of p70S6K, a downstream target of mTOR, was increased by 83.2% when compared with controls

265-

ALA,

Alpha-Lipoic Acid Reduces Cell Growth, Inhibits Autophagy, and Counteracts Prostate Cancer Cell Migration and Invasion: Evidence from In Vitro Studies

in-vitro,

Pca,

LNCaP

 ALA (25–1000 μM) for 48 h

in-vitro,

Pca,

DU145

ROS↓, ALA decreased ROS production, SOD1 and GSTP1 protein expression
SOD↓, SOD1, DU145
GSTP1/GSTπ↓,
NRF2↓, significantly reduced the cytosolic and nuclear content of the transcription factor Nrf2
p62↓, du145
p62↑, LNCaP
SOD↑, LNCaP
p‑mTOR↑, revealed that in both cancer cells, ALA, by upregulating pmTOR expression, reduced the protein content of two autophagy initiation markers, Beclin-1 and MAPLC3.
Beclin-1↓,
ROS↑, Interestingly, in LNCaP cells, we observed an almost significant increase in ROS content (p = 0.06) after ALA compared to the control, concomitantly with a significant upregulation of the antioxidant enzyme SOD1 after 48 h.
SOD1↑,

3396-

ART/DHA,

Progress on the study of the anticancer effects of artesunate

Review,

Var,

TumCP↓, reported inhibitory effects on cancer cell proliferation, invasion and migration.
TumCI↓,
TumCMig↓,
Apoptosis↑, ART has been reported to induce apoptosis, differentiation and autophagy in colorectal cancer cells by impairing angiogenesis
Diff↑,
TumAuto↑,
angioG↓,
TumCCA↑, inducing cell cycle arrest (11), upregulating ROS levels, regulating signal transduction [for example, activating the AMPK-mTOR-Unc-51-like autophagy activating kinase (ULK1) pathway in human bladder cancer cells]
ROS↑,
AMPK↑,
mTOR↑,
ChemoSen↑, ART has been shown to restore the sensitivity of a number of cancer types to chemotherapeutic drugs by modulating various signaling pathways
Tf↑, ART could upregulate the mRNA levels of transferrin receptor (a positive regulator of ferroptosis), thus inducing apoptosis and ferroptosis in A549 non-small cell lung cancer (NSCLC) cells.
Ferroptosis↑,
Ferritin↓, ferritin degradation, lipid peroxidation and ferroptosis
lipid-P↑,
CDK1↑, Cyclin-dependent kinase 1, 2, 4 and 6
CDK2↑,
CDK4↑,
CDK6↑,
SIRT1↑, Sirt1 levels
COX2↓,
IL1β↓, IL-1? ?
survivin↓, ART can selectively downregulate the expression of survivin and induce the DNA damage response in glial cells to increase cell apoptosis and cell cycle arrest, resulting in increased sensitivity to radiotherapy
DNAdam↑,
RadioS↑,

1076-

ART/DHA,

The Potential Mechanisms by which Artemisinin and Its Derivatives Induce Ferroptosis in the Treatment of Cancer

Review,

NA,

Ferroptosis↑,
ROS↑, interaction between heme-derived iron and ART will result in the production of ROS
ER Stress↑,
i-Iron↓, DHA can cause intracellular iron depletion in a time- and dose-dependent manner
TumAuto↑,
AMPK↑,
mTOR↑,
P70S6K↑,
Fenton↑,
lipid-P↑,
ROS↑,
ChemoSen↑, combination of ART and Nrf2 inhibitors to promote ferroptosis may have more efficient anticancer effects without damaging normal cells.
NRF2↑, Liu et al. discovered that ART covalently targets Keap1 at Cys151 to activate the Nrf2-dependent pathway [94
NRF2↓, inhibition of Nrf2-related gene expression accelerated erastin and sorafenib-induced ferroptosis [45]. More importantly, an accumulating body of research suggests that ART may induce ferroptosis in cancer cells by regulating the above molecules.

2677-

BBR,

Liposome-Encapsulated Berberine Alleviates Liver Injury in Type 2 Diabetes via Promoting AMPK/mTOR-Mediated Autophagy and Reducing ER Stress: Morphometric and Immunohistochemical Scoring

in-vivo,

Diabetic,

Rats

*hepatoP↑, berberine (Lip-BBR) to aid in ameliorating hepatic damage and steatosis, insulin homeostasis, and regulating lipid metabolism in type 2 diabetes (T2DM)
*LC3II↑, Lip-BBR treatment promoted autophagy via the activation of LC3-II and Bclin-1 proteins and activated the AMPK/mTOR pathway in the liver tissue of T2DM rats.
*Beclin-1↑,
*AMPK↑,
*mTOR↑,
*ER Stress↓, It decreased the endoplasmic reticulum stress by limiting the CHOP, JNK expression, oxidative stress, and inflammation.
*CHOP↓,
*JNK↓,
*ROS↓,
*Inflam↓,
*BG↓, Oral supplementation of diabetic rats either by Lip-BBR or Vild, 10 mg/kg of each, significantly (p < 0.001) lowered the blood glucose levels of tested diabetic rats compared to the diabetic group.
*SOD↑, when the diabetic rats received Lip-BBR, the decrements were less pronounced compared to the diabetic group by 1.16 fold, 2.52 fold, and 67.57% for SOD, GPX, and CAT, respectively.
*GPx↑,
*Catalase↑,
*IL10↑, Treatment of the diabetic rats with Lip-BBR significantly (p < 0.001) elevated serum IL-10 levels by 37.01% compared with diabetic rats.
*IL6↓, Oral supplementation of Lip-BBR could markedly (p < 0.0001) reduce the elevated serum levels of IL-6 and TNF-α when it is used as a single treatment by 55.83% and 49.54%,
*TNF-α↓,
*ALAT↓, ALT, AST, and ALP in the diabetic group were significantly higher (p < 0.0001) by 88.95%, 81.64%, and 1.8 fold, respectively, compared with those in the control group, but this was reversed by the treatment with Lip-BBR
*AST↓,
*ALP↓,

2047-

Buty,

Sodium butyrate inhibits migration and induces AMPK-mTOR pathway-dependent autophagy and ROS-mediated apoptosis via the miR-139-5p/Bmi-1 axis in human bladder cancer cells

in-vitro,

CRC,

T24/HTB-9

0-10mM

in-vitro,

Nor,

SV-HUC-1

in-vitro,

Bladder,

5637

in-vivo,

NA,

200 mg/kg/day, i.g., n = 5

mice

HDAC↓, Sodium butyrate (NaB) is a histone deacetylase inhibitor and exerts remarkable antitumor effects in various cancer cells
AntiTum↑,
TumCMig↓, NaB inhibited migration
AMPK↑, induced AMPK/mTOR pathway-activated autophagy and reactive oxygen species (ROS) overproduction via the miR-139-5p/Bmi-1 axis
mTOR↑,
TumAuto↑,
ROS↑, NaB initiates ROS overproduction
miR-139-5p↑, NaB upregulates miR-139-5p and depletes Bmi-1 in bladder cancer cells
BMI1↓,
TumCI?, NaB significantly inhibited cell migration dose-dependently
E-cadherin↑, E-cadherin was markedly increased, while the expression of N-cadherin, Vimentin, and Snail was decreased
N-cadherin↓,
Vim↓,
Snail↓,
cl‑PARP↑, increased expression levels of cleaved PARP, cleaved caspase-3, and Bax and the concurrent decrease in Bcl-2 and Bcl-xl
cl‑Casp3↑,
BAX↑,
Bcl-2↓,
Bcl-xL↓,
MMP↓, impairs mitochondrial membrane potential
PINK1↑, activates the PINK1/ PARKIN pathway
PARK2↑,
TumMeta↓, NaB inhibits tumor metastasis and growth in vivo
TumCG↓,
LC3II↑, a significant increase in the levels of cleaved caspase3, p-AMPK, and LC3B-II along with decreased Bmi-1 and Vimentin
p62↓, elevated LC3B-II levels and degradation of p62
eff↓, NAC abolished the impairment of MMP and ROS overproduction. Interestingly, NAC also significantly inhibited apoptosis induced by NaB

2017-

CAP,

Spice Up Your Kidney: A Review on the Effects of Capsaicin in Renal Physiology and Disease

Review,

Var,

RenoP↑, observed experimental benefits in preventing acute kidney injury
AntiTum↑, anti-tumoral properties of capsaicin on different types of cancer cells are well-acknowledged
AMPK↑, activating the AMPK/mTOR
mTOR↑,
PD-1↓, capsaicin promotes the inhibition of the PD-L1/PD-1 checkpoint
PD-L1↓,

4773-

CoQ10,

Coenzyme Q10 inhibits the activation of pancreatic stellate cells through PI3K/AKT/mTOR signaling pathway

in-vitro,

Nor,

Isolated PSCs from C57BL/6 mice were treated with various dosages of CoQ10 (1, 10, and 100μM) and different time (24h, 48h, and 72 h).

*other↓, Our finding suggests that CoQ10 inhibits the activation of PSCs by suppressing autophagy through activating the PI3K/AKT/mTOR signaling pathway.
*PI3K↑, PI3K/AKT/mTOR signaling pathway were dose-dependently upregulated with increased CoQ10 concentrations
*Akt↑,
*mTOR↑,
*ROS↓, In this study, CoQ10 significantly reduced the intracellular level of ROS in PSCs.

3631-

Cro,

Investigation of the neuroprotective effects of crocin via antioxidant activities in HT22 cells and in mice with Alzheimer's disease

in-vitro,

AD,

HT22

in-vivo,

AD,

mice

*ROS↓, suppressed intracellular reactive oxygen species (ROS) accumulation and Ca2+ overload compared with untreated cells.
*Ca+2↓, crocin strongly inhibited the overload of Ca2+ compared with the l-Glu-damaged HT22 cells,
*BAX↓, crocin significantly decreased the expression levels of Bax, Bad and cleaved caspase-3
*BAD↓,
*Casp3↓,
*cognitive↑, crocin substantially improved the cognition and memory abilities of the mice as measured by their coordination of movement in an open field test,
*memory↑,
*Aβ↓, Crocin improved cognitive abilities of AD mice, and reduced Aβ deposition in their brains
*GPx↑, crocin was able to reduce the Aβ1-42 content in the mouse brains, increase the levels of glutathione peroxidase, superoxide dismutase, acetylcholine and choline acetyltransferase,
*SOD↑,
*ChAT↑,
*Ach↑,
*AChE↓, and reduce the levels of ROS and acetylcholinesterase in the serum, cerebral cortex and hypothalamus compared with untreated mice.
*ROS↓,
*p‑Akt↑, crocin upregulated the phosphorylation levels of Akt and mTOR in 24-h l-Glu-exposed cells.
*p‑mTOR↑,
*neuroP↑, crocin-mediated neuroprotection of l-Glu-damaged HT22 cells.

1860-

dietFMD,

Chemo,

Fasting-mimicking diet blocks triple-negative breast cancer and cancer stem cell escape

in-vitro,

BC,

SUM159

in-vitro,

BC,

4T1

PI3K↑, FMD activates PI3K-AKT, mTOR, and CDK4/6 as survival/growth pathways, which can be targeted by drugs to promote tumor regression.
Akt↑,
mTOR↑,
CDK4↑,
CDK6↑,
hyperG↓, FMD cycles also prevent hyperglycemia and other toxicities caused by these drugs.
TumCG↓, cycles of FMD significantly slowed down tumor growth, reduced tumor size, and caused an increased expression of intratumor Caspase3
TumVol↓,
Casp3↑,
BG↓, confirming our hypothesis that lowering intracellular glucose levels (through reduced extracellular levels or reduced uptake) reduces CSC survival
eff↑, 2DG potentiated the effect of FMD both in terms of delaying tumor progression and in decreasing the number of mammospheres derived by tumor masses,
eff∅, metformin did not show any additive or synergistic antitumor effect when combined with the FMD, thus suggesting that FMD and metformin have redundant effects on blood glucose levels
PKA↓, We have previously shown that prolonged fasting reduces the activity of protein kinase A (PKA) in different types of normal cells
KLF5↓, PKA inhibition resulted in the downregulation of KLF5, a potential therapeutic target for TNBC
p‑GSK‐3β↑, (GSK3β) phosphorylation
Nanog↓, stemness-associated genes NANOG and OCT4, and KLF2 and TBX3,
OCT4↓,
KLF2↓,
eff↑, Combining FMD cycles with PI3K/AKT/mTOR inhibitors results in long-term animal survival and reduces treatment-induced side effects
ROS↑, FMD resulted in an increased expression of pro-apoptotic molecules, such as BIM, and ASK1, a critical cellular stress sensor frequently activated by ROS, whose production was previously shown to be increased by the FMD
BIM↑,
ASK1↑,
PI3K↑, FMD cycles upregulate PI3K-AKT and mTOR pathways and downregulate CCNB-CDK1 while upregulating CCND-CDK4/6 signaling axes
Akt↑,
mTOR↑,
CDK1↓,
CDK4↑,
CDK6↑,
eff↑, combining STS with pictilisib, ipatasertib, and rapamycin, selective inhibitors for PI3K, AKT, and mTOR, respectively, resulted in enhanced cancer cell death and reduction of mammosphere numbers in SUM159 cells

2860-

FIS,

Fisetin induces autophagy in pancreatic cancer cells via endoplasmic reticulum stress- and mitochondrial stress-dependent pathways

in-vitro,

PC,

PANC1

in-vitro,

PC,

Bxpc-3

in-vitro,

Nor,

hTERT-HPNE

in-vivo,

NA,

mice

AMPK↑, We found that the AMPK/mTOR signaling pathway was enhanced after fisetin treatment
mTOR↑,
UPR↑, RNA-seq analysis revealed that the unfolded protein response pathway, which is activated by ER stress, was enriched
ER Stress↑, Fisetin induced ER stress in pancreatic cancer cells
selectivity↑, results showed that fisetin was less cytotoxic to normal cells compared with pancreatic cancer cells
TumCP↓, fisetin inhibited the proliferation of PANC-1 cells
PERK↑, expression of PERK, ATF4, and ATF6 were also upregulated by fisetin
ATF4↑,
ATF6↑,

292-

HCA,

Hydroxycitric Acid Inhibits Chronic Myelogenous Leukemia Growth through Activation of AMPK and mTOR Pathway

in-vitro,

AML,

K562

 11.34 mM

ACLY↓,
AMPK↑,
mTOR↑,
eIF2α↑,
ATFs↑, ATF4
TumCG↓,

1918-

JG,

ROS -mediated p53 activation by juglone enhances apoptosis and autophagy in vivo and in vitro

in-vitro,

Liver,

HepG2

1-30uM

in-vivo,

NA,

4mg/kg

mice were intraperitoneally injected with 10%
dimethyl sulfoxide (DMSO) or JG (4 mg/kg) every other day for ten
times in tota

TumCG↓, JG significantly inhibited tumor growth in vivo
TumCP↓, JG effectively inhibited cell proliferation and induced apoptosis through extrinsic pathways
Apoptosis↑,
TumAuto↑, JG treatment induced autophagy flux
AMPK↑, activiting the AMPK-mTOR signaling pathway
mTOR↑,
P53↑, JG enhanced p53 activation
H2O2↑, JG enhanced the generation of hydrogen peroxide (H2O2)
ROS↑, JG caused apoptosis and autophagy via activating the ROS-mediated p53 pathway in human liver cancer cells in vitro and in vivo
toxicity↝, a slight loss in body weight was observed after JG injection (Fig. 1D), suggesting that JG might has slight side effects.
p62↓, rmarkable decrease of p62 level was observed after 30uM JG treatment
DR5↑,
Casp8↑,
PARP↑,
cl‑Casp3↑,

5117-

JG,

https://pubmed.ncbi.nlm.nih.gov/31283929/

vitro+vivo,

Liver,

TumCG↓, Here, the present results showed that JG significantly inhibited tumor growth in vivo.
TumCP↓, JG effectively inhibited cell proliferation and induced apoptosis through extrinsic pathways.
Apoptosis↑,
TumAuto↑, We also observed that JG treatment induced autophagy flux via activiting the AMPK-mTOR signaling pathway.
AMPK↑,
mTOR↑,
P53↑, JG enhanced p53 activation by increasing down-regulation of ubiquitin-mediated degradation
H2O2↑, JG enhanced the generation of hydrogen peroxide (H2O2) and superoxide anion radical (O2• -).
ROS↑, JG caused apoptosis and autophagy via activating the ROS-mediated p53 pathway in human liver cancer cells in vitro and in vivo

2643-

MCT,

Medium Chain Triglycerides enhances exercise endurance through the increased mitochondrial biogenesis and metabolism

Review,

Nor,

*Akt↑, increased mitochondrial biogenesis and metabolism is mediated through the activation of Akt and AMPK signaling pathways and inhibition of TGF-β signaling pathway.
*AMPK↓,
*TGF-β↓, MCT downregulates TGF-β signaling
eff↑, beneficial effect of dietary MCT in exercise performance through the increase of mitochondrial biogenesis and metabolism.
*BioEnh↑, Furthermore, addition of the combination of chilli and MCT to meals increased diet-induced thermogenesis by over 50% in heathy normal-weight humans
*ATP↑, a key regulator of energy metabolism and mitochondrial membrane ATP synthase (ATP5α) were significantly upregulated by MCT.
*PGC-1α↑, also observed a significant increase in protein level of PGC-1α and ATP5α
*p‑mTOR↑, increased levels in both total and phosphorylated Akt and mTOR
*SMAD3↓, a compensatory response of the huge reduction in Smad3.

2243-

MF,

Pulsed electromagnetic fields increase osteogenetic commitment of MSCs via the mTOR pathway in TNF-α mediated inflammatory conditions: an in-vitro study

in-vitro,

Nor,

mesenchymal stem cells (MSCs)

*eff↑, PEMF exposure increased cell proliferation and adhesion
*mTOR↑, PEMFs contribute to activation of the mTOR pathway via upregulation of the proteins AKT, MAPP kinase, and RRAGA, suggesting that activation of the mTOR pathway is required for PEMF-stimulated osteogenic differentiation.
*Akt↑,
*PKA↑, PEMFs increase the activity of certain kinases belonging to known intracellular signaling pathways, such as the protein kinase A (PKA) and the MAPK ERK1/2
*MAPK↑,
*ERK↑,
*BMP2↑, PEMFs stimulation also upregulates BMP2 expression in association with increased differentiation in mesenchymal stem cells (MSCs
*Diff↑,
*PKCδ↓, Decrease in PKC protein (involved on Adipogenesis)
*VEGF↑, Increase on VEGF (involved on angiogenesis)
*IL10↑, PEMF induced a significant increase of in vitro expression of IL-10 (that exerts anti-inflammatory activity)

486-

MF,

mTOR Activation by PI3K/Akt and ERK Signaling in Short ELF-EMF Exposed Human Keratinocytes

in-vitro,

Nor,

HaCaT

50 Hz, 1 mT for 1 h

*mTOR↑,
*PI3K↑, HaCaT cells exposed for 1h to 50Hz/1mT showed an increased percentage of cells in the S phase, through a significantly activation of the PI3K, JNK and ERK pathways
*Akt↑,
*p‑ERK↑,
*other↑, increases in the percentage of cells in the S phase and decrease in the percentage of cells in G0/G1 phase
*p‑JNK↑,
*p‑P70S6K↑,

3007-

RosA,

Hepatoprotective effects of rosmarinic acid: Insight into its mechanisms of action

Review,

NA,

*ROS↓, antioxidant properties as a ROS scavenger and lipid peroxidation inhibitor, anti-inflammatory, neuroprotective and antiangiogenic among others.
*lipid-P↓,
*Inflam↓,
*neuroP↑,
*angioG↓,
*eff↑, The hepatoprotective effects of RA alone and in combination with caffeic acid (CA) was reported in t-BHP-induced oxidative liver damage
*AST↓, significant reduction of indicators of hepatic toxicity, such as AST, ALT, GSSG, lipid peroxidation.
*ALAT↓,
*GSSG↓,
*eNOS↓, It also reduced the liver content of eNOS/iNOS and NO, attenuated NF-κB activation
*iNOS↓,
*NO↓,
*NF-kB↓,
*MMP2↓, It inhibited MMP-2 activity and suppressed ROS generation and lipid peroxidation.
*MDA↓, It also decreased malondialdehyde (MDA) and TNF-α levels while increasing GSH levels as well as SOD and GSH-Px activities in the livers and kidneys.
*TNF-α↓,
*GSH↑,
*SOD↑,
*IL6↓, RA decreased the hepatic level of IL-6, TNF-Alpha, and PGE2, as well as the activity of COX-2 It also decreased hepatic RAGE and sorbitol levels, and GLO-1 activity
*PGE2↓,
*COX2↓,
*mTOR↑, In the study, it was observed that RA stimulated hepatocyte proliferation. Specifically activated the mTOR signaling pathway during liver regeneration and rescued PH-impaired liver functions

4729-

Se,

Selenium regulates Nrf2 signaling to prevent hepatotoxicity induced by hexavalent chromium in broilers

*ROS↓, Studies have reported that selenium (Se), which is one of the essential trace elements of the poultry and participates in the oxidative metabolism, can alleviate Cr(Ⅵ)-induced organ damage by inhibiting oxidative stress,
*NRF2↑, levels of Nrf2, glutathione peroxidase 1 (GPx-1), NAD(P)H: quinone oxidoreductase 1 (NQO1), and mechanistic target of rapamycin (mTOR) in the Se&Cr group was upregulated
*GPx1↑,
*NQO1↑,
*mTOR↑,
*Beclin-1↓, along with decreased expression of Beclin 1, ATG5 and LC3 compared to the Cr group.
*ATG5↓,
*LC3s↓,
*hepatoP↑,

4745-

SeNPs,

Chemo,

Translational Selenium Nanoparticles Promotes Clinical Non-small-cell Lung Cancer Chemotherapy via Activating Selenoprotein-driven Immune Manipulation

Study,

NSCLC,

Risk↓, In this study, it is found that selenium (Se) depletion and immune dysfunction are present in patients with advanced NSCLC compared with healthy volunteers
TumCD↑, translational SeNPs can promote the proliferation of NK cells and enhance its cytotoxicity against cancer cells by activating mTOR signaling pathway
mTOR↑,
AntiTum↑, driven by GPXs to regulate the secretion of cytokines to achieve an antitumor response.
ChemoSen↑, Investigator-initiated Trial shows that translational SeNPs supplementation in combination with bevacizumab/cisplatin/pemetrexed exhibits enhanced therapeutic efficacy with an objective response rate of 83.3% and a disease control rate of 100%

1479-

SFN,

Sulforaphane triggers Sirtuin 3-mediated ferroptosis in colorectal cancer cells via activating the adenosine 5'-monophosphate (AMP)-activated protein kinase/ mechanistic target of rapamycin signaling pathway

in-vitro,

CRC,

HCT116

Ferroptosis↑, sulforaphane triggered the ferroptosis of HCT-116 cells by activating the SIRT3/AMPK/mTOR axis
SIRT3↑,
AMPK↑,
mTOR↑,
tumCV↓, SIRT3 overexpression reduced cell viability and increased intracellular levels of ROS, MDA, and iron
ROS↑,
MDA↑,
Iron↑,

3318-

SIL,

Pharmaceutical prospects of Silymarin for the treatment of neurological patients: an updated insight

Review,

AD,

Review,

Park,

*hepatoP↑, widely studied as a hepatoprotective drug for various liver disorders.
*neuroP↑, research studies have shown its putative neuroprotective nature against various brain disorders, including psychiatric, neurodegenerative, cognitive, metabolic and other neurological disorders
*TLR4↓, Silymarin treatment has shown anti-inflammatory action in AD models by suppressing toll-like receptor 4 (TLR4) pathways and decreasing the increased mRNA levels of TNF-α, IL-1β and NF-κB
*TNF-α↓,
*IL1β↓,
*NF-kB↓,
*memory↑, improvement in memory los
*cognitive↑, finally leading to normal cognitive functions
*NRF2↑, upregulating the Nrf-2/HO-1 signaling in mice model
*HO-1↑,
*ROS↓, inhibition of oxidative stress in the brain
*Akt↑, Figure 4
*mTOR↑,
*SOD↑,
*Catalase↑,
*GSH↑,
*IL10↑,
*IL6↑,
*NO↓,
*MDA↓,
*AChE↓,
*MAPK↓,
*BDNF↑, Silymarin supplementation improved learning and memory in diabetes-induced cognitively impaired rats by elevating BDNF levels

2232-

SK,

Shikonin Induces Autophagy and Apoptosis in Esophageal Cancer EC9706 Cells by Regulating the AMPK/mTOR/ULK Axis

in-vitro,

ESCC,

EC9706

2.26 ± 0.12 µM

tumCV↓, Shikonin exposure repressed cell viability and migration and invasion capabilities and caused EC9706 cell autophagy and apoptosis by activating the AMPK/mTOR/ULK axis.
TumCMig↓,
TumCI↓,
TumAuto↑,
Apoptosis↑,
Bcl-2↓, Bcl-2 protein expressions were decreased; nevertheless, the protein expression of Bax, cleaved caspase3, cleaved caspase-8, and cleaved PARP were elevated with increasing concentrations of shikonin
BAX↑,
cl‑Casp3↑,
cl‑Casp8↑,
cl‑PARP↑,
AMPK↑, Shikonin-Induced Autophagy and Apoptosis Through Activation of AMPK/mTOR/ULK Pathway
mTOR↑,
TumVol↓, The tumor diameter is reduced by more than 25%, the response rate is 37%, and the 1-year survival rate is 47%
OS↑,
LC3I↑, Similarly, shikonin can upregulate the protein expression of LC3 in EC9706 cells

4860-

Uro,

Urolithins–gut Microbial Metabolites with Potential Health Benefits

Review,

Nor,

Review,

AD,

Review,

Park,

*ROS↓, Urolithins have been shown to protect cells from oxidative stress, reduce inflammation, and inhibit tumor growth.
*Inflam↓, Urolithins, particularly Urolithin A, have shown potent anti-inflammatory effects, which are crucial in managing chronic inflammatory diseases
TumCG↓,
*neuroP↑, They also have neuroprotective effects, potentially mitigating neurodegenerative diseases like Alzheimer's and Parkinson's.
*cardioP↑, Additionally, urolithins may contribute to cardiovascular health by reducing cholesterol levels and improving endothelial function.
*LDL↓,
*BioAv↝, bioavailability and production of urolithins can vary significantly among individuals due to differences in gut microbiota composition.
*BioAv↓, Due to poor water solubility and susceptibility to enzymatic degradation, urolithin bioavailability remains a challenge.
*BioAv↑, Compared to non-encapsulated UA, liposomal formulations resulted in significantly higher intestinal absorption and plasma concentrations. PEGylated liposomes further prolonged circulation time and enhanced therapeutic efficacy
*SIRT1↑, In neurodegenerative diseases caused by aging, Uro-A prevents brain aging by activating the SIRT1/mTOR signaling pathway in experimental animals
*mTOR↑,
*BDNF↑, UA administration was associated with increased Brain-Derived Neurotrophic Factor (BDNF) levels, reduced neuroinflammation, and improved cognitive performance
*cognitive↑,

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 ⓘ

Catalase↑, 2, GPx↑, 2, GPx1↑, 1, GSH↑, 2, GSSG↓, 1, HO-1↑, 1, lipid-P↓, 1, MDA↓, 2, NQO1↑, 1, NRF2↑, 2, ROS↓, 8, SOD↑, 4,

Mitochondria & Bioenergetics ⓘ

ATP↑, 1, PGC-1α↑, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 2, AMPK↓, 1, AMPK↑, 1, LDL↓, 1, SIRT1↑, 1,

Cell Death ⓘ

Akt↑, 5, p‑Akt↑, 1, BAD↓, 1, BAX↓, 1, BMP2↑, 1, Casp3↓, 1, iNOS↓, 1, JNK↓, 1, p‑JNK↑, 1, MAPK↓, 1, MAPK↑, 1,

Transcription & Epigenetics ⓘ

Ach↑, 1, other↓, 1, other↑, 1,

Protein Folding & ER Stress ⓘ

CHOP↓, 1, ER Stress↓, 1,

Autophagy & Lysosomes ⓘ

ATG5↓, 1, Beclin-1↓, 1, Beclin-1↑, 1, LC3II↑, 1, LC3s↓, 1,

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1, ERK↑, 1, p‑ERK↑, 1, mTOR↑, 8, p‑mTOR↑, 2, p‑P70S6K↑, 1, PI3K↑, 2,

Migration ⓘ

Ca+2↓, 1, MMP2↓, 1, PKA↑, 1, PKCδ↓, 1, SMAD3↓, 1, TGF-β↓, 1,

Angiogenesis & Vasculature ⓘ

angioG↓, 1, eNOS↓, 1, NO↓, 2, VEGF↑, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, IL10↑, 3, IL1β↓, 1, IL6↓, 2, IL6↑, 1, Inflam↓, 3, NF-kB↓, 2, PGE2↓, 1, TLR4↓, 1, TNF-α↓, 3,

Synaptic & Neurotransmission ⓘ

AChE↓, 2, BDNF↑, 2, ChAT↑, 1,

Protein Aggregation ⓘ

Aβ↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↑, 1, BioAv↝, 1, BioEnh↑, 1, eff↑, 2,

Clinical Biomarkers ⓘ

ALAT↓, 2, ALP↓, 1, AST↓, 2, BG↓, 1, IL6↓, 2, IL6↑, 1,

Functional Outcomes ⓘ

cardioP↑, 1, cognitive↑, 3, hepatoP↑, 3, memory↑, 2, neuroP↑, 4,
Total Targets: 87

Scientific Paper Hit Count for: mTOR, mammalian target of rapamycin

2 Alpha-Lipoic-Acid
2 Artemisinin
2 Chemotherapy
2 Juglone
2 Magnetic Fields
1 Silver-NanoParticles
1 Berberine
1 Butyrate
1 Capsaicin
1 Coenzyme Q10
1 Crocetin
1 diet FMD Fasting Mimicking Diet
1 Fisetin
1 HydroxyCitric Acid
1 MCToil
1 Rosmarinic acid
1 Selenium
1 Selenium NanoParticles
1 Sulforaphane (mainly Broccoli)
1 Silymarin (Milk Thistle) silibinin
1 Shikonin
1 Urolithin

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#:209  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

mTOR Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

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 ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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