Emodin / ATM Cancer Research Results

EMD, Emodin: Click to Expand ⟱

Features:

Organic compound isolated from rhubarb, buckthorn, knotweed. It has laxative, anticancer, antibacterial, antiinflammatory, and antiviral activities, and is used in traditional Chinese medicine.
Emodin, an anthraquinone derivative found in various plants (e.g., rhubarb, Polygonum cuspidatum).

Pathways:
- Generation of Reactive Oxygen Species (ROS)
- Upregulation Bax downregulation of Bcl‑2, caspase activation and cyt_c release.
- Induce cell cycle arrest at various checkpoints (commonly G0/G1 or G2/M phases.
- Can inhibit NF‑κB activation
– MAPK Pathways
– PI3K/Akt Pathway
- Metalloproteinases (MMPs)

-ic50 cancer cells 10-50uM, normal cells higher(supports a therapeutic window)

Rank	Pathway / Target Axis	Direction	Label	Primary Effect	Notes / Cancer Relevance	Ref
1	Reactive oxygen species (ROS)	↑ ROS	Driver	Upstream cytotoxic trigger	Emodin induces ROS in cancer cells; ROS increase is positioned upstream of mitochondrial dysfunction and death signaling.	(ref)
2	Mitochondrial integrity (ΔΨm)	↓ ΔΨm	Driver	Mitochondrial dysfunction	Emodin decreases mitochondrial membrane potential (ΔΨm), consistent with mitochondria-dependent killing.	(ref)
3	Intrinsic apoptosis (caspase cascade)	↑ apoptosis (↑ caspases / ↑ PARP cleavage)	Driver	Execution-phase cell death	Emodin activates caspase-dependent apoptosis with mitochondrial involvement in colon cancer models.	(ref)
4	AMPK → AKT/mTOR axis	↑ AMPK / ↓ AKT-mTOR signaling	Secondary	Growth/metabolic suppression	NSCLC study reports AMPK activation with inhibition of AKT/mTOR alongside apoptosis and ROS increase (consistent directionality).	(ref)
5	NF-κB signaling	↓ NF-κB activation (↓ p65 nuclear translocation; ↓ IκBα phosphorylation/degradation)	Secondary	Reduced pro-survival/inflammatory transcription	Emodin inhibits TNF-α–induced NF-κB activation by blocking IκBα phosphorylation/degradation and p65 nuclear activity.	(ref)
6	STAT3 signaling	↓ STAT3 activation (↓ phosphorylation)	Secondary	Reduced survival/proliferation signaling	HCC study shows emodin suppresses STAT3 activation (and discusses upstream kinase modulation), supporting directionality as STAT3↓.	(ref)
7	HIF-1α hypoxia program	↓ HIF-1α (↓ biosynthesis; not via transcription/stability)	Adaptive	Reduced hypoxia tolerance	Pancreatic cancer study: emodin decreases HIF-1α by decreasing biosynthesis (explicit mechanism stated).	(ref)
8	Aerobic glycolysis (Warburg output)	↓ glycolysis (↓ ECAR / ↓ glycolytic dependence)	Phenotypic	Metabolic suppression	Renal cancer paper reports emodin inhibits aerobic glycolysis (and links killing to a non-apoptotic death mode in that model).	(ref)
9	HDAC inhibition (epigenetic enzyme activity)	↓ HDAC activity	Secondary	Epigenetic modulation	Direct biochemical evidence: emodin inhibits HDAC activity in vitro (fast-on/slow-off kinetics reported).	(ref)
10	NRF2 / HO-1 antioxidant response	↑ NRF2 / ↑ HO-1 (context-dependent stress response)	Adaptive	Counter-response to redox stress	HCC model reports emodin increases NRF2 and HO-1 expression; interpret as adaptive/compensatory (not necessarily the cytotoxic driver).	(ref)

ATM, similar to Serine-protein kinase ATM (Ataxia telangiectasia mutated) (A-T, mutated); ataxia telangiectasia mutated: Click to Expand ⟱

Source: CGL-Driver Genes

Type: TSG

ATM is considered a moderate cancer risk gene. A mutation in a moderate risk gene is just one risk factor that can contribute to cancer development. ATM has traditionally been assigned the role of a tumor suppressor. However, in both humans and mice, lymphoma and leukemia are the only clear-cut examples of cancer development caused by ATM deficiency(13). Its roles in other types of cancer, especially solid tumors, are much less clear.
ATM, a master regulator of DNA damage response.

Scientific Papers found: Click to Expand⟱

1326-

EMD,

Emodin induces a reactive oxygen species-dependent and ATM-p53-Bax mediated cytotoxicity in lung cancer cells

in-vitro,

Lung,

A549

Apoptosis↑, ROS↑, P53↑, BAX↑, ATM↑,

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,

Cell Death ⓘ

Apoptosis↑, 1, BAX↑, 1,

DNA Damage & Repair ⓘ

ATM↑, 1, P53↑, 1,
Total Targets: 5

Pathway results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: ATM, similar to Serine-protein kinase ATM (Ataxia telangiectasia mutated) (A-T, mutated); ataxia telangiectasia mutated

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