cMyc Cancer Research Results

cMyc, cellular-MYC oncogene: Click to Expand ⟱

Source:

Type: oncogene

The MYC proto-oncogenes are among the most commonly activated proteins in human cancer. The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell. The c-Myc oncogene is a ‘master regulator’ of both cellular growth and metabolism in transformed cells.
-C-myc is a common oncogene that enhances aerobic glycolysis in the cancer cells by transcriptionally activating GLUT1, HK2, PKM2 and LDH-A

Inhibitors (downregulate):
Curcumin
Resveratrol: downregulate c-Myc expression.
Epigallocatechin Gallate (EGCG)
Quercetin
Berberine: decrease c-Myc expression and repress its transcriptional activity.

Scientific Papers found: Click to Expand⟱

4388-

AgNPs,

Differential Cytotoxic Potential of Silver Nanoparticles in Human Ovarian Cancer Cells and Ovarian Cancer Stem Cells

in-vitro,

Cerv,

47.5 nm

tumCV↓, the numbers of A2780 (bulk cells) and ALDH+/CD133+ colonies were significantly reduced
CSCs↓,
selectivity↑, induced apoptosis in pancreatic CSCs and cancer cell lines, but had no effect on human normal pancreatic epithelial cells
Apoptosis↑,
ROS↑, figure 5, AgNPs induces apoptosis by oxidative stress
LDH↓, figure 5 (leakage outside the cell increases)
Casp3↑, AgNPs treated cells shows up-regulation of caspase-3, bax, bak, and c-myc, genes
BAX↑,
Bak↑,
cMyc↑,
MMP↓, and loss of mitochondrial membrane potential.

5553-

BBM,

A review on berbamine–a potential anticancer drug

Review,

Var,

P-gp↓, Treatment with berbamine decreased P-glycoprotein (P-gp) expression and down-regulated expression of MDR1 (multi-drug resistance1) and survivin mRNA in K562/A02 cells
MDR1↓,
survivin↓,
NF-kB↓, decrease expression of nuclear factor-B (NF-B), phosphoIB, IKK, and survivin.
TumCP↓, In a chronic myeloid leukemia cell line KU812, berbamine inhibited cell proliferation in a time- and dose-dependent manner, with IC50 values for treatments of 24, 48, and 72 h at 5.83, 3.43, and 0.75 μg/ml, respectively.
TumCCA↑, Berbamine induced cell cycle arrest at the G1 phase and also induced apoptosis.
Apoptosis↑,
SMAD3↑, The compound up-regulated transcriptions of Smad3 and p21, and increased protein levels of both total Smad3 and phosphorylated Smad3.
P21↑,
cycD1/CCND1↓, The protein levels of cyclin D1 and c-Myc were reduced.
cMyc↑,
Bcl-2↓, The levels of the anti-apoptotic proteins Bcl-2 and Bcl-xL were decreased, and the level of the pro-apoptotic protein Bax was increased.
Bcl-xL↓,
BAX↑,
CaMKII ↓, The compound has been shown to specifically bind to the ATP-binding pocket of calmodulin kinase (CAMK)II, inhibit its phosphorylation, and trigger apoptosis.
ChemoSen↑, Berbamine also significantly enhanced the activity of anticancer drugs like trichostatin A and celecoxib.
MMP2↓, EBB down-regulated the activities and mRNA levels of matrix metalloproteinases (MMP) 2 and 9, and up-regulated the mRNA levels of tissue inhibitor of metalloproteinases (TIMP) 1.
MMP9↓,
TIMP1↑,
cl‑Casp3↑, induction of apoptosis, including activation and cleavage of caspases 3, 8, 9 and PARP.
cl‑Casp9↑,
cl‑Casp8↑,
cl‑PARP↑,
IL6↓, BBD inhibited autocrine IL-6 production, and down-regulated membrane IL-6 receptor (IL-6R) expression.
ROS↑, Production of reactive oxygen species (ROS) was increased by BBMD3 in these cells.

975-

Est,

Estrogen inhibits autophagy and promotes growth of endometrial cancer by promoting glutamine metabolism

vitro+vivo,

UEC,

GLS↑, in estrogen-sensitive UEC cell (UECC) (an ER inhibitor antagonist) could reverse these effects.
cMyc↑, three MYC subtypes (c-MYC, n-MYC and l-MYC) were increased after estrogen treatment
GlutMet↑,
tumCV↑,
TumAuto↓,

2825-

FIS,

Exploring the molecular targets of dietary flavonoid fisetin in cancer

Review,

Var,

*Inflam↓, present in fruits and vegetables such as strawberries, apple, cucumber, persimmon, grape and onion, was shown to possess anti-microbial, anti-inflammatory, anti-oxidant
*antiOx↓, fisetin possesses stronger oxidant inhibitory activity than well-known potent antioxidants like morin and myricetin.
*ERK↑, inducing extracellular signal-regulated kinase1/2 (ERK)/c-myc phosphorylation, nuclear NF-E2-related factor-2 (Nrf2), glutamate cystine ligase and glutathione (GSH) levels
*p‑cMyc↑,
*NRF2↑,
*GSH↑,
*HO-1↑, activate Nrf2 mediated induction of hemeoxygenase-1 (HO-1) important for cell survival
mTOR↓, in our studies on fisetin in non-small lung cancer cells, we found that fisetin acts as a dual inhibitor PI3K/Akt and mTOR pathways
PI3K↓,
Akt↓,
TumCCA↑, fisetin treatment to LNCaP cells resulted in G1-phase arrest accompanied with decrease in cyclins D1, D2 and E and their activating partner CDKs 2, 4 and 6 with induction ofWAF1/p21 and KIP1/p27
cycD1/CCND1↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,
CDK6↓,
P21↑,
p27↑,
JNK↑, fisetin could inhibit the metastatic ability of PC-3 cells by suppressing of PI3 K/Akt and JNK signaling pathways with subsequent repression of matrix metalloproteinase-2 (MMP-2) and MMP-9
MMP2↓,
MMP9↓,
uPA↓, fisetin suppressed protein and mRNA levels of MMP-2 and urokinase-type plasminogen activator (uPA) in an ERK-dependent fashion.
NF-kB↓, decrease in the nuclear levels of NF-B, c-Fos, and c-Jun was noted in fisetin treated cells
cFos↓,
cJun↓,
E-cadherin↑, upregulation of E-cadherin and down-regulation of vimentin and N-cadherin.
Vim↓,
N-cadherin↓,
EMT↓, EMT inhibiting potential of fisetin has been reported in melanoma cells
MMP↓, The shift in mitochondrial membrane potential was accompanied by release of cytochrome c and Smac/DIABLO resulting in activation of the caspase cascade and cleavage of PARP
Cyt‑c↑,
Diablo↑,
Casp↑,
cl‑PARP↑,
P53↑, fisetin with induction of p53 protein
COX2↓, Fisetin down-regulated COX-2 and reduced the secretion of prostaglandin E2 without affecting COX-1 protein expression.
PGE2↓,
HSP70/HSPA5↓, It was shown that the induction of HSF1 target proteins, such as HSP70, HSP27 and BAG3 were inhibited in HCT-116 cells exposed to heat shock at 43 C for 1 h in the presence of fisetin
HSP27↓,
DNAdam↑, DNA fragmentation, an increase in the number of sub-G1 phase cells, mitochondrial membrane depolarization and activation of caspase-9 and caspase-3.
Casp3↑,
Casp9↑,
ROS↑, This was associated with production of intracellular ROS
AMPK↑, Fisetin induced AMPK signaling
NO↑, fisetin induced cytotoxicity and showed that fisetin induced apoptosis of leukemia cells through generation of NO and elevated Ca2+ activating the caspase
Ca+2↑,
mTORC1↓, Fisetin was shown to inhibit the mTORC1 pathway and its downstream components including p70S6 K, eIF4B and eEF2 K.
p70S6↓,
ROS↓, Others have also noted a similar decrease in ROS with fisetin treatment.
ER Stress↑, Induction of ER stress upon fisetin treatment, evident as early as 6 h, and associated with up-regulation of IRE1, XBP1s, ATF4 and GRP78, was followed by autophagy which was not sustained
IRE1↑,
ATF4↑,
GRP78/BiP↑,
eff↑, Combination of fisetin and the BRAF inhibitor sorafenib was found to be extremely effective in inhibiting the growth of BRAF-mutated human melanoma cells
eff↑, synergistic effect of fisetin and sorafenib was observed in human cervical cancer HeLa cells,
eff↑, Similarly, fisetin in combination with hesperetin induced apoptosis
RadioS↑, pretreatment with fisetin enhanced the radio-sensitivity of p53 mutant HT-29 cancer cells,
ChemoSen↑, potential of fisetin in enhancing cisplatin-induced cytotoxicity in various cancer models
Half-Life↝, intraperitoneal (ip) dose of 223 mg/kg body weight the maximum plasma concentration (2.53 ug/ml) of fisetin was reached at 15 min which started to decline with a first rapid alpha half-life of 0.09 h and a longer half-life of 3.12 h.

2914-

LT,

Therapeutic Potential of Luteolin on Cancer

Review,

Var,

3–50 µM in vitro

*antiOx↑, As an antioxidant, Luteolin and its glycosides can scavenge free radicals caused by oxidative damage and chelate metal ions
*IronCh↑,
*toxicity↓, The safety profile of Luteolin has been proven by its non-toxic side effects, as the oral median lethal dose (LD50) was found to be higher than 2500 and 5000 mg/kg in mice and rats, respectively, equal to approximately 219.8−793.7 mg/kg in humans
*BioAv↓, One major problem related to the use of flavonoids for therapeutic purposes is their low bioavailability.
*BioAv↑, Resveratrol, which functions as the inhibitor of UGT1A1 and UGT1A9, significantly improved the bioavailability of Luteolin by decreasing the major glucuronidation metabolite in rats
DNAdam↑, Luteolin’s anticancer properties, which involve DNA damage, regulation of redox, and protein kinases in inhibiting cancer cell proliferation
TumCP↓,
DR5↑, Luteolin was discovered to promote apoptosis of different cancer cells by increasing Death receptors, p53, JNK, Bax, Cleaved Caspase-3/-8-/-9, and PARP expressions
P53↑,
JNK↑,
BAX↑,
cl‑Casp3↑,
cl‑Casp8↑,
cl‑Casp9↑,
cl‑PARP↑,
survivin↓, downregulating proteins involved in cell cycle progression, including Survivin, Cyclin D1, Cyclin B, and CDC2, and upregulating p21
cycD1/CCND1↓,
CycB/CCNB1↓,
CDC2↓,
P21↑,
angioG↓, suppress angiogenesis in cancer cells by inhibiting the expression of some angiogenic factors, such as MMP-2, AEG-1, VEGF, and VEGFR2
MMP2↓,
AEG1↓,
VEGF↓,
VEGFR2↓,
MMP9↓, inhibit metastasis by inhibiting several proteins that function in metastasis, such as MMP-2/-9, CXCR4, PI3K/Akt, ERK1/2
CXCR4↓,
PI3K↓,
Akt↓,
ERK↓,
TumAuto↑, can promote the conversion of LC3B I to LC3B II and upregulate Beclin1 expression, thereby causing autophagy
LC3B-II↑,
EMT↓, Luteolin was identified to suppress the epithelial to mesenchymal transition by upregulating E-cadherin and downregulating N-cadherin and Wnt3 expressions.
E-cadherin↑,
N-cadherin↓,
Wnt↓,
ROS↑, DNA damage that is induced by reactive oxygen species (ROS),
NICD↓, Luteolin can block the Notch intracellular domain (NICD) that is created by the activation of the Not
p‑GSK‐3β↓, Luteolin can inhibit the phosphorylation of the GSK3β induced by Wnt, resulting in the prevention of GSK3β inhibition
iNOS↓, Luteolin in colon cancer and the complications associated with it, particularly the decreasing effect on the expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2)
COX2↓,
NRF2↑, Luteolin has been identified to increase the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), which is a crucial transcription factor with anticarcinogenic properties related
Ca+2↑, caused loss of the mitochondrial membrane action potential, enhanced levels of mitochondrial calcium (Ca2+),
ChemoSen↑, Luteolin enhanced the effect of one of the most effective chemotherapy drugs, cisplatin, on CRC cells
ChemoSen↓, high dose of Luteolin application negatively affected the oxaliplatin-based chemotherapy in a p53-dependent manner [52]. They suggested that the flavonoids with Nrf2-activating ability might interfere with the chemotherapeutic efficacy of anticancer
IFN-γ↓, decreased the expression of interferon-gamma-(IFN-γ)
RadioS↑, suggested that Luteolin can act as a radiosensitizer, promoting apoptosis by inducing p38/ROS/caspase cascade
MDM2↓, Luteolin treatment was associated with increased p53 and p21 and decreased MDM4 expressions both in vitro and in vivo.
NOTCH1↓, Luteolin suppressed the growth of lung cancer cells, metastasis, and Notch-1 signaling pathway
AR↓, downregulating the androgen receptor (AR) expression
TIMP1↑, Luteolin inhibits the migration of U251MG and U87MG human glioblastoma cell lines by downregulating MMP-2 and MMP-9 and upregulating the tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2.
TIMP2↑,
ER Stress↑, Luteolin caused oxidative stress and ER stress in the Hep3B cells,
CDK2↓, Luteolin’s ability to decrease Akt, polo-like kinase 1 (PLK1), cyclin B1, cyclin A, CDC2, cyclin-dependent kinase 2 (CDK2) and Bcl-xL
Telomerase↓, Luteolin dose-dependently inhibited the telomerase levels and caused the phosphorylation of NF-κB and the target gene of NF-κB, c-Myc to suppress the human telomerase reverse transcriptase (hTERT)
p‑NF-kB↑,
p‑cMyc↑,
hTERT/TERT↓,
RAS↓, Luteolin was found to suppress the expressions of K-Ras, H-Ras, and N-Ras, which are the activators of PI3K
YAP/TEAD↓, Luteolin caused significant inhibition of yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ)
TAZ↓,
NF-kB↓, Luteolin was found to have a strong inhibitory effect on the NF-κB
NRF2↓, Luteolin-loaded nanoparticles resulted in a significant reduction in the Nrf2 levels compared to Luteolin alone.
HO-1↓, The expressions of the downstream genes of Nrf2, Ho1, and MDR1 were also reduced, where inhibition of Nrf2 expression significantly increased the cell death of breast cancer cells
MDR1↓,

2472-

RES,

Resveratrol Restores Sirtuin 1 (SIRT1) Activity and Pyruvate Dehydrogenase Kinase 1 (PDK1) Expression after Hemorrhagic Injury in a Rat Model

in-vivo,

Nor,

rat

*SIRT1↑, However, resveratrol treatment along with resuscitation fluid restored SIRT1 activity.
*PGC-1α↑, When resveratrol was administered 10 min after the start of resuscitation, the protein level of SIRT1, PGC-1α and c-Myc in the nuclear fraction was restored.
*cMyc↑,
*PDK1↓, The experiments demonstrated a significant increase in PDK1 after T-H, which was abolished by resveratrol treatment

4833-

Uro,

Unveiling the potential of Urolithin A in Cancer Therapy: Mechanistic Insights to Future Perspectives of Nanomedicine

Review,

Var,

392 to 566 µM across various breast cancer cell lines

Review,

AD,

Review,

IBD,

BioAv↝, Urolithin A (UA), a metabolite derived from ellagic acid through gut microbiota metabolism, has emerged as a compelling anticancer agent.
TumAuto↝, UA has multiple mechanisms of action, including the regulation of autophagy, enhancement of mitochondrial function, and inhibition of tumor progression and metastatic pathways.
TumCG↓,
TumMeta↓,
ChemoSen↑, Additionally, its chemo-, immuno-, and radio-sensitization properties further increase its therapeutic advantages
Imm↑,
RadioS↑,
BioAv↑, Nanotechnology-driven approaches, such as nanoparticle formulations, lipids, and powder formulations, have successfully increased the solubility, stability, bioavailability, precise targeted delivery to cancer tissues
other↝, While sparingly soluble in water, UA shows better solubility in organic solvents, such as ethanol and dimethyl sulfoxide.
eff↓, prone to degradation at extreme pH values or high temperatures.
*antiOx↓, UA has gained increasing attention for its pharmacological properties, including anti-oxidant, anti-inflammatory, and anti-cancer activities.
*Inflam↓,
AntiCan↓,
AntiAge↑, UA has potential as a key component in antiaging interventions.
chemoP↑, UA can counteract age-related muscle wasting and enhance physical performance, making it a valuable therapeutic for improving muscle health and combating sarcopenia
*neuroP↑, UA has neuroprotective properties because of its ability to reduce neuroinflammation, improve mitochondrial function, and mitigate oxidative stress,
*ROS↓,
*cognitive↑, suggesting its potential application in neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, and other age-related cognitive disorders)
*lipid-P↓, UA to reduce lipid peroxidation, combat oxidative stress, and improve endothelial function, promoting its role in cardiovascular health
*cardioP↑,
*TNF-α↓, exerts anti-inflammatory effects by suppressing the production of proinflammatory cytokines, such as TNF-α and IL-6, which can be employed for the management of chronic inflammatory conditions (such as rheumatoid arthritis and inflammatory bowel dise
*IL6↓,
GutMicro↑, Given that UA formation and bioactivity are influenced by the gut microbiota, its supplementation could promote a healthier gut microbiome, with potential therapeutic benefits for a wide range of conditions, including irritable bowel syndrome.
TumCCA↑, UA has potent anticancer effects through cell cycle arrest, apoptosis induction, and the modulation of oncogenic signaling pathways.
Apoptosis↑,
angioG↓, regulate the tumor microenvironment by inhibiting angiogenesis and inflammation
NF-kB↓, UA inhibited key signaling pathways, such as the NF-κB and PI3K/AKT pathways, which are critical for tumor progression
PI3K↓,
Akt↓,
Casp↑, UA also promoted apoptosis via the activation of caspases and the downregulation of survival proteins such as Survivin
survivin↓,
TumCP↓, inhibited MCF-7 cell proliferation in vitro and significantly reduced 27-HC-induced tumor growth in vivo.
cycD1/CCND1↓, UA induced cell cycle arrest by downregulating cyclin D1 and c-MYC and promoted apoptosis by increasing the expression of proapoptotic proteins such as Bax while reducing antiapoptotic BCL2 levels.
cMyc↑,
BAX↑,
Bcl-2↓,
COX2↓, UA, a metabolite of pomegranate mesocarp, synergistically reduced COX-2 expression by ~70% and increased cleaved caspase-3 levels
P53↑, UA induces the expression of tumor suppressor proteins such as p53 and p38-MAPK
p38↑,
*ROS↓, UA demonstrates significant antioxidant activity by reducing reactive oxygen species levels and enhancing the activities of key antioxidant enzymes, such as superoxide dismutase and glutathione peroxidase.
*SOD↑,
*GPx↑,
SIRT1↑, UA induced cell cycle arrest and apoptosis while enhancing the expression of key tumor suppressors, including Sirtuin 1 (Sirt1) and Forkhead box protein O1 (FOXO1)
FOXO1↑,
eff↑, UA preferentially accumulates in prostate and intestinal tissues, suggesting its targeted bioactivity.
ChemoSen↑, UA has emerged as a potent chemosensitizing agent that enhances the efficacy of conventional cancer therapies.

Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

AntiAge↑, 1, AntiCan↓, 1, chemoP↑, 1,
Total Targets: 125

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↓, 2, antiOx↑, 1, GPx↑, 1, GSH↑, 1, HO-1↑, 1, lipid-P↓, 1, NRF2↑, 1, ROS↓, 2, SOD↑, 1,

Metal & Cofactor Biology ⓘ

IronCh↑, 1,

Mitochondria & Bioenergetics ⓘ

PGC-1α↑, 1,

Core Metabolism/Glycolysis ⓘ

cMyc↑, 1, p‑cMyc↑, 1, PDK1↓, 1, SIRT1↑, 1,

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,

Immune & Inflammatory Signaling ⓘ

IL6↓, 1, Inflam↓, 2, TNF-α↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↑, 1,

Clinical Biomarkers ⓘ

IL6↓, 1,

Functional Outcomes ⓘ

cardioP↑, 1, cognitive↑, 1, neuroP↑, 1, toxicity↓, 1,
Total Targets: 26

Scientific Paper Hit Count for: cMyc, cellular-MYC oncogene

1 Silver-NanoParticles
1 Berbamine
1 Estrogen
1 Fisetin
1 Luteolin
1 Resveratrol
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#:35  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

cMyc Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

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 ⓘ

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 ⓘ

Metal & Cofactor Biology ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Proliferation, Differentiation & Cell State ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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