Ursolic acid / Cyt‑c Cancer Research Results

UA, Ursolic acid: Click to Expand ⟱
Features:
Natural compound found in apples and rosemary.
Ursolic acid (UA) is a pentacyclic triterpenoid found in many plants (notably apple peel, rosemary, thyme, holy basil, and other herbs). In cancer models it is best described as a multi-target signaling modulator with prominent effects on NF-κB inflammation/survival transcription, STAT3, PI3K/AKT/mTOR, and MAPK pathways, with downstream outcomes including cell-cycle arrest, apoptosis, anti-angiogenesis, and reduced invasion/EMT. A practical translational constraint is poor aqueous solubility and low oral bioavailability, so many strong in-vitro µM effects may not map cleanly to typical oral exposure without formulation.

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 NF-κB inflammatory / survival transcription NF-κB ↓; COX-2/iNOS/cytokines/Bcl-2 family/MMPs ↓ (reported) Inflammation tone ↓ (context) R, G Anti-inflammatory + anti-survival transcription One of the most frequently reported UA effects across tumor models; downstream impacts include reduced pro-survival and pro-metastatic gene programs.
2 STAT3 axis (JAK/STAT3 signaling) STAT3 activity ↓ (reported); downstream targets ↓ ↔ R, G Oncogenic transcription suppression UA is often reported to suppress STAT3 signaling, contributing to reduced proliferation/survival signaling.
3 PI3K → AKT (± mTOR) survival axis PI3K/AKT ↓; mTORC1 tone ↓ (reported; model-dependent) ↔ R, G Growth/survival modulation Commonly listed mechanism; direction and strength vary by cell line and exposure.
4 MAPK re-wiring (ERK / JNK / p38) Stress-MAPK modulation (context-dependent) ↔ P, R, G Signal reprogramming JNK/p38 activation and ERK modulation are reported variably; avoid fixed arrows unless tied to a specific model.
5 Cell-cycle checkpoints (Cyclins/CDKs; p21/p27) Cell-cycle arrest ↑ (G1/S or G2/M; reported); Cyclin D1/CDKs ↓ (context) ↔ G Cytostasis Often downstream of NF-κB/STAT3/PI3K signaling suppression.
6 Intrinsic apoptosis (mitochondrial/caspase linked) Apoptosis ↑; Bax ↑; Bcl-2 ↓; caspases ↑ (reported) ↔ (generally less activation) G Cell death execution Common downstream endpoint; can be coupled to stress signaling and survival pathway suppression.
7 Angiogenesis signaling (VEGF / HIF-1α outputs) VEGF ↓; angiogenic outputs ↓ (reported) ↔ G Anti-angiogenic support Typically phenotype-level effects tied to NF-κB/PI3K/HIF programs.
8 Invasion / metastasis programs (MMPs / EMT) MMP2/MMP9 ↓; EMT markers ↓; migration/invasion ↓ (reported) ↔ G Anti-invasive phenotype Often downstream of NF-κB/STAT3 changes; not universal across all tumors.
9 ROS / redox modulation ROS direction variable; redox stress or buffering reported (context) Oxidative injury ↓ in some non-tumor stress models P, R, G Stress modulation UA is not a reliable “pro-oxidant killer”; redox effects depend on dose, model, and baseline oxidative state.
10 Bioavailability / formulation constraint Systemic exposure often limited (poor solubility) — — Translation constraint UA is highly lipophilic with poor aqueous solubility; many formulations (e.g., nanoparticles, phospholipid complexes) are explored to improve exposure.

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

  • P: 0–30 min (rapid signaling interactions)
  • R: 30 min–3 hr (acute stress-response + transcription signaling shifts)
  • G: >3 hr (gene-regulatory adaptation and phenotype-level outcomes)
Cyt‑c, cyt-c Release into Cytosol: Click to Expand ⟱
Source:
Type:
Cytochrome c
** The term "release of cytochrome c" ** an increase in level for the cytosol.
Small hemeprotein found loosely associated with the inner membrane of the mitochondrion where it plays a critical role in cellular respiration. Cytochrome c is highly water-soluble, unlike other cytochromes. It is capable of undergoing oxidation and reduction as its iron atom converts between the ferrous and ferric forms, but does not bind oxygen. It also plays a major role in cell apoptosis.

The term "release of cytochrome c" refers to a critical step in the process of programmed cell death, also known as apoptosis.
In its new location—the cytosol—cytochrome c participates in the apoptotic signaling pathway by helping to form the apoptosome, which activates caspases that execute cell death.
Cytochrome c is a small protein normally located in the mitochondrial intermembrane space. Its primary role in healthy cells is to participate in the electron transport chain, a process that helps produce energy (ATP) through oxidative phosphorylation.
Mitochondrial outer membrane permeability leads to the release of cytochrome c from the mitochondria into the cytosol.
The release of cytochrome c is a pivotal event in apoptosis where cytochrome c moves from the mitochondria to the cytosol, initiating a chain reaction that leads to programmed cell death.

On the one hand, cytochrome c can promote cancer cell survival and proliferation by regulating the activity of various signaling pathways, such as the PI3K/AKT pathway. This can lead to increased cell growth and resistance to apoptosis, which are hallmarks of cancer.
On the other hand, cytochrome c can also induce apoptosis in cancer cells by interacting with other proteins, such as Apaf-1 and caspase-9. This can lead to the activation of the intrinsic apoptotic pathway, which can result in the death of cancer cells.
Overexpressed in Breast, Lung, Colon, and Prostrate.
Underexpressed in Ovarian, and Pancreatic.
Scientific Papers found: Click to Expand⟱
3790- UA,    Therapeutic applications of ursolic acid: a comprehensive review and utilization of predictive tools
*Inflam↓, *antiOx↑, AntiCan↑, *neuroP↑, *hepatoP↑, *cardioP↑, *MMP↑, *ROS↓, *PGC-1α↑, *BDNF↑, *cognitive↑, Bcl-2↓, Cyt‑c↑, DR5↑, Casp9↑, Casp8↑, Casp3↑, TumCCA↑, *BioAv↓, *Dose↝, *Half-Life↓, *Half-Life↓,

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:


Cell Death ⓘ

Bcl-2↓, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   DR5↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,  
Total Targets: 8

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,   PGC-1α↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   Dose↝, 1,   Half-Life↓, 2,  

Functional Outcomes ⓘ

cardioP↑, 1,   cognitive↑, 1,   hepatoP↑, 1,   neuroP↑, 1,  
Total Targets: 13

Scientific Paper Hit Count for: Cyt‑c, cyt-c Release into Cytosol
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#:164  Target#:77  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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