Naringin / TumCCA Cancer Research Results

NarG, Naringin: Click to Expand ⟱
Features:
Flavonoid glycoside. Responsible for the bitterness of grapefruit.
Naringin is a flavonoid glycoside predominantly found in citrus fruits such as grapefruit and oranges. It is known for its antioxidant, anti-inflammatory, and potential anticancer properties.
It is hydrolyzed in vivo to naringenin, which exhibits antioxidant and anti-inflammatory activities and modulates signaling pathways (e.g., Nrf2 and NF-κB). In preclinical cancer models, naringin/naringenin is associated with cell-cycle arrest, apoptosis, and reduced invasion/metastasis, often linked to upstream modulation of survival pathways (PI3K/AKT) and stress MAPKs. Oral systemic exposure is limited due to metabolism and conjugation.
-Antioxidant Activity
-Induction of Apoptosis
-Cell Cycle Arrest (often G1 or G2/M)
-Anti-inflammatory Effects

-**a natural bioenhancer(effects vary) and reported to enhance the bioavailability of drugs by inhibiting cytochrome P450 (CYP3A4 especially grape fruit juice) and P-glycoprotein (P-gp). Naringin/naringenin can inhibit CYP3A4 and P-glycoprotein, contributing to grapefruit–drug interactions and potentially increasing exposure of certain medications.
-Usually paired with other bioflavonoids such as quercetin, hesperidin and rutin.

-Mainly obtained from grapefruit
-Including enhanced solubility, improved bioavailability and targeted delivery.
-Antioxidant
-Inhibition of CYP19(weak/modest). Naringin suppresses the PI3K/AKT signalling pathway
-Wnt/β-catenin, PI3K/Akt, NF-ĸB, and TGF-β pathways
-Up-regulation of adenosine monophosphate-activated protein kinase (AMPK), and inhibition of gluconeogenesis
-Antioxidant effects, by modulating reactive oxygen species (ROS) levels and increasing superoxide dismutase (SOD)
-Naringenin can reduce carcinogenesis through pleiotropic processes such as antioxidative, apoptotic-inducing ROS generation, and cell cycle arrest
-Revealed new mechanisms underlying the hypolipidemic effects of naringin and naringenin, including regulation of lipid digestion, reverse cholesterol transport, and low-density lipoprotein receptor expression
-Low bioavailability (approximately 8.8%) when administered orally. Bioavailability: citrus flavonoid glycosides are hydrolyzed in the gut; systemic plasma levels are often much lower than in vitro MICs.

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Nrf2/ARE antioxidant response Stress adaptation modulation (context-dependent) Nrf2 ↑; antioxidant enzymes ↑ R, G Endogenous antioxidant upshift Naringin and its aglycone naringenin are widely reported to activate Nrf2, elevate HO-1 and other antioxidant defenses, and reduce oxidative injury in many models.
2 NF-κB inflammatory signaling NF-κB ↓; pro-inflammatory cytokines ↓ (reported) Inflammation tone ↓ R, G Anti-inflammatory signaling Consistent evidence shows naringin/naringenin reduces pro-inflammatory signaling and cytokine expression in tumor and non-tumor contexts.
3 PI3K/AKT/mTOR survival axis PI3K/AKT ↓ (reported; model-dependent) ↔ R, G Growth/survival modulation Modulation of survival pathways is observed in various cancer‐cell studies, but effects vary by cell type and context.
4 Cell cycle control (Cyclins/CDKs) Cell-cycle arrest ↑ (G1/S or G2/M; reported) ↔ G Cytostasis Often reported as reduced proliferation and cell cycle arrest following upstream signaling changes.
5 Intrinsic apoptosis (mitochondrial/caspase linked) Apoptosis ↑; caspase activation ↑ (reported) ↔ G Execution of cell death Observed in many in vitro models, usually downstream of signaling modulation and stress pathways.
6 MAPK re-wiring (ERK / JNK / p38) MAPK modulation (context-dependent) ↔ P, R, G Stress/mitogenic signaling adjustment MAPK effects vary by assay and cell type; avoid fixed up/down arrows without a specific citation.
7 Invasion / metastasis programs (MMPs/EMT) MMPs ↓; migration/invasion ↓ (reported) ↔ G Anti-invasive phenotype Downstream phenotype changes reported in some models; linked to NF-κB/MAPK modulation.
8 Angiogenesis signaling (VEGF & related) Angiogenic outputs ↓ (reported) ↔ G Anti-angiogenic support Later phenotype outcomes; direction is often model-dependent.
9 Reactive oxygen species modulation Redox buffering; ROS direction variable ↔ P, R, G Redox modulation (context-dependent) Naringin is classically antioxidant; ROS changes in cancer models vary and are not reliably pro-oxidant under typical conditions.
10 Bioavailability / metabolism constraint Systemic exposure limited; rapid metabolism/conjugation — — Translation constraint Naringin’s glycoside form is hydrolyzed to naringenin; phase II conjugates circulate. Native systemic levels are often low compared with in vitro effective concentrations.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (rapid biochemical/signaling interactions)
  • R: 30 min–3 hr (acute signaling and transcription modulation)
  • G: >3 hr (gene-regulatory adaptation and phenotype outcomes)
TumCCA, Tumor cell cycle arrest: Click to Expand ⟱
Source:
Type:
Tumor cell cycle arrest refers to the process by which cancer cells stop progressing through the cell cycle, which is the series of phases that a cell goes through to divide and replicate. This arrest can occur at various checkpoints in the cell cycle, including the G1, S, G2, and M phases. S, G1, G2, and M are the four phases of mitosis.
Scientific Papers found: Click to Expand⟱
1803- NarG,    Naringin and naringenin as anticancer agents and adjuvants in cancer combination therapy: Efficacy and molecular mechanisms of action, a comprehensive narrative review
- Review, Var, NA
JAK↓, STAT↓, PI3K↓, Akt↓, mTOR↓, NF-kB↓, COX2↓, NOTCH↓, TumCCA↑,
1807- NarG,    A Systematic Review of the Preventive and Therapeutic Effects of Naringin Against Human Malignancies
- Review, NA, NA
AntiTum↑, TumCP↓, tumCV↓, TumCCA↑, Mcl-1↓, RAS↓, e-Raf↓, 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↑, ROS↑, MAPK↑, STAT3↓, chemoP↑,
1799- NarG,    Naringenin as potent anticancer phytocompound in breast carcinoma: from mechanistic approach to nanoformulations based therapeutics
- Review, NA, NA
TumCCA↑, BioAv↑, Half-Life∅, TNF-α↓, Casp8↑, BAX↑, Bak↑, EGF↓, mTOR↓, PI3K↓, ERK↓, Akt↓, NF-kB↓, VEGF↓, angioG↓, antiOx↑, EMT↓, OS↑, MAPK↓, ChemoSen↑, MMP9↓, MMP2↓, ROS↑, ROS↑, GSH↓, Casp3↑, ROS↑,
1798- NarG,    Naringenin: A potential flavonoid phytochemical for cancer therapy
- Review, NA, NA
*Inflam↓, *antiOx↓, neuroP↑, hepatoP↑, AntiCan↑, Apoptosis↑, TumCCA↑, angioG↓, ROS↝, SOD↑, TGF-β↓, Treg lymp↓, IL1β↓, *BioAv↝, ChemoSen↑, cardioP↑,
1797- NarG,    Naringin inhibits growth potential of human triple-negative breast cancer cells by targeting β-catenin signaling pathway
- in-vitro, BC, MDA-MB-231
TumCG↓, β-catenin/ZEB1↓, AntiTum↑, Apoptosis↑, TumCCA↑, P21↑, survivin↓,
1015- NarG,    Naringin induces endoplasmic reticulum stress-mediated apoptosis, inhibits β-catenin pathway and arrests cell cycle in cervical cancer cells
- in-vitro, Cerv, SiHa - in-vitro, Cerv, HeLa - in-vitro, Cerv, C33A
ER Stress↑, p‑eIF2α↑, CHOP↑, PARP1↑, Casp3↑, β-catenin/ZEB1↓, GSK‐3β↓, p‑β-catenin/ZEB1↓, p‑GSK‐3β↓, TumCCA↑, P21↑, p27↑,

Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   CYP1A1↑, 1,   GSH↓, 1,   lipid-P↓, 1,   ROS↑, 5,   ROS↝, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics ⓘ

EGF↓, 1,   e-Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

GLO-I↓, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 1,   Apoptosis↑, 2,   Bak↑, 1,   BAX↑, 2,   Bcl-2↓, 1,   Casp↑, 1,   Casp3↑, 2,   Casp8↑, 1,   MAPK↓, 1,   MAPK↑, 1,   Mcl-1↓, 1,   p27↑, 1,   p38↓, 1,   survivin↓, 2,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   p‑eIF2α↑, 1,   ER Stress↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,   PARP1↑, 1,  

Cell Cycle & Senescence ⓘ

P21↑, 2,   TumCCA↑, 6,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   ERK↓, 1,   GSK‐3β↓, 1,   p‑GSK‐3β↓, 1,   mTOR↓, 2,   p‑mTOR↓, 1,   NOTCH↓, 1,   PI3K↓, 2,   RAS↓, 1,   STAT↓, 1,   STAT3↓, 1,   TumCG↓, 1,   Wnt↓, 1,  

Migration ⓘ

AntiAg↑, 1,   MMP2↓, 2,   MMP9↓, 2,   TGF-β↓, 1,   TIMP1↑, 1,   TIMP2↑, 1,   Treg lymp↓, 1,   TumCP↓, 1,   VCAM-1↓, 1,   β-catenin/ZEB1↓, 2,   β-catenin/ZEB1↑, 1,   p‑β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   VEGF↓, 2,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL1β↓, 1,   JAK↓, 1,   NF-kB↓, 2,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↑, 2,   Half-Life∅, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 2,   cardioP↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   OS↑, 1,  
Total Targets: 76

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,  
Total Targets: 3

Scientific Paper Hit Count for: TumCCA, Tumor cell cycle arrest
6 Naringin
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#:128  Target#:322  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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