lipoGen Cancer Research Results

lipoGen, lipogenesis: Click to Expand ⟱
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Lipogenesis is the metabolic process by which simple substrates like acetyl-CoA are converted into fatty acids, which are then assembled into complex lipids. This process is essential for producing cell membranes, signaling molecules, and energy storage forms, such as triglycerides. In normal physiology, lipogenesis is tightly regulated by nutritional and hormonal signals to meet the needs of different tissues.
Key enzymes (e.g. acetyl-CoA carboxylase [ACC], fatty acid synthase [FASN]) involved in lipogenesis. Several enzymes play critical roles in lipogenesis, including acetyl-CoA carboxylase (ACC), which catalyzes the rate-limiting formation of malonyl-CoA, and fatty acid synthase (FASN), which catalyzes the assembly of fatty acids. Transcription factors such as SREBP1 (sterol regulatory element-binding protein 1) also regulate the expression of lipogenic genes.

Cancer cells often upregulate lipogenesis, even under conditions where normal cells might rely on dietary fat. This metabolic reprogramming supports rapid cell proliferation by providing the necessary lipids for new cellular membranes and energy storage. Elevated activity of enzymes like ACC and FASN is frequently observed in tumors.
High lipogenic activity in tumors has been correlated with aggressive phenotypes. Elevated expression of lipogenic enzymes is often associated with increased cell proliferation, invasion, and resistance to apoptosis. Consequently, tumors showing robust lipogenesis may be linked to poorer overall prognosis.
Scientific Papers found: Click to Expand⟱
1199- CBD,    Cannabidiol improves muscular lipid profile by affecting the expression of fatty acid transporters and inhibiting de novo lipogenesis
- in-vivo, Obesity, NA
lipoGen↓,

3241- EGCG,    Epigallocatechin gallate triggers apoptosis by suppressing de novo lipogenesis in colorectal carcinoma cells
- in-vitro, CRC, HCT116 - in-vitro, CRC, HT29 - in-vitro, Liver, HepG2 - in-vitro, Liver, HUH7
tumCV↓, EGCG treatment decreased cell viability and increased mitochondrial damage‐triggered apoptosis in both HCT116 and HT‐29 cancer cells
mtDam↑,
Apoptosis↑,
ATP↓, Suppression of ATP synthesis by EGCG
lipoGen↓, depletion of lipogenesis in the DNL pathway,
eff↑, Antiproliferative activity of EGCG and 5FU reduces tumor progression in a nude mouse xenograft model

1186- Gb,    Ginkgolic acid suppresses the development of pancreatic cancer by inhibiting pathways driving lipogenesis
- in-vitro, PC, NA - in-vitro, Nor, HUVECs - in-vivo, PC, NA
tumCV↓,
*toxicity∅, little toxicity on normal cells, e.g, HUVEC cells
TumCMig↓,
TumCI↓,
Apoptosis↑,
AMPK↑,
lipoGen↓,
ACC↓,
FASN↓,

1625- HCA,    In S. cerevisiae hydroxycitric acid antagonizes chronological aging and apoptosis regardless of citrate lyase
- Review, Nor, NA
CRM↑, Hydroxycitric acid (HCA) is considered a bona fide CRM since it depletes acetyl-CoA pools by acting as a competitive inhibitor of ATP citrate lyase (ACLY), ultimately repressing protein acetylation and promoting autophagy.
ACLY↓, competitive inhibitor of ATP citrate lyase (ACLY)
TumAuto↑, promoting autophagy.
Inflam↓, reduce inflammation and tumour development
TumCG↓,
toxicity∅, HCA appear to have a low or negligible impact in terms of acute or chronic toxicity, genotoxicity, reproductive failure and teratogenicity
lipoGen↓, decreases lipogenesis, insulin resistance, inflammation and oxidative stress
*ROS↓, H2O2 treatment: Strikingly, the molecule was able to largely prevent the massive cell death (PI+ cells) caused by the intense oxidative stress. In parallel there was a sharp increase of live cells with high ROS levels
*OCR↓, chronic exposure to 5 mM HCA (from cell seeding) down-regulated yeast OCR

1630- HCA,    Chemistry and biochemistry of (-)-hydroxycitric acid from Garcinia
- Review, NA, NA
ACLY↓, HCA was shown to be a potent inhibitor of ATP citrate lyase
FASN↓, Extensive animal studies indicated that (-)-HCA suppresses the fatty acid synthesis, lipogenesis, food intake, and induced weight loss.
lipoGen↓,
Weight↓,

2052- PB,    Lipid-regulating properties of butyric acid and 4-phenylbutyric acid: Molecular mechanisms and therapeutic applications
- Review, NA, NA
*HDAC↓, BA appears to function as a histone deacetylase (HDAC) inhibitor while PBA acts as a chemical chaperone and/or a HDAC inhibitor.
*Half-Life↑, In humans, the plasma concentration of BA decreased quickly with a half-life of approximately 5 min once the infusion had ended
*Half-Life↑, The mean half-lives of PBA, PAA and PAGN in blood plasma were 0.7, 1.2 and 1.7 h, respectively, after an intravenous infusion of sodium phenylbutyrate to human subjects and 1, 1.8 and 2.8 h in serum, respectively, after an oral PB 9 to 45 g/day
*lipoGen↓, in vivo studies have shown that PBA ameliorated fructose-induced hepatosteatosis by inhibiting lipogenesis.
*ER Stress↓, PBA blocked fructose-driven expression of SREBP1c and its target genes by attenuating ER stres
*FAO↑, BA and PBA promote fatty acid β-oxidation
*ROS↓, Moreover, PBA prevented palmitate-induced autophagy-dependent reactive oxygen species (ROS) formation further supporting the protective role of PBA against lipotoxicity.
*BioAv↑, The absolute bioavailability of PBA averaged 78% in human subjects following the oral administrations of 9-45 g/day

1193- SM,    Cryptotanshinone from the Salvia miltiorrhiza Bunge Attenuates Ethanol-Induced Liver Injury by Activation of AMPK/SIRT1 and Nrf2 Signaling Pathways
- in-vivo, Alcohol, NA - in-vitro, Liver, HepG2
*p‑AMPK↑,
*SIRT1↑,
*NRF2↑,
*CYP2E1↓,
*lipoGen↓,
*ROS↓,
*Inflam↓,


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

ACC↓, 1,   ACLY↓, 2,   AMPK↑, 1,   CRM↑, 1,   FASN↓, 2,   lipoGen↓, 5,  

Cell Death ⓘ

Apoptosis↑, 2,  

Transcription & Epigenetics ⓘ

tumCV↓, 2,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Migration ⓘ

TumCI↓, 1,   TumCMig↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,  

Functional Outcomes ⓘ

toxicity∅, 1,   Weight↓, 1,  
Total Targets: 18

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

CYP2E1↓, 1,   NRF2↑, 1,   ROS↓, 3,  

Mitochondria & Bioenergetics ⓘ

OCR↓, 1,  

Core Metabolism/Glycolysis ⓘ

p‑AMPK↑, 1,   FAO↑, 1,   lipoGen↓, 2,   SIRT1↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   Half-Life↑, 2,  

Functional Outcomes ⓘ

toxicity∅, 1,  
Total Targets: 14

Scientific Paper Hit Count for: lipoGen, lipogenesis
2 HydroxyCitric Acid
1 Cannabidiol
1 EGCG (Epigallocatechin Gallate)
1 Ginkgo biloba
1 Phenylbutyrate
1 Salvia miltiorrhiza
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

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