P450 Cancer Research Results

P450, cytochrome P450 (CYP) family: Click to Expand ⟱
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The cytochrome P450 (CYP) family includes many isoenzymes that play key roles in metabolizing endogenous substances (like hormones) and xenobiotics (including drugs and toxins). Changes in the expression of these enzymes in various cancers can affect carcinogen activation, drug metabolism, and overall tumor biology, influencing both cancer risk and prognosis.

CYP1B1
– Frequently overexpressed in several cancers including breast, ovarian, prostate, and colorectal cancers.
– Its expression is often low in normal tissues, making it a potential target for selective cancer therapies.

2. CYP3A4 and CYP3A5
These enzymes are highly expressed in the liver, but their expression is also observed in extrahepatic tissues.
– In cancer, CYP3A enzymes can be variably expressed; for instance, CYP3A4 may be upregulated in some liver cancers but downregulated in others.

3. CYP2E1
– CYP2E1 is expressed in the liver and extrahepatic tissues.
– Elevated CYP2E1 activity can lead to increased production of reactive oxygen species (ROS), contributing to DNA damage and cancer progression.

4. CYP19A1 (Aromatase)
– Aromatase converts androgens to estrogens and is expressed in adipose tissue as well as in certain tumors such as breast cancer.
– Its local expression in breast tumors can increase estrogen levels, promoting hormone-dependent tumor growth.

5. CYP2C Family (e.g., CYP2C8, CYP2C9, CYP2C19)
– These enzymes are involved in metabolizing various drugs and are expressed in the liver and intestines.
– Their expression levels can be altered in different tumor types, potentially affecting drug metabolism.

CYP450 enzymes are a large family with diverse roles in cancer biology.
• Their expression in cancers (e.g., CYP1B1, CYP3A4/5, CYP2E1, CYP19A1) has been linked to both the development and progression of tumors, as well as influencing responses to therapy.
Scientific Papers found: Click to Expand⟱
3268- Lyco,    Lycopene as a Natural Antioxidant Used to Prevent Human Health Disorders
- Review, AD, NA
*BioAv↓, Lycopene bioavailability can be decreased by ageing, and some of the pathological states, such as cardiovascular diseases (CVDs)
*AntiCan↑, For instance, it has been shown that a higher dietary intake and circulating concentration of lycopene have protective effects against prostate cancer (PCa), in a dose-dependent way
*ROCK1↓, It remarkably lessened the expression of ROCK1, Ki-67, ICAM-1 and ROCK2,
*Ki-67↓,
*ICAM-1↓,
*cardioP↑, Lycopene is a cardioprotective nutraceutical.
*antiOx↑, Lycopene is a well-known antioxidant.
*NQO1↑, Furthermore, lycopene supplementation improves mRNA expressions of the NQO-1 and HO-1 as antioxidant enzymes.
*HO-1↑,
*TNF-α↓, downregulate inflammatory cytokines (i.e., TNF-α, and IL-1β) in the hippocampus of the mice.
*IL22↓,
*NRF2↑, Lycopene decreased neuronal oxidative damage by activating Nrf2, as well as by inactivating NF-κB translocation in H2O2-related SH-SY5Y cell model
*NF-kB↓,
*MDA↓, significantly reduced the malondialdehyde (MDA)
*Catalase↑, Furthermore, it improved the catalase (CAT), superoxide dismutase (SOD), and GSH levels, and antioxidant capacity [109].
*SOD↑,
*GSH↑,
*cognitive↑, Lycopene administration considerably improved cognitive defects, noticeably reduced MDA levels and elevated GSH-Px activity, and remarkably reduced tau
*tau↓,
*hepatoP↑, Lycopene was also found to be effective against hepatotoxicity by acting as an antioxidant, regulating total glutathione (tGSH) and CAT concentrations
*MMP2↑, It also elevated MMP-2 down-regulation
*AST↓, lowering the liver enzymes levels, like aspartate transaminase (AST), alanine transaminase (ALT), LDL, free fatty acid, and MDA.
*ALAT↓,
*P450↑, Moreover, tomato powder has been shown to have a protective agent against alcohol-induced hepatic injury by inducing cytochrome p450 2E1
*DNAdam↓, lycopene decreased DNA damage
*ROS↓, It has been revealed that they inhibited ROS production, protected antioxidant enzymes, and reversed hepatotoxicity in rats’ liver
*neuroP↑, lycopene consumption relieved cognitive defects, age-related memory loss, neuronal damage, and synaptic dysfunction of the brain.
*memory↑,
*Ca+2↓, Lycopene suppressed the 4-AP-invoked release of glutamate and elevated intra-synaptosomal Ca2+ level.
*Dose↝, an in vivo study revealed that lycopene (6.5 mg/day) was effective against cancer in men [147]. However, lycopene dose should be increased up to 10 mg/day, in the case of advanced PCa.
*Dose↑, lycopene supplementation (15 mg/day, for 12 weeks) in an old aged population improved immune function through increasing natural killer cell activity by 28%
*Dose↝, Finally, according to different epidemiological studies, daily lycopene intake can be suggested to be 2 to 20 mg per day
*toxicity∅, A toxicological study on rats showed the no-observed-adverse-effect level at the highest examined dose (i.e., 1.0% in the diet)
PGE2↓, Lycopene doses of 0, 10, 20, and 30 µM were used to treat human colorectal cancer cell. Prostaglandin E2 (PGE2), and NO levels declined after lycopene administration,
CDK2↓, Treatment with lycopene reduced cell hyperproliferation induced by UVB and ultimately promoted apoptosis and reduced CDK2 and CDK4 complex in SKH-1 hairless mice
CDK4↓,
STAT3↓, lycopene reduced the STAT3 expression in ovarian tissues
NOX↓, (SK-Hep-1) cells and indicated a substantial reduction in NOX activity. Moreover, it inhibits the protein expression of NOX4, NOX4 mRNA and ROS intracellular amounts
NOX4↓,
ROS↓,
*SREBP1↓, Lycopene decreases the fatty acid synthase (FAS), sterol regulatory element-binding protein 1c (SREBP-1c), and Acetyl-CoA carboxylase (ACC1) expression in HFD mice.
*FASN↓,
*ACC↓,

3001- RosA,    Therapeutic Potential of Rosmarinic Acid: A Comprehensive Review
- Review, Var, NA
TumCP↓, including in tumor cell proliferation, apoptosis, metastasis, and inflammation
Apoptosis↑,
TumMeta↓,
Inflam↓,
*antiOx↑, RA is therefore considered to be the strongest antioxidant of all hydroxycinnamic acid derivatives
*AntiAge↑, , it also exerts powerful antimicrobial, anti-inflammatory, antioxidant and even antidepressant, anti-aging effects
*ROS↓, RA and its metabolites can directly neutralize reactive oxygen species (ROS) [10] and thereby reduce the formation of oxidative damage products.
BioAv↑, RA is water-soluble, and according to literature data, the efficacy of secretion of this compound in infusions is about 90%
Dose↝, Accordingly, it is possible to consume approximately 110 mg RA daily, i.e., approximately 1.6 mg/kg for adult men weighing 70 kg.
NRF2↑, liver cancer cell line, HepG2, transfected with plasmid containing ARE-luciferin gene, RA predominantly enhances ARE-luciferin activity and promotes nuclear factor E2-related factor-2 (Nrf2) translocation from cytoplasm to the nucleus
P-gp↑, and also increases MRP2 and P-gp efflux activity along with intercellular ATP level
ATP↑,
MMPs↓, RA concurrently induced necrosis and apoptosis and stimulated MMP dysfunction activated PARP-cleavage and caspase-independent apoptosis.
cl‑PARP↓,
Hif1a↓, inhibits transcription factor hypoxia-inducible factor-1α (HIF-1α) expression
GlucoseCon↓, it also suppressed glucose consumption and lactate production in colorectal cells
lactateProd↓,
Warburg↓, may suppress the Warburg effects through an inflammatory pathway involving activator of transcription-3 (STAT3) and signal transducer of interleukin (IL)-6
TNF-α↓, RA supplementation also reduced tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2) and IL-6 levels, and modulated p65 expression [
COX2↓,
IL6↓,
HDAC2↓, RA induced the cell cycle arrest and apoptosis in prostate cancer cell lines (PCa, PC-3, and DU145) [31]. These effects were mediated through modulation of histone deacetylases expression (HDACs), specifically HDAC2;
GSH↑, RA can also inhibit adhesion, invasion, and migration of Ls 174-T human colon carcinoma cells through enhancing GSH levels and decreasing ROS levels
ROS↓,
ChemoSen↑, RA also enhances chemosensitivity of human resistant gastric carcinoma SGC7901 cells
*BG↓, RA significantly increased insulin index sensitivity and reduced blood glucose, advanced glycation end-products, HbA1c, IL-1β, TNFα, IL-6, p-JNK, P38 mitogen-activated protein kinase (MAPK), and NF-κB levels
*IL1β↓,
*TNF-α↓,
*IL6↓,
*p‑JNK↓,
*p38↓,
*Catalase↑, The reduced activities of CAT, SOD, glutathione S-transferases (GST), and glutathione peroxidase (GPx) and the reduced levels of vitamins C and E, ceruloplasmin, and GSH in plasma of diabetic rats were also significantly recovered by RA application
*SOD↑,
*GSTs↑,
*VitC↑,
*VitE↑,
*GSH↑,
*GutMicro↑, protective effects of RA (30 mg/kg) against hypoglycemia, hyperlipidemia, oxidative stress, and an imbalanced gut microbiota architecture was studied in diabetic rats.
*cardioP↑, Cardioprotective Activity: RA also reduced fasting serum levels of vascular cell adhesion molecule 1 (VCAM-1), inter-cellular adhesion molecule 1 (ICAM-1), plasminogen-activator-inhibitor-1 (PAI-1), and increased GPX and SOD levels
*ROS↓, Finally, in H9c2 cardiac muscle cells, RA inhibited apoptosis by decreasing intracellular ROS generation and recovering mitochondria membrane potential
*MMP↓,
*lipid-P↓, At once, RA suppresses lipid peroxidation (LPO) and ROS generation, whereas in HSC-T6 cells it increases cellular GSH.
*NRF2↑, Additionally, it significantly increases Nrf2 translocation
*hepatoP↑, Hepatoprotective Activity
*neuroP↑, Nephroprotective Activity
*P450↑, RA also reduced CP-produced oxidative stress and amplified cytochrome P450 2E1 (CYP2E1), HO-1, and renal-4-hydroxynonenal expression.
*HO-1↑,
*AntiAge↑, Anti-Aging Activity
*motorD↓, A significantly delays motor neuron dysfunction in paw grip endurance tests,


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↑, 1,   NOX4↓, 1,   NRF2↑, 1,   ROS↓, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,  

Core Metabolism/Glycolysis ⓘ

GlucoseCon↓, 1,   lactateProd↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC2↓, 1,   STAT3↓, 1,  

Migration ⓘ

MMPs↓, 1,   TumCP↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,  

Barriers & Transport ⓘ

P-gp↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IL6↓, 1,   Inflam↓, 1,   PGE2↓, 1,   TNF-α↓, 1,  

Cellular Microenvironment ⓘ

NOX↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↑, 1,   Dose↝, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  
Total Targets: 29

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   Catalase↑, 2,   GSH↑, 2,   GSTs↑, 1,   HO-1↑, 2,   lipid-P↓, 1,   MDA↓, 1,   NQO1↑, 1,   NRF2↑, 2,   ROS↓, 3,   SOD↑, 2,   VitC↑, 1,   VitE↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACC↓, 1,   ALAT↓, 1,   FASN↓, 1,   SREBP1↓, 1,  

Cell Death ⓘ

p‑JNK↓, 1,   p38↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,  

Migration ⓘ

Ca+2↓, 1,   Ki-67↓, 1,   MMP2↑, 1,   ROCK1↓, 1,  

Immune & Inflammatory Signaling ⓘ

ICAM-1↓, 1,   IL1β↓, 1,   IL22↓, 1,   IL6↓, 1,   NF-kB↓, 1,   TNF-α↓, 2,  

Synaptic & Neurotransmission ⓘ

tau↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   Dose↑, 1,   Dose↝, 2,   P450↑, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   BG↓, 1,   GutMicro↑, 1,   IL6↓, 1,   Ki-67↓, 1,  

Functional Outcomes ⓘ

AntiAge↑, 2,   AntiCan↑, 1,   cardioP↑, 2,   cognitive↑, 1,   hepatoP↑, 2,   memory↑, 1,   motorD↓, 1,   neuroP↑, 2,   toxicity∅, 1,  
Total Targets: 51

Scientific Paper Hit Count for: P450, cytochrome P450 (CYP) family
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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