| Features: | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Caffeic acid is a polyphenol antioxidant found in coffee, fruits, vegetables, and herbs. It may have anti-inflammatory, anticancer, anti-aging, and other health benefits. Caffeic acid (CA) is a dietary hydroxycinnamic acid found widely in plant foods and in coffee largely as chlorogenic acids (caffeoylquinic acids). CA is generally antioxidant / anti-inflammatory and is frequently reported to modulate Nrf2 and NF-κB signaling, with downstream effects on survival pathways (PI3K/AKT), MAPKs, cell cycle, and apoptosis in preclinical cancer models. A notable mechanistic nuance is a context-dependent pro-oxidant effect described in the presence of copper (Cu), where CA can drive oxidative DNA damage in vitro (often discussed as potentially relevant to tumors with higher copper levels). -Caffeic acid phenethyl ester, the main representative component of propolis -Black chokeberry 141.14 mg/100 g F -Sunflower seed, meal 8.17 mg/100 g FW -Common sage, dried 26.40 mg/100 g FW -Ceylan cinnamon 24.20 mg/100 g FW -Nutmeg 16.30 mg/100 g FW -Dual capacity of CA to act as an antioxidant during carcinogenesis and as a pro-oxidant against cancer cells, promoting their apoptosis or sensitizing them to chemotherapeutic drugs. Pathways: -Caffeic acid is a potent antioxidant -Caffeic acid may also exhibit pro-oxidant behavior. At higher concentrations( 50–100 µM ?) or/and in the presence of transition metal ions (such as copper or iron), caffeic acid can participate in Fenton-like reactions, potentially leading to increased ROS generation. -Shown to inhibit NF-κB activation -Inhibitory effects on MAPK/ERK Pathway -PI3K/Akt Signaling Pathway -Activation of the Nrf2/ARE pathway -Cell cycle arrest at various checkpoints -Angiogenesis Inhibition Caffeic acid typically shows low oral bioavailability (sometimes only a few percent of the ingested dose is systemically available) and a short plasma half-life (around 1–2 hours in animal models). Caffeic acid — Caffeic acid is a dietary hydroxycinnamic acid polyphenol present in coffee, fruits, vegetables, and many herbs, and is also generated from hydrolysis of chlorogenic acids. It is formally classified as a small-molecule plant phenolic acid with redox-active, anti-inflammatory, and signal-modulating properties. Standard abbreviations include CA for caffeic acid; it should be distinguished from CAPE (caffeic acid phenethyl ester), which is a different propolis-derived ester with overlapping but not identical pharmacology. In cancer research, CA is best viewed as a pleiotropic preclinical modulator of inflammatory signaling, stress adaptation, metabolism, apoptosis, invasion, and angiogenesis, with translation limited by rapid conjugation and generally low free-aglycone systemic exposure. Primary mechanisms (ranked):
Bioavailability / PK relevance: CA is absorbable in humans, but after oral intake much of the circulating material appears rapidly as sulfate, glucuronide, and methylated metabolites rather than persistent free aglycone. Peak plasma timing is typically early, and delivery is constrained less by gut uptake than by fast metabolic conversion and short-lived free exposure. In-vitro vs systemic exposure relevance: Many anticancer studies use tens of micromolar CA, and some mechanistic claims depend on 50–100 µM or higher conditions that are not reliably reproduced as sustained free systemic exposure after ordinary oral intake. Accordingly, anti-inflammatory/adjuvant interpretations translate better than claims requiring strong direct tumor-cidal free-drug concentrations; metal-assisted pro-oxidant effects are especially context-dependent. Clinical evidence status: Primarily preclinical. The cancer evidence base consists mainly of cell and animal studies, with some adjunct/chemosensitization signals. Human oncology evidence remains very limited; at least one registered esophageal squamous cell carcinoma trial has been reported, but caffeic acid is not an established anticancer drug or standard adjunct. Mechanistic matrix
Time-Scale Flag (TSF): P / R / G
|
| Source: |
| Type: |
| Vimentin, a major constituent of the intermediate filament family of proteins, is ubiquitously expressed in normal mesenchymal cells and is known to maintain cellular integrity and provide resistance against stress. Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure. In many epithelial-derived tumors (carcinomas), elevated Vimentin expression is often observed in cancer cells that have undergone EMT. This upregulation is characteristic of a shift toward a mesenchymal state, which is associated with reduced cell–cell adhesion and increased motility. Vimentin expression is also noted in the tumor stroma, reflecting the presence and activation of mesenchymal cells such as cancer-associated fibroblasts (CAFs). This dual expression can contribute to the remodeling of the tumor microenvironment. The degree of Vimentin expression may vary depending on the tumor type, grade, and stage. More aggressive and advanced tumors tend to show higher levels of Vimentin expression. High Vimentin expression has been correlated with poor clinical outcomes in several cancers, including breast, colorectal, prostate, and lung cancers. Elevated Vimentin levels are typically associated with higher tumor grade, increased invasiveness, enhanced metastatic potential, and a greater risk of recurrence. As a component of the EMT signature, high Vimentin expression can serve as an indicator of a more aggressive tumor phenotype and is often associated with reduced overall survival. - vimentin up-regulation is often used as a marker of EMT in cancer |
| 1652- | CA, | Caffeic Acid and Diseases—Mechanisms of Action |
| - | Review, | Var, | NA |
| 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 |
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#:51 Target#:336 State#:% Dir#:1
wNotes=0 sortOrder:rid,rpid