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| Dichloroacetate (DCA) is a metabolic modulator that targets the altered metabolic state of cancer cells by inhibiting PDKs. This action impacts several key pathways: • Reversal of the Warburg effect • Restoration of mitochondrial function and promotion of apoptosis • suppresses glycolysis and promotes oxidative phosphorylation, thereby increasing mitochondrial ROS-mediated apoptosis in tumor cells • Increase in ROS production leading to oxidative stress • Inhibition of cell cycle progression • Modulation of HIF-1α signaling: DCA might decrease HIF-1α stabilization, thereby reducing the expression of genes that support glycolysis, angiogenesis, and survival under low-oxygen conditions. -DCA has been primarily used in treating congenital lactic acidosis—a rare genetic disorder characterized by the buildup of lactic acid in the body. -DCA is an anti-diabetic and lipid-lowering drug, as well as treating myocardial and cerebrovascular ischemia. -Do not add DCA to hot or warm beverages. DCA is unstable at higher temperatures -Caffeinated increases effectiveness -Vitamin B1 reduces neuropathy (500mg-2500mg/day) -Possibly 20 grams of citric acid 20 minutes before taking DCA -Procaine, Diclofenac or Sulindac to increase SMCT1 -Omeprazole 80mg/day to increase DCA effectiveness -Scorpion venom to increase DCA effectiveness -Metformin 1000mg to 1500mg/day -Propranolol (Ref.) -Fenbendazole shows strong synergy when combined to DCA, So it may make very much sense to combine the two. "Note: DCA is not tumor cell specific,> and therefore the same shift in glucose metabolism that occurs in cancer cells will also take place in immune cells, leading to induction of Tregs (Ref.). In order to avoid this possibility, while using DCA I would also use Treg inhibitors such as Cimetidine (Ref.) or low dose Cyclophosphamide (Ref.)." Dose: 10mg/kg/day and increase slowly to about 25mg/kg/day:(1/2morn,1/2evening) take 5 days on, 2 off? OR 2wks on/ 1wk off: https://www.thedcasite.com/dca_dosage.html Done by mixing it in water and drinking, suggested that DCA not be taken on an empty stomach. **** DCA-induced apoptosis in cancer cells requires sodium-coupled monocarboxylates transporter SLC5A8 (SMCT1) -Inhibitors of DNA methylation induce reactivation of SLC5A8 -Procaine is a DNA-demethylating agent with growth-inhibitory effects in human cancer cells. -SMCT1 was found to be stimulated by some other NSAIDs (diclofenac, meclofenamate and sulindac), by activin A143 and by the probiotic Lactobacillus plantarum. SMCT1 has been found to be inhibited by some NSAIDs (ibuprofen, ketoprofen, fenoprofen, naproxen135 and indomethacin94), phytochemicals (resveratrol and quercetin) **** Hence these should be avoided with DCA. (also AVOID Bromide, iodide and sulfite ) **** GSTZ1 an/or chloride anion transport inhibitors also reduce resistance to DCA (if the tumor expresses GSTZ1 and contains a high chloride anions level, the GSTZ1 will be stable, maintaining the resistance to DCA). -Dichloroacetate-dca-treatment-strategy GSTZ1 an/or chloride anion transport inhibitors. . -Etacrynic acid is a Cl(-)-ATPase inhibitor -Lansoprazole and Omeprazole inhibit chloride channels. -Chlorotoxin found in scorpion venom (see my post on scorpion venom) can also inhibit chlorine channels Sources: https://northernhealthproducts.com/shop/ https://www.dcalab.com/
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| SLC5A8 (also known as SMCT1) is a sodium-coupled monocarboxylate transporter. SLC5A8 (SMCT1) is a sodium-coupled monocarboxylate transporter and a candidate tumor suppressor. It mediates uptake of butyrate, pyruvate, and related metabolites, enabling HDAC inhibition and promoting apoptosis / growth suppression in cancer cells. It is frequently silenced by DNA methylation, especially in colorectal cancer, and has also been implicated in breast, lung, cervical, gastric, thyroid, brain, and kidney cancers. - Many studies suggest that SLC5A8 functions as a tumor suppressor. In normal tissues, SLC5A8 contributes to the cellular uptake of short-chain fatty acids (SCFAs) like butyrate. Butyrate is known to have histone deacetylase inhibitor activity, which can modulate gene expression in a way that suppresses tumor growth. -In cancer, loss or silencing of SLC5A8 is often observed. Epigenetic mechanisms such as DNA hypermethylation of the SLC5A8 promoter region are commonly cited as a reason for its downregulation. SLC5A8 is commonly downregulated in a variety of cancers. Its loss, often due to promoter hypermethylation, correlates with poorer outcomes in several tumor types, suggesting a tumor suppressor role. While sustained expression of SLC5A8 appears to be protective and is associated with a better prognosis in some cancers, the field is still evolving. Inhibitors of DNA methylation induce reactivation of SLC5A8. procaine is a DNA-demethylating agent with growth-inhibitory effects in human cancer cells. |
| 1885- | DCA, | Role of SLC5A8, a plasma membrane transporter and a tumor suppressor, in the antitumor activity of dichloroacetate |
| - | in-vitro, | CRC, | HCT116 | - | in-vitro, | CRC, | SW-620 | - | in-vitro, | CRC, | HT-29 |
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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