Ursolic acid / P21 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)
P21, P21: Click to Expand ⟱
Source:
Type: Proapototic
cyclin-dependent kinase inhibitor p21 (also known as p21 WAF1/Cip1) promotes cell cycle arrest in response to many stimuli.
P21 is a cyclin-dependent kinase inhibitor that plays a crucial role in regulating the cell cycle. It is encoded by the CDKN1A gene and is a key player in the cellular response to stress, including DNA damage.
P21 is often considered a tumor suppressor because its expression is upregulated in response to p53 activation, a well-known tumor suppressor protein. When DNA damage occurs, p53 can activate the transcription of the CDKN1A gene, leading to increased levels of P21, which helps prevent the proliferation of damaged cells.
In many cancers, the p53 pathway is disrupted, leading to decreased levels of P21. p21 is a apoptotic marker protein.
Cell cycle arrest gene p21
Scientific Papers found: Click to Expand⟱
15- CUR,  UA,    Effects of curcumin and ursolic acid in prostate cancer: A systematic review
- Review, Pca, NA
NF-kB↝, Akt↝, AR↝, Apoptosis↝, Bcl-2↝, Casp3↝, BAX↝, P21↝, ROS↝, Bcl-xL↝, JNK↝, MMP2↝, P53↝, PSA↝, VEGF↝, COX2↝, cycD1/CCND1↝, EGFR↝, IL6↝, β-catenin/ZEB1↝, mTOR↝, NRF2↝, AP-1↝, Cyt‑c↝, PI3K↝, PTEN↝, Cyc↝, TNF-α↝,

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:


Redox & Oxidative Stress ⓘ

NRF2↝, 1,   ROS↝, 1,  

Cell Death ⓘ

Akt↝, 1,   Apoptosis↝, 1,   BAX↝, 1,   Bcl-2↝, 1,   Bcl-xL↝, 1,   Casp3↝, 1,   Cyt‑c↝, 1,   JNK↝, 1,  

DNA Damage & Repair ⓘ

P53↝, 1,  

Cell Cycle & Senescence ⓘ

Cyc↝, 1,   cycD1/CCND1↝, 1,   P21↝, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↝, 1,   PI3K↝, 1,   PTEN↝, 1,  

Migration ⓘ

AP-1↝, 1,   MMP2↝, 1,   β-catenin/ZEB1↝, 1,  

Angiogenesis & Vasculature ⓘ

EGFR↝, 1,   VEGF↝, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↝, 1,   IL6↝, 1,   NF-kB↝, 1,   PSA↝, 1,   TNF-α↝, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↝, 1,  

Clinical Biomarkers ⓘ

AR↝, 1,   EGFR↝, 1,   IL6↝, 1,   PSA↝, 1,  
Total Targets: 32

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: P21, P21
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#:234  State#:%  Dir#:4
  wNotes=0  sortOrder:rid,rpid

 

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