Ferulic acid / FIS1 Cancer Research Results

FA, Ferulic acid: Click to Expand ⟱
Features:
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
            
Type of corn p-coumaric acidferulic acid
   mg/kg, DW mg/kg, DW
Yellow dent 18.9 265
American blue N.D. 927
Mexican blue 1.3 202
white 6.6 2484
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
Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Nrf2 → HO-1 / ARE antioxidant response Stress adaptation modulation (context-dependent) Nrf2 ↑; HO-1 ↑; antioxidant defenses ↑ R, G Endogenous antioxidant upshift FA is repeatedly reported to promote Nrf2 nuclear translocation and HO-1 induction; this is one of the most defensible “core” mechanisms.
2 NF-κB inflammatory transcription (COX-2 / iNOS / cytokines) NF-κB ↓; COX-2/iNOS and pro-inflammatory cytokine programs ↓ (reported) Inflammation tone ↓ (tissue protective) R, G Anti-inflammatory signaling Often described as downstream of redox changes and upstream of reduced inflammatory mediators; direction is consistent across many inflammation models.
3 ROS / oxidative stress tone Oxidative stress ↓ (often); ROS direction can vary by tumor model Oxidative injury ↓ P, R, G Redox buffering (context-dependent) FA is classically antioxidant; in tumor systems, effects may be secondary to signaling changes and vary with baseline redox instability.
4 Cell-cycle control (Cyclin D1 / CDK4/6; checkpoints) Cell-cycle arrest ↑ (reported); Cyclin D1 ↓; proliferation ↓ G Cytostasis Frequently reported as later phenotype-level outcomes; direction and checkpoint phase (G1 vs G2/M) vary by model.
5 Apoptosis (intrinsic caspase-linked; p53 axis in some models) Apoptosis ↑; caspase activation ↑ (reported); p53/p21 ↑ (model-dependent) ↔ (generally less activation) G Cell death execution Apoptosis is commonly observed in cancer models but is not as “signature-direct” as for mitochondrial toxins; best treated as downstream/conditional.
6 MAPK re-wiring (ERK / JNK / p38) MAPK modulation (context-dependent) P, R, G Signal reprogramming MAPK direction depends on whether FA is acting primarily as anti-inflammatory/anti-stress vs antiproliferative; avoid hard arrows for p38/JNK/ERK unless model-specific.
7 PI3K → AKT (± mTOR) survival axis PI3K/AKT modulation (reported; model-dependent) R, G Survival/growth modulation Often listed in anticancer summaries; treat as “reported” rather than universal primary mechanism.
8 Invasion / metastasis programs (MMPs / migration) MMPs ↓; migration/invasion ↓ (reported) G Anti-invasive phenotype Observed as later outcomes (gene expression + phenotype assays) and commonly linked to NF-κB/MAPK context.
9 Radiation/chemo injury mitigation (supportive care framing) Adjunct potential: may reduce treatment-associated oxidative/inflammatory injury (context) Tissue protection ↑ (reported) G Cytoprotection Animal models report radioprotective/anti-inflammatory effects; present as supportive/adjunct rather than standalone anticancer therapy.
10 Bioavailability / metabolism constraint (conjugation; food-matrix dependence) Systemic exposure variable; much appears as glucuronide/sulfate conjugates Translation constraint FA is absorbed and rapidly metabolized; “bioavailability” varies widely with food matrix and binding to polysaccharides in grains.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (primary/rapid effects; early redox interactions / rapid signaling shifts)
  • R: 30 min–3 hr (acute stress-response + transcription signaling shifts)
  • G: >3 hr (gene-regulatory adaptation and phenotype-level outcomes)


FIS1, Mitochondrial fission 1 protein: Click to Expand ⟱
Source:
Type:

FIS1 — Mitochondrial fission 1 protein
FIS1 is a mitochondrial outer-membrane fission adaptor/receptor linked to DRP1-mediated mitochondrial dynamics. In cancer, FIS1 is an emerging target because mitochondrial fission supports proliferation, survival adaptation, metastatic behavior, and tumor-initiating/stem-like phenotypes in some models. Recent TNBC evidence suggests FIS1 is required for expansion of tumor-initiating cells and that FIS1 loss suppresses TIC activity without broadly collapsing mitochondrial function, making it a potentially more selective mitochondrial dynamics target than global DRP1 inhibition.

-Often pro-tumor, Supports mitochondrial fragmentation/dynamics in stress-adapted cells

FIS1 is relevant to Alzheimer’s disease as part of the pathological mitochondrial fission program. AD models and human tissue studies show an imbalance toward mitochondrial fission, involving increased DRP1 and FIS1 and reduced fusion proteins such as MFN1, MFN2, and OPA1. Aβ and phosphorylated tau are linked to abnormal DRP1-mediated mitochondrial fragmentation, and increased DRP1/FIS1 interaction has been reported in Aβ-treated neurons and AD patient-derived fibroblasts.
-Direction: Usually increased or overactive in AD-like pathology

Natural Product Reported FIS1 / Fission Effect Evidence Strength for FIS1 Cancer Relevance Database Classification Suggested Note
Curcumin Reported to decrease FIS1 and DRP1-associated mitochondrial fission in several mitochondrial injury models. Moderate to strong Indirect; FIS1-specific cancer evidence is limited. FIS1/DRP1 mitochondrial fission down-modulator Best-supported natural product to link with FIS1, but still mostly non-cancer evidence.
EGCG Reported to decrease FIS1 or regulate the DRP1/FIS1 mitochondrial dynamics axis in neuroprotection and injury models. Moderate Indirect; stronger evidence for mitochondrial quality control than cancer-specific FIS1 targeting. Possible FIS1 down-modulator Useful to tag under mitochondrial fission, mitophagy, and oxidative-stress adaptation.
Urolithin A Reported to decrease FIS1 and DRP1 while improving mitophagy and mitochondrial quality control. Moderate Indirect; mostly neurodegeneration/mitophagy evidence. FIS1/DRP1-associated mitochondrial quality-control modulator Better classified under mitophagy and mitochondrial quality control
Melatonin Often reported to reduce pathological DRP1/FIS1-mediated mitochondrial fission, but effects can be context-dependent. Moderate Indirect; cancer relevance is complex and context-dependent. Context-dependent mitochondrial dynamics modulator “normalizes mitochondrial dynamics” rather than simple FIS1 inhibition.
Resveratrol Can reduce pathological DRP1/FIS1 fission in some injury models, but may increase Fis1/Drp1 expression in aging-repair contexts. Mixed Indirect; direction may vary by model and dose. Context-dependent FIS1/DRP1 modulator not a simple FIS1 inhibitor; more a mitochondrial dynamics normalizer.
Quercetin Associated with FIS1 targeting in omics/computational studies; direct experimental FIS1 modulation is weaker. Weak to moderate Indirect; not validated as a FIS1-targeted anticancer compound. Putative FIS1-associated modulator Suitable as a low-confidence or “possible” FIS1 link.
Sulforaphane Inhibits mitochondrial fission mainly through DRP1-related mechanisms; direct FIS1 modulation is unclear. Weak for FIS1 specifically Indirect; relevant to cancer metabolism and oxidative stress, but not FIS1-specific. Broader DRP1/fission pathway modulator mitochondrial fission rather than direct FIS1 modulation.
Berberine Reported to inhibit DRP1-mediated mitochondrial fission; FIS1 is mainly implicated as part of the pathway rather than directly modulated. Weak for FIS1 specifically Indirect; potentially relevant to cancer metabolism but not validated through FIS1. Broader DRP1/fission pathway modulator not a direct FIS1 modulator unless using a broader mitochondrial fission category.


Scientific Papers found: Click to Expand⟱
6416- CUR,  QC,  FA,  RES,  EGCG  Natural products targeting mitochondria: emerging therapeutics for age-associated neurological disorders
- Review, AD, NA
*DRP1/DNM1L↓, *FIS1↓, *MFN2↑, *OPA1↑, *DRP1/DNM1L↓, *FIS1↓, *OPA1↑, *MFN1↑, *MFN2↑, *DRP1/DNM1L↓, *FIS1↓, *MFN1↑, *MFN2↑, *memory↑, *mtDam↓, *DRP1/DNM1L↓, *FIS1↓,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


NA, unassigned

DRP1/DNM1L↓, 4,   FIS1↓, 4,   MFN1↑, 2,   MFN2↑, 3,   OPA1↑, 2,  

Mitochondria & Bioenergetics

mtDam↓, 1,  

Functional Outcomes

memory↑, 1,  
Total Targets: 7

Scientific Paper Hit Count for: FIS1, Mitochondrial fission 1 protein
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#:77  Target#:1486  State#:%  Dir#:%
wNotes=0 sortOrder:rid,rpid

 

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