CBR1 Cancer Research Results

CBR1, carbonyl reductase 1: Click to Expand ⟱
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CBR1 (carbonyl reductase 1) is an NADPH-dependent enzyme involved in carbonyl compound metabolism, oxidative-stress regulation, and the reduction of several anticancer drugs. In the chemotherapy context, CBR1 can convert anthracyclines such as doxorubicin and daunorubicin into less active alcohol metabolites, including doxorubicinol and daunorubicinol, which may contribute to reduced anticancer potency and increased cardiotoxicity. Therefore, CBR1 inhibition or downregulation may act as a chemosensitizing strategy for anthracycline-treated cancers. However, CBR1 is also reported to suppress invasion and metastasis in some cancers, including gynecologic cancer models, where low CBR1 expression has been associated with poorer prognosis. For database interpretation, CBR1 should be treated as a context-dependent target: downregulation may be beneficial for anthracycline chemosensitization, while loss of CBR1 may be unfavorable in tumors where CBR1 restrains EMT, invasion, or metastasis.



Scientific Papers found: Click to Expand⟱
6135- CHr,    Chrysin as a Multifunctional Therapeutic Flavonoid: Emerging Insights in Pathogenesis Management: A Narrative Review
- Review, Var, NA - Review, AD, NA
Inflam↓, various cancers has been demonstrated and it modulates cell signaling pathways, including inflammation, angiogenesis, apoptosis, autophagy, and the cell cycle.
angioG↓,
Apoptosis↑,
TumAuto↑,
TumCCA↑,
BioAv↓, Despite its promising pharmacological activities, the clinical utility of chrysin remains limited due to its poor bioavailability, low solubility, limited permeability, and rapid metabolism.
Half-Life↓,
BioAv↓, The oral bioavailability of chrysin has been reported to range from 0.003% to 0.02%, with a maximum plasma concentration between 12 and 64 nM
*ROS↓, The study reported that chrysin administration protected the kidneys and liver of rats from oxidative damage induced by chronic ethanol consumption
*hepatoP↑, Hepatoprotective Potential
*RenoP↑, The renal protective effect of chrysin was related to increasing the antioxidant enzyme activities and decreasing the regulation of serum renal toxicity markers.
TET1↑, chrysin meaningfully induced the expression of TET1 in GC cells.
MMP9↓, hrysin might contribute to its anticancer effects by regulating MMP-9 expression.
cMyc↓, Both c-Myc and Ki-67 expressions were found to be suppressed in the tumor tissues treated with chrysin and G1-treated tumor tissues
Ki-67↓,
CBR1↓, chrysin directly interacts with CBR1, inhibiting its enzymatic activity at both the molecular and cellular levels.
ROS↑, This inhibition led to elevated intracellular ROS levels, triggering ROS-dependent autophagy
ChemoSen↑, chrysin enhances pancreatic cancer cell sensitivity to gemcitabine by inducing ferroptosis death, both in vitro and in vivo
Bax:Bcl2↑, chrysin increased the Bax/Bcl-2 expression ratio in ATC cells following treatment
PUMA↑, PUMA and Notch-1 were activated, and Slug was inactivated by chrysin treatment
NOTCH1↑,
*AntiDiabetic↑, Anti-Diabetic Potential
*neuroP↑, Neuroprotective Effects
*GABA↑, treatment of chrysin improves levels of GABA, monoamines, glutamic acid, and their metabolites in three brain regions, while also inhibiting DNA fragmentation markers like 8-HdG as well as BDNF.
*DNAdam↓,
*BDNF↑,
*memory↑, protective effects of chrysin against memory impairments associated with hippocampal neurogenesis
*AGEs↓, figure 6
*Aβ↓,
*cardioP↑, Cardioprotective Effects
*AntiArt↑, Anti-Arthritis Potential
eff↑, combination potential was higher than apigenin or chrysin alone.
eff↑, combination of quercetin enhanced the toxic effects of chrysin on the cell lines
*eff↑, neuroprotective synergistic effects of chrysin and kaempferol revealed therapeutic potential in mitigating cerebral ischemi
RadioS↑, study reported that treatment of MDA-MB-231 cells with chrysin in combination with radiation therapy (RT) caused synergistic antitumor properties.
eff↑, the combination of metformin and chrysin demonstrated pronounced synergistic cytotoxic effects on cancer cells
ChemoSen↑, chrysin was combined with a low dose of cisplatin, the resulting growth inhibition was significantly enhanced.
eff↑, demonstrating greater potency than chrysin or silver nanoparticles alone [198].


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 ⓘ

CBR1↓, 1,  

Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   Bax:Bcl2↑, 1,   PUMA↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

NOTCH1↑, 1,  

Migration ⓘ

Ki-67↓, 1,   MMP9↓, 1,   TET1↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   ChemoSen↑, 2,   eff↑, 4,   Half-Life↓, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

Ki-67↓, 1,  
Total Targets: 20

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

AntiArt↑, 1,  

Redox & Oxidative Stress ⓘ

ROS↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,   GABA↑, 1,  

Protein Aggregation ⓘ

AGEs↓, 1,   Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   cardioP↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 1,   RenoP↑, 1,  
Total Targets: 14

Scientific Paper Hit Count for: CBR1, carbonyl reductase 1
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#:1470  State#:%  Dir#:1
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