Vitamin C (Ascorbic Acid) / GLUT1 Cancer Research Results

VitC, Vitamin C (Ascorbic Acid): Click to Expand ⟱
Features:
High-dose vitamin C: Some studies have suggested that high-dose vitamin C may be effective in treating certain types of cancer, such as ovarian cancer and pancreatic cancer.
Symptoms of vitamin C deficiency include fatigue, weakness, poor wound healing, ecchymoses, xerosis, lower extremity edema, and musculoskeletal pain—most of them are often observed in end-stage cancer patients. -Vitamin C is an essential nutrient involved in the repair of tissue, the formation of collagen, and the enzymatic production of certain neurotransmitters. It is required for the functioning of several enzymes and is important for immune system function.
-Ascorbic Acid, Different levels in different Organs
Homeostasis ranging from about 0.2 mM in the muscle and heart, and up to 10 mM in the brain and adrenal gland. -(Note the Oncomagnetic success in the brain also was then under conditions of high Vitamin C)

-Ascorbic acid is an electron donor
Ascorbic Acid, can be a Pro-oxidant
"The pro-oxidative activity of ascorbic acid (Figure 2) is associated with the interaction with transition metal ions (especially iron and copper). Under conditions of high, millimolar ascorbate concentration, vitamin C catalyzes the reduction of free transition metal ions, which causes the formation of oxygen radicals."
Ascorbic Acid, formation of H2O2 (Hydrogen Peroxide)
Many studies indicate the toxicity of ascorbate to cancer cells. Much evidence indicates that the underlying phenomenon is the pro-oxidative activity of ascorbate, which induces the formation of H2O2 and oxidative stress.
"ascorbate at concentrations achieved only by i.v. administration may be a pro-drug for formation of H(2)O(2)"
-High dose VitC therapy may not be for those with kidney problems
-Oral supplement up to 10g/day?
-Direct regulator of TET↑
-caution for (G6PD-) deficient patients receiving vitamin C infusions

-Note plasma half-life 30mins to 1hr, 1.5-2hr elimination half-life.
oral BioAv water soluble, but has limitiations as 100mg yeilds 60uM/L in plasma, but 1000mg only yeilds 85uM/L. mM concentration are required for effectiveness on cancer cells. Hence why IV administration is common. Boosting HIF increases the intracellular uptake of oxidized VitC
Pathways:
- high dose induces ROS production in cancer cells. Otherwise well known antioxidant in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Caspases↑, DNA damage↑, cl-PARP↑,
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, TrxR↓**, SOD↓, GSH↓ Catalase↓ HO1↓ GPx↓
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, VEGF↓, NF-κB↓,
- reactivate genes thereby inhibiting cancer cell growth : P53↑, TET↑
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, ERK↓, EMT↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓,
- Others: PI3K↓, AKT↓, STAT↓, AMPK, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Hepatoprotective,

- Selectivity: Cancer Cells vs Normal Cells
Selenium supplementation may protect cells against iron-dependent cell death by supporting increased expression of selenoproteins, including GPX4, which defend against oxidative stress. Meaning it may decrease effectiveness of high dose VitC.(#4468)
GLUT1, Glucose Transporter 1: Click to Expand ⟱
Source:
Type: protein
Also known as SLC2A1
An important hallmark in cancer cells is the increase in glucose uptake. GLUT1 is an important target in cancer treatment because cancer cells upregulate GLUT1, a membrane protein that facilitates the basal uptake of glucose in most cell types, to ensure the flux of sugar into metabolic pathways.
GLUT1 is a member of the facilitated glucose transporter family and is widely expressed in various tissues, including red blood cells, brain, and cancer cells.
GLUT1 has been shown to be overexpressed in many types of tumors, including breast, lung, and colon cancer. This overexpression may contribute to the development and progression of cancer by promoting glucose uptake and energy production in cancer cells.
GLUT1 is a protein that facilitates the transport of glucose across cell membranes. GLUT1 plays a role in the regulation of glucose metabolism in diabetes.
GLUT1 plays a role in the regulation of glucose metabolism in diabetes.
GLUT1 is also known to be involved in the Warburg effect.
GLUTs are expressed 10–12-fold higher in cancer cells than in healthy tissues, especially in highly proliferative and malignant tumors.

Downregulators:
-Resveratrol: associated with reduced GLUT1 expression.
-Curcumin: downregulate GLUT1 in various cancer cell lines
-Quercetin: downregulating the expression and function of GLUT1.
-EGCG: suppress GLUT1 expression
-Berberine: linked to decreased expression or activity of GLUT1.
Scientific Papers found: Click to Expand⟱
3133- VitC,    Vitamin C supplementation had no side effect in non-cancer, but had anticancer properties in ovarian cancer cells
- in-vitro, Ovarian, NA
*SVCT-2↑, *GLUT1↓, SVCT-2↓, GLUT1↑, TumCP↓, CDK2↓, PARP↓, selectivity↑,
3136- VitC,    Vitamin C uncouples the Warburg metabolic switch in KRAS mutant colon cancer
- in-vitro, Colon, SW48 - in-vitro, Colon, LoVo
ERK↓, p‑PKM2↓, GLUT1↓, Warburg↓, TumCD↑, eff↑, ROS↓, cMyc↓,
3146- VitC,    Vitamin C protects against hypoxia, inflammation, and ER stress in primary human preadipocytes and adipocytes
- in-vivo, Nor, NA
*Obesity↓, *ER Stress↓, *Inflam↓, Hif1a↓, VEGF↓, GLUT1↓, GRP78/BiP↓,
3145- VitC,    Vitamin C inhibits the growth of colorectal cancer cell HCT116 and reverses the glucose‐induced oncogenic effect by downregulating the Warburg effect
- in-vitro, CRC, HCT116
Warburg↓, TumCG↓, Glycolysis↓, GlucoseCon↓, ATP↓, lactateProd↓, selectivity↑, GLUT1↓, PKM2↓, LDHA↓, mTOR↓,
3141- VitC,    High-dose Vitamin C inhibits PD-L1 expression by activating AMPK in colorectal cancer
- in-vitro, CRC, HCT116
Glycolysis↓, eff↑, PD-L1↓, AMPK↑, HK2↓, NF-kB↓, Warburg↓, tumCV↓, GLUT1↓, PKM2↓, LDHA↓, CD4+↑, CD8+↑,
3140- VitC,    Vitamin-C-dependent downregulation of the citrate metabolism pathway potentiates pancreatic ductal adenocarcinoma growth arrest
- in-vitro, PC, MIA PaCa-2 - in-vitro, Nor, HEK293
citrate↓, FASN↓, ACLY↓, LDH↓, Glycolysis↓, Warburg↓, PDK1↓, GLUT1↓, LDHA↓, ECAR↓, PDH↑, eff↑,
1067- VitC,    Vitamin C activates pyruvate dehydrogenase (PDH) targeting the mitochondrial tricarboxylic acid (TCA) cycle in hypoxic KRAS mutant colon cancer
- in-vivo, CRC, NA
PDK1↓, Hif1a↓, GLUT1↓, ATP↓, MMP↓,
623- VitC,    The Involvement of Ascorbic Acid in Cancer Treatment
- Review, NA, NA
ROS↑, GLUT1↓, ATP↓,

Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 3,   MMP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACLY↓, 1,   AMPK↑, 1,   citrate↓, 1,   cMyc↓, 1,   ECAR↓, 1,   FASN↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 3,   HK2↓, 1,   lactateProd↓, 1,   LDH↓, 1,   LDHA↓, 3,   PDH↑, 1,   PDK1↓, 2,   PKM2↓, 2,   p‑PKM2↓, 1,   Warburg↓, 4,  

Cell Death ⓘ

TumCD↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

GRP78/BiP↓, 1,  

DNA Damage & Repair ⓘ

PARP↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   mTOR↓, 1,   TumCG↓, 1,  

Migration ⓘ

TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 2,   VEGF↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 7,   GLUT1↑, 1,   SVCT-2↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   NF-kB↓, 1,   PD-L1↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 3,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

LDH↓, 1,   PD-L1↓, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 43

Pathway results for Effect on Normal Cells:


Protein Folding & ER Stress ⓘ

ER Stress↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,   SVCT-2↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

Obesity↓, 1,  
Total Targets: 5

Scientific Paper Hit Count for: GLUT1, Glucose Transporter 1
8 Vitamin C (Ascorbic Acid)
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#:166  Target#:566  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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