MYCN Cancer Research Results

MYCN, MYCN proto-oncogene: Click to Expand ⟱
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MYCN (MYCN proto-oncogene; N-Myc) is a member of the MYC family of basic helix-loop-helix transcription factors that regulates genes involved in cell growth, proliferation, metabolism, ribosome biogenesis, differentiation and apoptosis. MYCN amplification or overexpression is strongly oncogenic and is particularly important in neuroblastoma, where amplification is associated with aggressive disease, increased tumour progression and poor prognosis. Increased MYCN activity promotes proliferative and metabolic programs, inhibits neuronal differentiation and can enhance glycolysis, angiogenesis, stemness and metastatic behaviour. Experimental MYCN suppression can reduce proliferation, promote differentiation and inhibit tumour growth. The typical cancer-associated direction is therefore up, while the desired anticancer modulation is down, transcriptional suppression or destabilization of the MYCN protein. MYCN is separate from MYC (c-Myc) and MYCL, which are related but distinct MYC-family oncogenes.



Scientific Papers found: Click to Expand⟱
7951- RT,  BuckWS,    The anticancer potential of the dietary polyphenol rutin: Current status, challenges, and perspectives
- Review, Nor, NA
*Dose↝, Though rutin is widely distributed in plants, buckwheat is considered as its major source
*BioAv↓, Rutin is not easily absorbed into the blood, since its sugar moiety blocks its passage through the intestinal epithelial layers, indicating its poor bioavailability compared to other flavonoid glycosides
*BioAv↓, several in vitro studies have reported the biodegradation of rutin by both intestinal and non-intestinal microorganisms including Pediococcus Q-05 (Kim et al. 1998), Cunninghamella echinulata ATCC 9244 (Araujo et al. 2013),
*BioAv↓, P-glycoprotein (P-gp) and multidrug resistance protein 1 (MRP1) located in the intestine expelled rutin out of the cell thereby negatively affect its absorption and decrease its bioavailability (Zhang et al. 2013). This explains the significant role
*BioAv↓, The results showed that rutin was recovered as glucuronides and/or sulfates of quercetin and as unconjugated quercetin aglycone, but no free rutin was found in plasma, corroborating the pharmacokinetic studies of rutin in rats
*BioAv↝, All these studies strongly suggest that quercetin glucuronide is the major metabolite formed and circulated in blood after the intake of rutin.
TumCP↓, Rutin has been shown to hinder the proliferation of diverse cancer cell types in vitro, including breast, glioma, pancreas, colon, liver, lung, skin, prostate, cervical, and ovarian cancer cells
Risk↓, Rutin has been reported to prevent different types of cancers in vivo, such as breast, colon, melanoma, prostate, lymphoma, and leukemia.
*radioP↑, Recent reports showed that rutin has protective effects against radiation-induced inflammation and prevents radiation-induced skin carcinogenesis.
chemoPv↑, Overall, rutin exhibits outstanding chemopreventive and radioprotective effects both in vitro and in vivo,
TumCCA↑, Rutin has been reported to arrest cell cycle progression in cancer cells. Rutin can inhibit cell cycle at different checkpoints, such as G1, G2/M, and S phases.
GSK‐3β↑, Rutin can induce apoptosis in A549 lung cancer cells by upregulating the expression of GSK 3b, a downstream regulator of Wnt/b-catenin signaling
Wnt↓,
β-catenin/ZEB1↓,
ROS↑, Figure 3
BAX↑,
Casp3↑,
Casp8↑,
Casp9↑,
PARP↑,
Beclin-1/ATG6↑,
ATG5↑,
LC3II↑,
DNMT1↓,
P21↑,
CDK1↑,
CycB/CCNB1↓,
TNF-α↑,
VEGF↓,
IL1β↓,
NF-kB↓,
AP-1↓,
MYCN↓,
AMPK↑,
MAPK↓,
PI3K↓,
Akt↓,
cMET↓,
P-gp/ABCB1↓,
MRP1/ABCC1↓,
ABCG2↓,
MMPs↓,
TNF-α↓,
iNOS↓,
COX2/PTGS2↓,
angioG↓, Moreover, administration of 200 mM/kg rutin can inhibit angiogenesis in B16F-10 melanoma bearing C57BL/6 mice through the prevention of capillary formation
STAT3↓, rutin’s ability to prevent STAT3 activation mediated cancer development.
*chemoP↑, Several studies have reported that rutin can alleviate the toxicities induced by cisplatin, a platinum-based anticancer drug in experimental animal models
*ROS↓, The possible mechanisms by which rutin might exert its protective effects are ROS inhibition, suppression of MDA levels, and downregulation of p53, caspase-3, caspase-9, and JNK/TNF/p38 MAPK pathways
*MDA↓,
*P53↓,
*Casp3↓,
*Casp9↓,
*JNK↓,
*TNF-α↓,
*p38↓,
*MAPK↓,
GSH↓, GSH level in tumor cells was decreased after combined treatment with rutin, indicating that rutin sensitized cancer cells to cisplatin.
ChemoSen↑,
*hepatoP↑, rutin could inhibit cyclophosphamide-induced hepatocytotoxicity, probably through the upregulation of antioxidant enzyme activities and downregulation of serum toxicity markers.
*COX1↓, Rutin protected intestine from methotrexate, an antimetabolite used in cancer therapy, and induced lesions by inhibiting the expression of COX-1, COX-2, and 15-lipoxygenase
*COX2/PTGS2↓,
*15-LOX/ALOX15↓,
RenoP↑, rutin might protect the kidney from doxorubicin-induced nephrotoxicity, probably by up-regulation of the activity of antioxidant enzymes.
*toxicity↓, According to clinical trials, the safe dosage of rutin is 500 mg/day (Sharma et al. 2013). Rutin is nontoxic both acutely and chronically and no evidence of injury has been found due to rutin administration


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

MYCN↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

GSH↓, 1,   ROS↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   BAX↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   iNOS↓, 1,   MAPK↓, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1/ATG6↑, 1,   LC3II↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNMT1↓, 1,   PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↑, 1,   CycB/CCNB1↓, 1,   P21↑, 1,   TumCCA↑, 1,  

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

cMET↓, 1,   GSK‐3β↑, 1,   PI3K↓, 1,   STAT3↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   MMPs↓, 1,   TumCP↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL1β↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ABCG2↓, 1,   ChemoSen↑, 1,   MRP1/ABCC1↓, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoPv↑, 1,   RenoP↑, 1,   Risk↓, 1,  
Total Targets: 43

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

15-LOX/ALOX15↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

MDA↓, 1,   ROS↓, 1,  

Cell Death(tgid=5) ⓘ

Casp3↓, 1,   Casp9↓, 1,   JNK↓, 1,   MAPK↓, 1,   p38↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   COX2/PTGS2↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 4,   BioAv↝, 1,   Dose↝, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoP↑, 1,   hepatoP↑, 1,   radioP↑, 1,   toxicity↓, 1,  
Total Targets: 19

Scientific Paper Hit Count for: MYCN, MYCN proto-oncogene
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#:1602  State#:%  Dir#:1
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