Ursolic acid / GlutMet 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)

GlutMet, Glutamine metabolism: Click to Expand ⟱

Source:

Type:

Glutamine metabolism plays a significant role in cancer biology, as many cancer cells exhibit altered metabolic pathways to support their rapid growth and proliferation.
Glutamine is a non-essential amino acid that serves as a vital nutrient for many cells, including cancer cells. It is involved in various metabolic processes, including protein synthesis, nucleotide synthesis, and energy production.
Warburg Effect: Cancer cells often rely on aerobic glycolysis (the Warburg effect) for energy production, even in the presence of oxygen. Glutamine metabolism can complement this process by providing intermediates for the tricarboxylic acid (TCA) cycle, which is crucial for energy production and biosynthesis.
Inhibitors of glutaminase (an enzyme that converts glutamine to glutamate) and other metabolic pathways are being explored in preclinical and clinical settings.

Key Enzymes in Glutamine Metabolism
Glutaminase (GLS)
Glutamate Dehydrogenase (GLUD)
Glutamine Synthetase (GS)
Asparagine Synthetase (ASNS)
Aminotransferases (e.g., GPT, GOT)

The expression of enzymes involved in glutamine metabolism is often elevated in various cancers and is generally associated with poorer prognosis.

Scientific Papers found: Click to Expand⟱

119-

UA,

CUR,

RES,

Combinatorial treatment with natural compounds in prostate cancer inhibits prostate tumor growth and leads to key modulations of cancer cell metabolism

in-vitro,

Pca,

DU145

in-vitro,

Pca,

PC3

ROS⇅, p‑STAT3↓, Src↓, AMPK↑, GlutMet↑, TCA↑, glut↓,

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 ⓘ

ROS⇅, 1,

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1, glut↓, 1, GlutMet↑, 1, TCA↑, 1,

Proliferation, Differentiation & Cell State ⓘ

Src↓, 1, p‑STAT3↓, 1,
Total Targets: 7

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: GlutMet, Glutamine metabolism

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