CYP1A1 Cancer Research Results

CYP1A1, Cytochrome P450 1A1: Click to Expand ⟱
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CYP1A1 (Cytochrome P450 1A1) is an enzyme that plays a significant role in the metabolism of various substances, including drugs, environmental pollutants, and procarcinogens. It is part of the cytochrome P450 family of enzymes, which are involved in the oxidative metabolism of a wide range of compounds.

Role in Cancer
Activation of Procarcinogens: CYP1A1 is known to convert certain procarcinogenic compounds, such as polycyclic aromatic hydrocarbons (PAHs) found in tobacco smoke and grilled meats, into their active forms. These metabolites can bind to DNA and form adducts, leading CYP1A1 expression is a significant factor in the context of various cancers, particularly those associated with environmental and lifestyle factors. to mutations and potentially initiating cancer.
Scientific Papers found: Click to Expand⟱
6082- CHOC,    Potential for preventive effects of cocoa and cocoa polyphenols in cancer
- Review, Var, NA
*ROS↓, Cocoa flavonoids have been demonstrated to influence several important biological functions in vitro and in vivo by their free radical scavenging ability
Apoptosis↑, or through the regulation of signal transduction pathways to stimulate apoptosis and to inhibit inflammation, cellular proliferation, apoptosis, angiogenesis and metastasis.
Inflam↓,
TumCP↓,
angioG↓,
TumMeta↓,
*Ca+2↓, oxidative stress in lead-exposed cells through the downregulation of ROS generation, decrease of intracellular calcium and prevented the alteration of the mitochondrial membrane potential
*MMP∅,
CYP1A1↑, A polyphenolic cocoa extract increased CYP1A1 mRNA and protein levels and enzymatic activity in MCF-7 and SKBR3 breast cancer cells
PGE2↓, Cocoa phenolic extract inhibited the inflammatory mediator prostaglandin E2 in human intestinal Caco-2 cells
TumCCA↑, Cocoa-derived pentameric procyanidin (pentamer) caused G0/G1 cell cycle arrest in human breast cancer MDA MB-231,
chemoPv↑, This study demonstrated that a co- coa-rich diet could prevent the early stage of chemically induced colorectal cancer in rats

1322- EMD,    The versatile emodin: A natural easily acquired anthraquinone possesses promising anticancer properties against a variety of cancers
- Review, Var, NA
Apoptosis↑,
TumCP↓,
ROS↑,
TumAuto↑,
EMT↓,
TGF-β↓,
DNAdam↑,
ER Stress↑,
TumCCA↑,
ATP↓,
NF-kB↓,
CYP1A1↑,
STAC2↓,
JAK↓,
PI3K↓,
Akt↓,
MAPK↓,
FASN↓,
HER2/EBBR2↓,
ChemoSen↑, DOX combined with emodin can improve the sensitivity of MDA-MB-231 and MCF-7 cells to chemotherapy
eff↑, emodin was reported to increase the anti-proliferative effect of an EGFR inhibitor (afatinib) against PC through downregulation of EGFR by promoting STAT3
ChemoSen↑, gemcitabine combined with emodin increased cell death
angioG↓,
VEGF↓,
MMP2↓,
eNOS↓,
FOXD3↑,
MMP9↓,
TIMP1↑,

1807- NarG,    A Systematic Review of the Preventive and Therapeutic Effects of Naringin Against Human Malignancies
- Review, NA, NA
AntiTum↑, antitumor ability of naringin
TumCP↓,
tumCV↓,
TumCCA↑,
Mcl-1↓,
RAS↓,
e-Raf↓, suppressing the Ras/Raf/extracellular
VEGF↓,
AntiAg↑,
MMP2↓,
MMP9↓,
TIMP2↑,
TIMP1↑,
p38↓,
Wnt↓,
β-catenin/ZEB1↑,
Casp↑,
P53↑,
BAX↑,
COX2↓,
GLO-I↓,
CYP1A1↑,
lipid-P↓,
p‑Akt↓,
p‑mTOR↓,
VCAM-1↓,
P-gp↓,
survivin↓,
Bcl-2↓,
ROS↑, ↑oxidative stress, Prostate DU145 cell line 50–250 μM
ROS↑, ↑ROS, Stomach (Gastric) AGS cell line, 1–3 mM
MAPK↑,
STAT3↓,
chemoP↑, flavonoids have excellent radical scavenging and iron-chelating properties (Kaiserová et al., 2007), and they can act as an effective modulator for DOX-induced toxicity

4922- PEITC,    Phenethyl Isothiocyanate: A comprehensive review of anti-cancer mechanisms
- Review, Var, NA
Risk↓, strong inverse relationship between dietary intake of cruciferous vegetables and the incidence of cancer.
AntiCan↑, Phenethyl isothiocyanate (PEITC) is present as gluconasturtiin in many cruciferous vegetables with remarkable anti-cancer effects.
TumCP↓, PEITC targets multiple proteins to suppress various cancer-promoting mechanisms such as cell proliferation, progression and metastasis
TumMeta↓,
ChemoSen↑, combination of PEITC with conventional anti-cancer agents is also highly effective in improving overall efficacy
*BioAv↑, ITCs are released from glucosinolates by the action of the enzyme myrosinase. The enzyme myrosinase can be activated by cutting or chewing the vegetables, but heating can destroy its activity
*other↝, Although water cress and broccoli are known to be the richest source, PEITC can also be obtained from turnips and radish
*Dose↝, In a study conducted with human volunteers, approximately 2 to 6 mg of PEITC was found to be released by the consumption of one ounce of watercress
Dose↓, significant anti-cancer effects can be achieved at micromolar concentrations of PEITC.
*BioAv↑, PEITC is highly bioavailable after oral administration. A single dose of 10–100 μmol/kg PEITC in rats resulted in bioavailability ranging between 90–114%
*Dose↝, Furthermore, about 928.5±250nM peak plasma concentration of PEITC was achieved in human subjects, after the consumption of 100g watercress.
*Half-Life↝, time to reach peak plasma concentration was observed to be 2.6h±1.1h with a t1/2 4.9±1.1h
*toxicity↝, long term studies are required to establish the safety profile of PEITC, since regular intake of PEITC can cause its accumulation resulting in cumulative effects, which could be toxic.
GSH↓, The conjugation of PEITC with intracellular glutathione and the subsequent removal of the conjugate result in depletion of glutathione and alteration in redox homeostasis leading to oxidative stress
ROS↑, PEITC-mediated generation of reactive oxygen species (ROS) is known to be a general mechanism of action leading to cytotoxic effects, especially specific to cancer cells
CYP1A1↑, PEITC on one hand causes induction of CYP1A1 and CYP1A2; however, it inhibits activity of certain CytP450 enzymes, such as CYP2E1, CYP3A4 and CYP2A3
CYP1A2↑,
P450↓,
CYP2E1↑,
CYP3A4↓,
CYP2A3/CYP2A6↓,
*ROS↓, PEITC treatment caused a significant increase in the activities of ROS detoxifying enzymes such as glutathione peroxidase1, superoxide dismutase 1 and 2. This was also confirmed in human study where subjects were administered watercress, a major sour
*GPx1↑,
*SOD1↑,
*SOD2↑,
Akt↓, PEITC inhibits Akt, a component of Ras signaling to inhibit tumor growth in several cancer types
EGFR↓, PEITC is also known to inhibit EGFR and HER2, which are important growth factors and regulators of Akt in different cancer models
HER2/EBBR2↓,
P53↑, PEITC-mediated activation of another tumor suppressor, p53 was observed in oral squamous cell carcinoma, causing G0/G1 phase arrest in multiple myeloma,
Telomerase↓, PEITC has been shown to inhibit telomerase activity in prostate and cervical cancer cells
selectivity↑, generation of reactive oxygen species (ROS), which also has been shown to be the basis of selectivity of PEITC toward cancer cells leaving normal cells undamaged [
MMP↓, ROS generation by PEITC leads to mitochondrial deregulation and modulation of proteins like Bcl2, BID, BIM and BAX, causing the release of cytochrome c into cytosol leading to apoptosis
Cyt‑c↑,
Apoptosis↑,
DR4↑, induction of death receptors and Fas-mediated apoptosis
Fas↑,
XIAP↓, PEITC-mediated suppression of anti-apoptotic proteins like XIAP and survivin, which are up-regulated in cancer cells
survivin↓,
TumAuto↑, PEITC induces autophagic cell death in cancer cells
Hif1a↓, PEITC directly or indirectly suppresses HIF1α
angioG↓, is possible that PEITC can block angiogenesis by non-hypoxic mechanisms also.
MMPs↓, Various studies with PEITC have shown suppression of invasion through inhibition of matrix metalloproteinases along with anti-metastatic effects caused by suppression of ERK kinase activity and transcriptional activity of NFkB
ERK↓,
NF-kB↓,
EMT↓, PEITC was also known to inhibit processes, such as epithelial to mesenchymal transition (EMT), cell invasion and migration, which are essential pre-requisites for metastasis
TumCI↓,
TumCMig↓,
Glycolysis↓, reduced rates of glycolysis in PEITC-treated cells and depletion of ATP lead to death in prostate cancer cells
ATP↓,
selectivity↑, PEITC (5μM) treatment suppressed glycolysis in the cancer cells, but no changes were observed in normal cells.
*antiOx↑, the antioxidant effect is achieved at very low ITC levels in normal cells as shown in various animal models
Dose↝, At higher concentrations, ITCs may generate ROS by depleting antioxidant levels. PEITC is known to cause ROS generation, which is the major mechanism of toxicity in cancer cells
other↝, There is a continuous leakage of electrons from the electron transport chain (ETC), which is major source of ROS production. PEITC causes generation of endogenous ROS by disrupting mitochondrial respiratory chain
OCR↓, PEITC also inhibits mitochondrial complex III activity and reduces the oxygen consumption rate in prostate cancer cells
GSH↓, PEITC binds to GSH and causes its depletion in cancer cells leading to ROS-induced cell damage
ITGB1↓, PEITC was found to inhibit major integrins, such as ITGB1, ITGA2 and ITGA6 in prostate cancer cells
ITGB6↓,
ChemoSen↑, Using pre-clinical studies, improved outcomes were observed when the conventional agents, such as docetaxel, metformin, vinblastine, doxorubicin and HDAC inhibitors were combined with PEITC

2216- SK,    Shikonin upregulates the expression of drug-metabolizing enzymes and drug transporters in primary rat hepatocytes
- in-vivo, Nor, NA
*NRF2↑, Shikonin effectively upregulates the transcription of CYP isozymes, phase II detoxification enzymes, and phase III membrane transporters and this function is at least partially through activation of AhR and Nrf2
*AhR↑,
*CYP1A1↑, shikonin dose-dependently increased the protein expression of CYP1A1, CYP1A2, CYP2C6, CYP2D1, and CYP3A2.
*CYP1A2↑,
*CYP2C6↑,
*CYP2D1↑,
*CYP3A2↑,
*NQO1↑, Compared with the controls, cells treated with 2 uM shikonin had 5.5-, 3.0-, and 2.0-fold higher UGT1A1, NQO1, and PGST protein levels


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

CYP1A1↑, 4,   CYP2E1↑, 1,   GSH↓, 2,   lipid-P↓, 1,   ROS↑, 4,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 2,   MMP↓, 1,   OCR↓, 1,   e-Raf↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

CYP3A4↓, 1,   FASN↓, 1,   GLO-I↓, 1,   Glycolysis↓, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 1,   Apoptosis↑, 3,   BAX↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   Cyt‑c↑, 1,   DR4↑, 1,   Fas↑, 1,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↓, 1,   p38↓, 1,   survivin↓, 2,   Telomerase↓, 1,  

Kinase & Signal Transduction ⓘ

FOXD3↑, 1,   HER2/EBBR2↓, 2,  

Transcription & Epigenetics ⓘ

other↝, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 2,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 2,   ERK↓, 1,   p‑mTOR↓, 1,   PI3K↓, 1,   RAS↓, 1,   STAT3↓, 1,   Wnt↓, 1,  

Migration ⓘ

AntiAg↑, 1,   ITGB1↓, 1,   ITGB6↓, 1,   MMP2↓, 2,   MMP9↓, 2,   MMPs↓, 1,   STAC2↓, 1,   TGF-β↓, 1,   TIMP1↑, 2,   TIMP2↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 4,   TumMeta↓, 2,   VCAM-1↓, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   EGFR↓, 1,   eNOS↓, 1,   Hif1a↓, 1,   VEGF↓, 2,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 1,   JAK↓, 1,   NF-kB↓, 2,   PGE2↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 4,   CYP1A2↑, 1,   CYP2A3/CYP2A6↓, 1,   Dose↓, 1,   Dose↝, 1,   eff↑, 1,   P450↓, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   HER2/EBBR2↓, 2,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   chemoP↑, 1,   chemoPv↑, 1,   Risk↓, 1,  
Total Targets: 87

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   CYP1A1↑, 1,   GPx1↑, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↓, 2,   SOD1↑, 1,   SOD2↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP∅, 1,  

Core Metabolism/Glycolysis ⓘ

CYP2C6↑, 1,   CYP3A2↑, 1,  

Cell Death ⓘ

AhR↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Migration ⓘ

Ca+2↓, 1,   CYP2D1↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   CYP1A2↑, 1,   Dose↝, 2,   Half-Life↝, 1,  

Functional Outcomes ⓘ

toxicity↝, 1,  
Total Targets: 20

Scientific Paper Hit Count for: CYP1A1, Cytochrome P450 1A1
1 Chocolate
1 Emodin
1 Naringin
1 Phenethyl isothiocyanate
1 Shikonin
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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