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| Brazilian Green Propolis often considered best • Derived from Baccharis dracunulifolia, this type is rich in artepillin C. • It has been widely researched for its anticancer, anti-inflammatory, and antioxidant properties. -Propolis common researched flavonoids :chrysin, pinocembrin, galangin, pinobanksin(Pinocembrin) -most representative phenolic acids were caffeic acid, p-coumaric acid, and ferulic acid, as well as their derivatives, DMCA and caffeic acid prenyl, benzyl, phenylethyl (CAPE), and cinnamyl esters -One of the most studied active compounds of a poplar-type propolis is caffeic acid phenethyl ester (CAPE) -caffeic acid phenethyl ester (CAPE), galangin, chrysin, nemorosone, propolin G, artepillin C, cardanol, pinocembrin, pinobanksin, chicoric acid, and phenolic acids (caffeic acid, ferulic acid, and coumaric acid), as well as luteolin, apigenin, myricetin, naringenin, kaempferol, quercetin, polysaccharides, tannins, terpenes, sterols, and aldehydes -content highly variable based on location and extraction Two main factors of interest: 1. affects interstitual fluild pH 2. high concentration raises ROS (Reactive Oxygen Species), while low concentration may reduce ROS - Artepillin-C (major phenolic compounds found in Brazilian green propolis (BGP)) - caffeic acid major source Propolis is chemically diverse (300+ compounds reported) and composition depends on botanical/geographic source. Antibacterial activity is documented in classic literature (often stronger against Gram+). CAPE from propolis has reported preferential tumor cytotoxicity in early landmark work (often cited in antimicrobial paper references) Do not combine with 2DG Pathways: -Propolis compounds (e.g., artepillin C, caffeic acid phenethyl ester [CAPE]) can trigger apoptosis (programmed cell death) in cancer cells. -Propolis has been shown to inhibit NF‑κB activation. -Propolis extracts can cause cell cycle arrest at specific checkpoints (e.g., G0/G1 or G2/M phases). -Enhance the body’s antitumor immune responses, for example by activating natural killer (NK) cells and modulating cytokine profiles. -Note half-life no standard, high variablity of content. BioAv poor water solubility, and low oral bioavailability. Pathways: - high concentration may induce ROS production, while low concentrations mya low it. This may apply to both normal and cancer cells. Normal Cells Example. (Also not sure if high level are acheivable in vivo due to bioavailability) - ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx, SOD↓, GSH↓ Catalase↓ HO1↓ GPx↓ --> - Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑, - lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : NLRP3↓, TNF-α↓, IL-6↓, IL-8↓ - inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, TGF-β↓, α-SMA↓, ERK↓ - reactivate genes thereby inhibiting cancer cell growth : HDAC↓, P53↑, - cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓, - inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1, - inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDH↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, GRP78↑, GlucoseCon↓ - inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, - Others: PI3K↓, AKT↓, STAT↓, β-catenin↓, AMPK, ERK↓, JNK, - Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective, - Selectivity: Cancer Cells vs Normal Cells
Time-Scale Flag (TSF): P / R / G
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| Cancer Stem Cells Phytochemicals (natural plant-derived compounds) that may affect CSCs: Curcumin — suppresses self-renewal and pathways (Wnt/Notch/Hedgehog). Resveratrol — shown to reduce CSC populations and sphere formation in multiple models. Sulforaphane (from broccoli sprouts) — reported to inhibit CSC properties and pathways; active in vitro and in vivo. EGCG (epigallocatechin-3-gallate, green tea) — reduces CSC markers and sphere formation in several cancer types. Quercetin — reported to inhibit CSC proliferation, self-renewal and invasiveness (breast, endometrial, others). Berberine — shown to suppress CSC “stemness” and reduce tumorigenic properties in multiple models. Genistein (soy isoflavone) — decreases CSC markers, sphere formation and stemness signaling in prostate/breast/other models. Honokiol (Magnolia bark) — shown to eliminate or suppress CSC-like populations in oral, colon, glioma models. Luteolin — inhibits stemness/EMT and reduces CSC markers and self-renewal in breast, prostate and other models. Withaferin A (from Withania somnifera / ashwagandha) — multiple preclinical reports show WA targets CSCs and reduces tumor growth/metastasis in models. Circadian disruption in cancer and regulation of cancer stem cells by circadian clock genes: An updated review Potential Role of the Circadian Clock in the Regulation of Cancer Stem Cells and Cancer Therapy Can we utilise the circadian clock to target cancer stem cells? |
| 1651- | CA, | PBG, | Caffeic acid and its derivatives as potential modulators of oncogenic molecular pathways: New hope in the fight against cancer |
| - | Review, | Var, | NA |
| 1662- | PBG, | The immunomodulatory and anticancer properties of propolis |
| - | 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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