P450 Cancer Research Results

P450, cytochrome P450 (CYP) family: Click to Expand ⟱
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Type:
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⟱
2852- FIS,    A comprehensive view on the fisetin impact on colorectal cancer in animal models: Focusing on cellular and molecular mechanisms
- Review, CRC, NA
Risk↓, Flavonoids, including fisetin, have been linked to a reduced risk of colorectal cancer (CRC)
P53↑, increased levels of p53 and decreased levels of murine double minute 2, contributing to apoptosis induction
MDM2↓,
COX2↓, fisetin inhibits the cyclooxygenase-2 and wingless-related integration site (Wnt)/epidermal growth factor receptor/nuclear factor kappa B signaling pathways
Wnt↓,
NF-kB↓,
CDK2↓, regulating the activities of cyclin-dependent kinase 2 and cyclin-dependent kinase 4, reducing retinoblastoma protein phosphorylation, decreasing cyclin E levels, and increasing p21 levels
CDK4↓,
p‑RB1↓,
cycE/CCNE↓,
P21↑,
NRF2↓, Pandey and Trigun revealed that fisetin induces apoptosis in CRC cells by inhibiting autophagy and suppressing Nrf2
ROS↑, Furthermore, fisetin elevated ROS levels and downregulated Nrf2 expression, indicating Nrf2 suppression in fisetin-induced apoptosis in CRC cells.
Casp8↑, fisetin treatment resulted in the upregulation of various molecular pathways, including cleaved caspase-8, Fas ligand, TRAIL, and DR5 levels, in the cancer cells
Fas↑,
TRAIL↑,
DR5↑,
MMP↓, Fisetin also caused mitochondrial membrane depolarization, leading to the release of Smac/DIABLO and cytochrome c
Cyt‑c↑,
selectivity↑, enhanced cellular uptake, and induction of apoptosis in cancer cells
P450↝, Fisetin also affected the activities of cytochrome P450 (CYP450 3A4) and glutathione-S-transferase
GSTs↝,
RadioS↑, fisetin pretreatment heightened the radiosensitivity of p53-mutant HT29 human CRC cells
Inflam↓, Fisetin suppresses inflammation in the colon and CRC
β-catenin/ZEB1↓, fisetin in treating colon cancer, revealing its capability to effectively downregulate β-catenin and COX-2
EGFR↓, fisetin decreased EGFR and NF-κB activation in HT29 cells
TumCCA↑, It induces cell cycle arrest, disrupting the transition from the G1 to the S phase, as well as causing G2/M phase arrest
ChemoSen↑, intervention with fisetin and 5-FU appeared to extend the lifespan of the experimental animals


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:


Redox & Oxidative Stress ⓘ

GSTs↝, 1,   NRF2↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

Casp8↑, 1,   Cyt‑c↑, 1,   DR5↑, 1,   Fas↑, 1,   MDM2↓, 1,   TRAIL↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycE/CCNE↓, 1,   P21↑, 1,   p‑RB1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

Wnt↓, 1,  

Migration ⓘ

β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   P450↝, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

EGFR↓, 1,  

Functional Outcomes ⓘ

Risk↓, 1,  
Total Targets: 29

Pathway results for Effect on Normal Cells:


Total Targets: 0

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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