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↓,

6683- DCA,    Dichloroacetate for Cancer Treatment: Some Facts and Many Doubts
- Review, Var, NA
PDK1↓, classic DCA target, pyruvate dehydrogenase kinase
lactateProd↓, reduce lactic acid production which would push the cell towards oxidative phosphorylation: this would be the supposed function of dichloroacetate (DCA).
Apoptosis↑, They found that DCA induced apoptosis and decreased proliferation by restoring mitochondrial oxidative metabolism, without toxicity to normal cells.
TumCP↓,
selectivity↑,
other↝, many clinics, usually called “DCA Clinics” have opened, mainly in Canada and Germany.
Dose↝, DCA is sold over the counter and is produced by many laboratories. The quality of the product from these laboratories is not well established. These particulars explain many of the doubts about DCA’s real value as a therapeutic tool.
BioAv↑, DCA is an orally available molecule that is quickly and almost completely absorbed by the digestive system
Half-Life↓, With a 10 mg/kg infusion the maximum plasma concentration achieved was between 19.9 μg/ml and 24.7 μg/ml with a half life of only 20 minutes. If the infused dose was increased to 20 mg/kg the plasma concentration was between 57.3 and 74.9 μg/ml with
Glycolysis↓, facilitates the switch from a glycolytic to an oxidative metabolism.
OXPHOS↑,
Casp↑, onversion to an oxidative metabolism by DCA, is an increase in caspase-mediated apoptosis
i-pH↓, pHi decreases (at least temporarily).
COX2↑, DCA increases the expression of COX2 and the latter increases tumor resistance to DCA. Therefore, a possible integrated treatment could be COX2 inhibitor co-administered with DCA
Hif1a↓, DCA suppresses HIF-1α activity and angiogenesis through the inhibition of PDK-II
angioG↓,
HMG-CoA↓, figure 7
GSTZ1↓,
OCR↑,
lipoGen↓,
fatigue↓,
survivin↓, Survivin (an inhibitor of apoptosis) expression was decreased and miR-375 (a microRNA which acts as a tumor suppressor) levels were increased.
miR-375↑,
eff↓, African Americans are known to respond poorly to therapy compared with Caucasian American patients.
CSCs↓, DCA can inhibit the cancer stem cell like characteristics of the cells and strongly influenced the metabolic pathway of the cells causing a shift from glycolysis to oxidative phosphorylation.
TumAuto↑, DCA induced autophagy in human colon cancer cells with ROS production and mTOR inhibition,
mTOR↓,
TumCI↓, DCA induced apoptosis, inhibited invasion, and angiogenesis. In mouse experiments in vivo with the melanoma allografts, DCA reduced volume and weight of tumors.
TumVol↓,
TumW↓,
ATP↓, DCA alone reduced glycolytic activity and intracellular ATP levels and inhibited cellular growth in melanoma cells.
Warburg↓, DCA was also found to interrupt the Warburg effect and decreased proliferation.
eff↑, The co-application of metformin and DCA suppressed human liver cancer cell proliferation inducing apoptosis through inhibition of mTORC1 and increased ROS in vitro and in vivo
e-pH↑, when measuring extracellular pH in vivo found that an initial increase in extracellular pH of tumors in mice when treated with DCA.
eff↑, To avoid the development of this type of metabolic resistance DCA should be given simultaneously with other metabolic drugs such as metformin [327] or 2 deoxyglucose.
eff↑, chronic co-administration of DCA with sodium bicarbonate to tumor bearing mice prolonged survival
other↝, High doses of thiamin (vit B1) have effects similar to those of DCA: reduced PDH phosphorylation, reduced lactate prod and increased casp3 activity with reduced proliferation in colon cancer cells. can vitB1 replace DCA as a nontoxic PDK inhibitor?
RadioS↑, Dong et al. [380] found that DCA radiosensitized esophageal carcinoma cells in vitro and in vivo through increased ROS accumulation.
toxicity↓, 25 mg/Kg/day may show a mild sedative effect or drowsiness. The most serious published side effect is reversible peripheral neuropathy
Dose↝, 10 to 50 mg/kg body weight/day has been found to be a safe dose. However, single nucleotide polymorphisms (SNPs) in the gene of the enzyme GSTZ1 cause difficulties in establishing a universal dose [409] as noted above.
eff↑, There is strong evidence showing that the association of metformin and DCA has significant cytotoxic effects.
eff↑, To this approach we must add a third compound: a COX2 inhibitor like celecoxib to decrease COX2 expression induced by DCA.
eff↑, the triple association of DCA, metformin and celecoxib, which has never been experimentally tested in patients, deserves well planned phase II clinical trials.
toxicity↝, DCA will never become a stand-alone chemotherapeutic compound. The fundamental reason for this statement is that the drug can only reach micromolar blood concentrations without toxicity and requires millimolar levels to be cytotoxic.
eff↓, DCA should not be used in association with allopurinol, NSAIDs, or flavonoids because they reduce cellular DCA uptake.

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 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

miR-375↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

GSTZ1↓, 1,   OXPHOS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↓, 2,   mtDam↑, 1,   OCR↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACC↓, 1,   ACLY↓, 2,   AMPK↑, 1,   CRM↑, 1,   FASN↓, 2,   Glycolysis↓, 1,   HMG-CoA↓, 1,   lactateProd↓, 1,   lipoGen↓, 6,   PDK1↓, 1,   Warburg↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 3,   Casp↑, 1,   survivin↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 2,   tumCV↓, 2,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 2,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CSCs↓, 1,   mTOR↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

TumCI↓, 2,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↑, 1,   Inflam↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

e-pH↑, 1,   i-pH↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   Dose↝, 2,   eff↓, 2,   eff↑, 7,   Half-Life↓, 1,   RadioS↑, 1,   selectivity↑, 1,  

Functional Outcomes(tgid=23) ⓘ

fatigue↓, 1,   toxicity↓, 1,   toxicity↝, 1,   toxicity∅, 1,   TumVol↓, 1,   TumW↓, 1,   Weight↓, 1,  
Total Targets: 49

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

CYP2E1↓, 1,   NRF2↑, 1,   ROS↓, 3,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

OCR↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

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

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

HDAC↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   Half-Life↑, 2,  

Functional Outcomes(tgid=23) ⓘ

toxicity∅, 1,  
Total Targets: 14

Scientific Paper Hit Count for: lipoGen, lipogenesis
2 HydroxyCitric Acid
1 Cannabidiol
1 Dichloroacetate
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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