Kaempferol / glucose Cancer Research Results

KaempF, Kaempferol: Click to Expand ⟱

Features:

Kaempferol = dietary flavonol polyphenol (aglycone; often present as glycosides such as kaempferol-3-O-glucoside). Sources: tea, kale, spinach, capers, broccoli, onions. Primary mechanisms (ranked):
1) PI3K/Akt/mTOR pathway inhibition → ↓ proliferation, ↓ survival signaling (core anti-tumor axis).
2) MAPK modulation (ERK/JNK/p38) → apoptosis or growth arrest (context-dependent).
3) NF-κB suppression → ↓ inflammatory and pro-survival transcription programs.
4) Pro-oxidant ROS induction at higher concentrations → mitochondrial apoptosis signaling.
Bioavailability/PK relevance: Oral absorption modest; extensive phase II metabolism (glucuronidation/sulfation); plasma typically low µM or sub-µM after dietary intake; many in-vitro studies use 10–100 µM (often exceeding achievable systemic exposure without specialized delivery).
Clinical evidence status: largely preclinical (cell + animal); limited human cancer trial data; strongest support in epidemiologic associations rather than interventional oncology RCTs.

Kaempferol—an abundant flavonoid found in various fruits, vegetables, and medicinal herbs—affects cancer cell behavior

Pathways:
-Inhibit the PI3K/Akt signaling
-Modulation of the MAPK pathway (including ERK1/2)
-Inhibit NF-κB Signaling Pathway
-can upregulate or activate p53-dependent pathways
-Inhibitory action on STAT
-Activation of AMPK
-Reduce VEGF
-Can induce oxidative stress in cancer cells (ROS)

Kaempferol — Cancer vs Normal Pathway Effects

Rank	Pathway / Axis	Cancer Cells (↑ / ↓ / ↔)	Normal Cells (↑ / ↓ / ↔)	TSF	Primary Effect	Notes / Interpretation
1	PI3K/Akt/mTOR	↓ proliferation; ↓ survival signaling	↔ / mild ↓ (cytoprotective context)	R→G	Growth suppression	Core mechanistic axis across multiple tumor models (breast, lung, colon, prostate).
2	MAPK (ERK, JNK, p38)	↑ JNK/p38 (pro-apoptotic); ↓ ERK (proliferative)	↔ (dose-dependent)	R	Apoptosis induction	Often stress-activated signaling; balance of ERK vs JNK determines outcome.
3	NF-κB	↓ transcription of inflammatory & anti-apoptotic genes	↓ inflammatory tone	R→G	Anti-inflammatory / anti-survival	Reduces cytokine signaling and tumor microenvironment support pathways.
4	ROS	↑ (high concentration; pro-oxidant apoptosis)	↔ / ↓ (antioxidant at low conc.)	P→R	Mitochondrial stress	Biphasic: antioxidant at dietary levels; pro-oxidant at higher in-vitro doses.
5	NRF2	↔ / ↓ (context-dependent)	↑ cytoprotective response	G	Redox adaptation	May activate antioxidant genes in normal cells; persistent activation in tumors could support resistance.
6	Intrinsic apoptosis (Bax/Bcl-2, caspases)	↑ Bax; ↓ Bcl-2; ↑ caspase-3/9	↔	R→G	Mitochondrial apoptosis	Common downstream convergence of ROS + PI3K suppression.
7	Ca²⁺ signaling	↑ mitochondrial Ca²⁺ (subset models)	↔	R	Apoptotic amplification	Not universal; observed in certain carcinoma lines.
8	HIF-1α / Angiogenesis	↓ HIF-1α; ↓ VEGF (model-dependent)	↔	G	Anti-angiogenic potential	Observed in hypoxia models; translational impact uncertain.
9	Ferroptosis	↔ (indirect; limited data)	↔	R	Redox-linked sensitivity (theoretical)	No consistent ferroptosis signature established.
10	Clinical Translation Constraint	Low oral bioavailability; rapid conjugation; in-vitro concentrations commonly exceed systemic exposure; limited human interventional oncology data.		—	PK / Evidence	Dietary intake likely below cytotoxic range; delivery systems (nano-formulations) under investigation.

TSF legend: P: 0–30 min | R: 30 min–3 hr | G: >3 hr

glucose, glucose: Click to Expand ⟱

Source:

Type:

Glucose

Scientific Papers found: Click to Expand⟱

2390-

KaempF,

Kaempferol Can Reverse the 5-Fu Resistance of Colorectal Cancer Cells by Inhibiting PKM2-Mediated Glycolysis

in-vitro,

CRC,

HCT8

eff↑, GlucoseCon↓, lactateProd↓, PKM2↓, Glycolysis↓, glucose↑,

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:

Core Metabolism/Glycolysis ⓘ

glucose↑, 1, GlucoseCon↓, 1, Glycolysis↓, 1, lactateProd↓, 1, PKM2↓, 1,

Drug Metabolism & Resistance ⓘ

eff↑, 1,
Total Targets: 6

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: glucose, glucose

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