Ursolic acid / glut 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)

glut, glutamine: Click to Expand ⟱

Source:

Type:

Glutamine is an amino acid that fuels various metabolic pathways, supporting bioenergetics, biosynthesis, and redox balance in cancer cells.

-Many breast tumors exhibit glutamine addiction, relying on enhanced glutamine uptake and metabolism to support rapid proliferation.

-In many tumor types—such as breast, lung, colorectal, liver, and pancreatic cancers—enhanced glutamine metabolism is often associated with a more aggressive phenotype, therapy resistance, and poorer patient outcomes.

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: glut, glutamine

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