pH Cancer Research Results

pH, : Click to Expand ⟱
Source:
Type:
Tumor Microenvironment: Cancer cells often thrive in a more acidic environment compared to normal cells. This is partly due to the metabolic processes of cancer cells, which can produce lactic acid and other acidic byproducts. The acidic microenvironment can promote tumor growth and invasion.
Many tumors exhibit an acidic microenvironment. This is largely due to the high rate of glycolysis (often referred to as the Warburg effect), even in the presence of oxygen, leading to lactate production. Acidification is thought to promote invasion, metastasis, and resistance to certain chemotherapies.
The body maintains a relatively stable pH in the blood (around 7.4). However, the pH of tissues can vary, and tumors can exhibit a lower pH.

-Normal tissues have a higher extracellular pH than intracellular pH, in cancer is exactly the opposite. (inversion of the pH gradient).

Cancer cells often overexpress proton pumps (such as V-ATPase) and transporters that actively extrude protons (H⁺) to maintain an intracellular pH conducive to their growth.
Inhibiting these pumps can lead to intracellular acidification and potentially induce apoptosis or render cancer cells more vulnerable to other treatments.
Normal pH levels in the body:
Nasal: ~6.3 pH
Mouth/saliva: 6.2-7.6 pH
Stomach: 1-3 pH
Small Intestine: 5.9-6.8 pH
Colon/Large Intestine: 6.8-7 pH


Scientific Papers found: Click to Expand⟱
4548- AgNPs,  Chit,    Synergistic combination of antioxidants, silver nanoparticles and chitosan in a nanoparticle based formulation: Characterization and cytotoxic effect on MCF-7 breast cancer cell lines
- in-vitro, BC, MCF-7
AntiCan↑, anti-cancer efficacy was observed against MCF-7 breast cancer cells having IC50 values of 53.36 ± 0.36 μg/mL (chitosan–ascorbic acid–glucose
EPR↑, we hypothesize that the nanoformulations can be up-taken readily by the cancer cells
pH↝, cancer cells are known to be acidic therefore the chitosan matrix can readily dissolve releasing the encapsulated components thereby triggering the subsequent death process in the cancerous cells

1880- DCA,    A Novel Form of Dichloroacetate Therapy for Patients With Advanced Cancer: A Report of 3 Cases
- Case Report, Var, NA
OS↑, 3 cases with patients who had recurrent cancers and for whom all conventional therapies had failed
angioG↓, (1) inhibition of angiogenesis
Hif1a↝, (2) alteration of expression of hypoxia-inducible factor 1-α (HIF1-α)
pH↝, (3) alteration of pH regulators vacuolar-type H + -ATPase (V-ATPase) and monocarboxylate transporter 1 (MCT1)
QoL↑, DCA has the potential to extend life without reducing patients’ quality of life with debilitating side effects or compromising physiological function, even for disease in a very advanced stage

1868- DCA,  MET,    Long-term stabilization of stage 4 colon cancer using sodium dichloroacetate therapy
- Case Report, NA, NA
eff↑, DCA therapy resulted in tumour stabilization of stage 4 colon cancer in a 57 years old female for a period of nearly 4 years, with no serious toxicity
toxicity∅,
MMP↓, In the initial 2007 paper by Bonnet et al[1], it was reported that DCA reduced mitochondrial membrane potential resulting in selective apoptosis in cancer cells.
Apoptosis↑,
selectivity↑,
pH↝, alteration of pH regulators V-ATPase and MCT1
Dose↝, The neuropathy risk with inclusion of natural neuroprotective agents was roughly 20% with 20-25 mg/kg per day dosing on a 2 wk on/1 wk off cycle.
Dose↝, 3 natural supplements were prescribed: Alpha lipoic acid (racemic) 500 mg i.v. with each DCA dose, oral R-alpha lipoic acid 150 mg 3 times a day, oral acetyl L-carnitine 500 mg 3 times a day, and oral benfotiamine 80 mg twice a day.
eff↑, Oral metformin was added to help sensitize the cancer to the chemotherapy, starting at 500 mg orally once a day with titration up to 500 mg 3 times a day

786- Mg,  VitC,    A narrative review on the role of magnesium in immune regulation, inflammation, infectious diseases, and cancer
Risk↓, boasts a significant anti-cancer effect.
*VitD↑, Mg is also essential for the synthesis and distribution of vitamin D
*pH↝, Additionally, the presence of Mg2+ plays a crucial role in regulating the levels of "intracellular free Ca2+ and intracellular pH"
*ROS↓, mitochondrial ROS inhibition (study in frail elderly patients)
TumCG↓, Mg in the diet slowed tumor development in young male rats
eff↑, Mg can enhance the anti-cancer effects of AA. (related to SVCT2 expression)

2202- SK,    Enhancing Tumor Therapy of Fe(III)-Shikonin Supramolecular Nanomedicine via Triple Ferroptosis Amplification
- in-vitro, Var, NA
Iron↑, After delivering into glutathione (GSH)-overexpressed tumor cells, FeShik will disassemble and release Fe2+ to induce cell death via ferroptosis.
Ferroptosis↑,
pH↝, GOx executes its catalytic activity to produce an acid environment and plenty of H2O2 for stimulating •OH generation via the Fenton reaction
H2O2↑,
ROS↑,
Fenton↑,
GSH↓, SRF will suppress the biosynthesis of GSH by inhibiting system Xc-, further deactivating the enzymatic activity of glutathione peroxidase 4 (GPX4).
GPx4↓,
lipid-P↑, Up-regulation of the oxidative stress level and down-regulation of GPX4 expression can dramatically accelerate the accumulation of lethal lipid peroxides, leading to ferroptosis amplification of tumor cells

3950- Taur,    Taurine Supplementation as a Neuroprotective Strategy upon Brain Dysfunction in Metabolic Syndrome and Diabetes
- Review, Diabetic, NA - Review, Stroke, NA - Review, AD, NA
*Ca+2↝, taurine homeostasis can impact a number of biological processes, such as osmolarity control, calcium homeostasis, and inhibitory neurotransmission, and have been reported in both metabolic and neurodegenerative disorders.
*neuroP↑, taurine can afford neuroprotection in individuals with obesity and diabetes.
*other↝, Notably, both methionine and cysteine produced from protein degradation can generate taurine as an end-product
*pH↝, Taurine might counteract extreme mitochondrial pH fluctuations and help preserve mitochondrial physiology.
*ROS∅, Taurine is not able to act as a radical scavenger
eff↑, Taurine also decreased the activity of glutathione peroxidase and manganese-superoxide dismutase upon tamoxifen toxicity, which contributed to decreasing mitochondrial oxidative stress, measured through lipid peroxidation, protein carbonyl content, a
*MMP↑, In sum, taurine supplementation is proposed to improve the function of the mitochondria, contributing to the preservation of mitochondrial membrane potential, proton gradient, and matrix pH that are critical for energy metabolism and efficient oxidat
*Apoptosis↓, Taurine was found to prevent apoptosis upon many noxious challenges
*other↝, The most striking neuroprotective effects of taurine were observed on the reduction of apoptotic rates and the improvement of neurological outcomes upon brain ischemia.
*ER Stress↓, prevention of mitochondrial and endoplasmic reticulum (ER) stress.
*Bcl-xL↓, reduction of anti-apoptotic Bcl-xL and the increase of the pro-apoptotic Bax, preventing cytochrome C release from the mitochondria, and inhibiting the activation of calpain and caspase-3
*BAX↑,
*Cyt‑c↑,
*cal2↓,
*Casp3↓,
*UPR↓, prevent ischemia/hypoxia-induced endoplasmic reticulum (ER) stress by inhibiting the unfolded protein response via transcription factor 6 (ATF6), protein kinase R-like ER kinase (PERK), and inositol-requiring enzyme 1 (IRE1) pathways
*other↝, Altogether, one might speculate that taurine loss in patients with AD is linked to worsened cognitive deterioration.
*NF-kB↓, ameliorated the diabetes-induced increase of the transcription factor NF-κβ, involved in inflammatory processes, and the diabetes-induced reduction of Nrf2 and glucose transporters Glut1 and Glut3 in the brain.
*NRF2↑,
*GLUT1↑,
*GLUT3↑,
*memory↑, In mice fed a fat-rich diet, which develop metabolic syndrome, we recently demonstrated that 3% (w/v) taurine supplemented in the drinking water for 2 months prevented memory impairment


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

Fenton↑, 1,   Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 1,   H2O2↑, 1,   Iron↑, 1,   lipid-P↑, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics

MMP↓, 1,  

Cell Death

Apoptosis↑, 1,   Ferroptosis↑, 1,  

Proliferation, Differentiation & Cell State

TumCG↓, 1,  

Angiogenesis & Vasculature

angioG↓, 1,   EPR↑, 1,   Hif1a↝, 1,  

Cellular Microenvironment

pH↝, 4,  

Drug Metabolism & Resistance

Dose↝, 2,   eff↑, 4,   selectivity↑, 1,  

Functional Outcomes

AntiCan↑, 1,   OS↑, 1,   QoL↑, 1,   Risk↓, 1,   toxicity∅, 1,  
Total Targets: 24

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

NRF2↑, 1,   ROS↓, 1,   ROS∅, 1,  

Mitochondria & Bioenergetics

MMP↑, 1,  

Cell Death

Apoptosis↓, 1,   BAX↑, 1,   Bcl-xL↓, 1,   Casp3↓, 1,   Cyt‑c↑, 1,  

Transcription & Epigenetics

other↝, 3,  

Protein Folding & ER Stress

ER Stress↓, 1,   UPR↓, 1,  

Migration

Ca+2↝, 1,   cal2↓, 1,  

Barriers & Transport

GLUT1↑, 1,   GLUT3↑, 1,  

Immune & Inflammatory Signaling

NF-kB↓, 1,   VitD↑, 1,  

Cellular Microenvironment

pH↝, 2,  

Clinical Biomarkers

VitD↑, 1,  

Functional Outcomes

memory↑, 1,   neuroP↑, 1,  
Total Targets: 22

Scientific Paper Hit Count for: pH,
2 Dichloroacetate
1 Silver-NanoParticles
1 chitosan
1 Metformin
1 Magnesium
1 Vitamin C (Ascorbic Acid)
1 Shikonin
1 Taurine
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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