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| Ferulic acid is an antioxidant found in some skin creams and serums. Foods: popcorn, bamboo, whole-grain rye bread, whole-grain oat flakes, sweet corn (cooked) Ferulic acid (FA) is a hydroxycinnamic acid abundant in plant cell walls (notably cereals/whole grains) with strong antioxidant and cytoprotective activity. Mechanistically, FA is frequently described as inducing Nrf2/HO-1 antioxidant programs and suppressing NF-κB-linked inflammation, with additional model-dependent anticancer effects (cell-cycle arrest, apoptosis, reduced invasion). Oral exposure is variable because FA is rapidly metabolized (often as conjugates) and bioaccessibility depends on the food matrix. -Ferulic acid found in dietary strand fractions, especially its free form, has important functions for protecting the human health. -AChE inhibitor (AD) -Cooking results in an increase in free ferulic acid quantity and in a reduction in bound ferulic acid quantity. Bamboo shoots 243.6 mg/100g Sugar-beet pulp 800 mg/100g Popcorn 313 mg/100g Wheat bran 500–1500mg/100g Whole wheat flour 100–300mg/100g
Pathway / Target Modulation by FA / Direction Aβ aggregation ↓ Inhibits fibril formation and destabilizes existing Aβ fibrils BACE‑1 & APP ↓ Reduces BACE-1 and APP expression; ↑ MMP‑2/‑9 expression promoting Aβ clearance Tau hyperphosphorylation Implicitly ↓ through modulation of Ca²⁺/CDK5/GSK3β pathways Ca²⁺ ↓ FA lowers STEP levels via chelation of Ca²⁺, suppressing PP2B → restores synaptic plasticity (AChE / BChE) ↓ Inhibition of AChE (FA IC₅₀~15 µM, derivatives IC₅₀ down to 0.006 µM); also BChE (MAO‑A/B) ↓ Inhibits MAO‑B (derivatives IC₅₀ ~0.3–0.7 µM), reducing ROS ROS ↓ Scavenges ROS, enhances antioxidant enzymes (e.g., catalase), ↓ MDA (COX‑2, 5‑LOX, NLRP3) ↓ Derivatives inhibit COX‑2/5‑LOX; derivative 13a ↓ NLRP3 inflammasome Iron/Cu²⁺ chelation ↓ Metal-induced Aβ aggregation via chelation by FA and derivatives Autophagy & Aβ clearance ↗ Suggested promotion of autophagy mechanisms targeting Aβ
Time-Scale Flag (TSF): P / R / G
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| Type: enzyme |
| PKM2 (Pyruvate Kinase, Muscle 2) is an enzyme that plays a crucial role in glycolysis, the process by which cells convert glucose into energy. PKM2 is a key regulatory enzyme in the glycolytic pathway, and it is primarily expressed in various tissues, including muscle, brain, and cancer cells. -C-myc is a common oncogene that enhances aerobic glycolysis in the cancer cells by transcriptionally activating GLUT1, HK2, PKM2 and LDH-A -PKM2 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 glycolysis and energy production in cancer cells. -inhibition of PKM2 may cause ATP depletion and inhibiting glycolysis. -PK exists in four isoforms: PKM1, PKM2, PKR, and PKL -PKM2 plays a role in the regulation of glucose metabolism in diabetes. -PKM2 is involved in the regulation of cell proliferation, apoptosis, and autophagy. – Pyruvate kinase catalyzes the final, rate-limiting step of glycolysis, converting phosphoenolpyruvate (PEP) to pyruvate with the production of ATP. – The PKM2 isoform is uniquely regulated and can exist in both highly active tetrameric and less active dimeric forms. – Cancer cells often favor the dimeric form of PKM2 to slow pyruvate production, thereby accumulating upstream glycolytic intermediates that can be diverted into anabolic pathways to support cell growth and proliferation. – Under low oxygen conditions, cancer cells rely on altered metabolic pathways in which PKM2 is a key player. – The shift to aerobic glycolysis (Warburg effect) orchestrated in part by PKM2 helps tumor cells survive and grow in hypoxic conditions. – Elevated expression of PKM2 is frequently observed in many cancer types, including lung, breast, colorectal, and pancreatic cancers. – High levels of PKM2 are often correlated with enhanced tumor aggressiveness, poor differentiation, and advanced clinical stage. PKM2 in carcinogenesis and oncotherapy Inhibitors of PKM2: -Shikonin, Resveratrol, Baicalein, EGCG, Apigenin, Curcumin, Ursolic Acid, Citrate (best known as an allosteric inhibitor of phosphofructokinase-1 (PFK-1), a key rate-limiting enzyme in glycolysis) potential to directly inhibit or modulate PKM2 is less well established Full List of PKM2 inhibitors from Database -key connected observations: Glycolysis↓, lactateProd↓, ROS↑ in cancer cell, while some result for opposite effect on normal cells. Tumor pyruvate kinase M2 modulators Flavonoids effect on PKM2 Compounds name IC50/AC50uM Effect Flavonols 1. Fisetin 0.90uM Inhibition 2. Rutin 7.80uM Inhibition 3. Galangin 8.27uM Inhibition 4. Quercetin 9.24uM Inhibition 5. Kaempferol 9.88uM Inhibition 6. Morin hydrate 37.20uM Inhibition 7. Myricetin 0.51uM Activation 8. Quercetin 3-b- D-glucoside 1.34uM Activation 9. Quercetin 3-D -galactoside 27-107uM Ineffective Flavanons 10. Neoeriocitrin 0.65uM Inhibition 11. Neohesperidin 14.20uM Inhibition 12. Naringin 16.60uM Inhibition 13. Hesperidin 17.30uM Inhibition 14. Hesperitin 29.10uM Inhibition 15. Naringenin 70.80uM Activation Flavanonols 16. (-)-Catechin gallateuM 0.85 Inhibition 17. (±)-Taxifolin 1.16uM Inhibition 18. (-)-Epicatechin 1.33uM Inhibition 19. (+)-Gallocatechin 4-16uM Ineffective Phenolic acids 20. Ferulic 11.4uM Inhibition 21. Syringic and 13.8uM Inhibition 22. Caffeic acid 36.3uM Inhibition 23. 3,4-Dihydroxybenzoic acid 78.7uM Inhibition 24. Gallic acid 332.6uM Inhibition 25. Shikimic acid 990uM Inhibition 26. p-Coumaric acid 22.2uM Activation 27. Sinapinic acids 26.2uM Activation 28. Vanillic 607.9uM Activation |
| 1654- | FA, | Molecular mechanism of ferulic acid and its derivatives in tumor progression |
| - | Review, | Var, | NA |
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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