lipidDe Cancer Research Results

lipidDe, Lipid Deposition: Click to Expand ⟱
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Lipid deposition refers to the process by which lipids (fats) accumulate in tissues.

Key Markers Implicated in Lipid Deposition with Prognostic Relevance
Fatty Acid Synthase (FASN):key enzyme in de novo lipogenesis, catalyzing the synthesis of palmitate.
-Frequently overexpressed in cancers, associated with aggressive tumor behavior, resistance to therapy, and poorer overall survival.

SREBP-1: A transcription factor that upregulates lipogenic genes (including FASN, ACC, and SCD1).
-Overactive in various cancers, correlates with enhanced lipogenesis, increased proliferation, and worse prognosis.

ACC:Catalyzes the conversion of acetyl-CoA to malonyl-CoA, a crucial step in fatty acid synthesis.
-Overactivity may contribute to increased lipid deposition in tumors, promoting growth and associated with poor outcomes.

SCD1: Catalyzes the desaturation of saturated fatty acids to monounsaturated fatty acids, important for membrane fluidity and signaling.
-Upregulated in cancers, linked to tumor progression, resistance to apoptosis, and a poorer prognosis.

CD36: A fatty acid translocase that facilitates the uptake of long-chain fatty acids and is involved in lipid storage.
-Overexpression in various cancer, associated with metastatic potential and worse clinical outcomes.

FABPs, (FABP4 and FABP5): Intracellular lipid chaperones that help transport fatty acids and other lipids within cells.
-Typically Increased expression in cancers, may correlate with increased lipid uptake/storage, contributing to tumor aggressiveness and poorer survival in some cancer types.

Lipid Droplet–Associated Proteins (Perilipins PLIN2 and PLIN3)
-Involved in the formation and regulation of lipid droplets, which serve as intracellular lipid storage organelles.
-Increased lipid droplet accumulation has been linked to chemotherapy resistance and a worse prognosis in certain cancers.
Tumor cells exploit lipid deposition to:
-Buffer oxidative stress
-Supply membranes for rapid proliferation
-Survive nutrient-poor or hypoxic environments


Scientific Papers found: Click to Expand⟱
2389- BA,    Baicalin alleviates lipid accumulation in adipocytes via inducing metabolic reprogramming and targeting Adenosine A1 receptor
- in-vitro, Obesity, 3T3
*ECAR↑, Baicalin promoted metabolic reprogramming in 3T3-L1 preadipocytes, characterized by increased ECAR and decreased OCR
*OCR↓,
*p‑AMPK↑, baicalin significantly altered cellular respiration by reducing mitochondrial oxygen consumption while enhancing glycolytic flux, accompanied by increased phosphorylation of AMPK and ACC, suggesting an adaptation to altered energy availability.
*p‑ACC↑,
*Glycolysis↑, significant enrichment in metabolic pathways such as glycolysis, gluconeogenesis, and lipid metabolism.
*lipidDe↓, inhibited the maturation of sterol regulatory element binding protein 1 (SREBP1) and finally alleviated lipid deposition.
*SREBP1↓,
*FAO↑, baicalin induces metabolic reprogramming of adipocytes by inhibiting glucose aerobic metabolism while enhancing anaerobic glycolysis and FAO.
*HK2↑, baicalin upregulated glycolytic enzymes, such as HK1, HK2, PKM2, and LDHA, while downregulating pyruvate dehydrogenase,
*PKM2↑,
*LDHA↑,
*PDKs↓,
*ACC↓, leading to decreased acetyl-CoA production and enhanced fatty acid β-oxidation.

1586- Citrate,    Extracellular Citrate Is a Trojan Horse for Cancer Cells
- in-vitro, Liver, HepG2
Dose?, At low concentration, citrate increased both histone H4 acetylation and lipid deposition; at high concentration, citrate inhibited both
ac‑H4↓,
lipidDe↓,
ACLY↓, Considering the strong demand for acetyl-CoA but not for OAA in tumor cells, the exogenous citrate would behave like a trojan horse that carries OAA inside the cells and reduces ACLY expression and cellular metabolism.
selectivity↑, in non-tumor cells, changes of acetylated histone level do not correspond to a change of ACLY expression, as instead shown by HepG2 cells.
*ACLY∅, In contrast, ACLY expression in IHH (normal)cells was not modified after citrate exposure, suggesting that, in this case, ACLY expression was not regulated by histone H4 acetylation
Glycolysis↓, strong inhibition of glycolysis, which leads to a decrease in NADH necessary for OAA reduction
NADH↓,
OAA↑, exogenous citrate would behave like a trojan horse that releases OAA in the cells, where it could exert its therapeutic effect also on hepatoma cells.
other↑, most important discovery is undoubtedly the demonstration that high concentrations of citrate decrease the availability of acetyl-CoA, a key molecule both in the metabolism of sugars and lipids


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

lipidDe↓, 1,   NADH↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACLY↓, 1,   Glycolysis↓, 1,   OAA↑, 1,  

Transcription & Epigenetics ⓘ

ac‑H4↓, 1,   other↑, 1,  

Drug Metabolism & Resistance ⓘ

Dose?, 1,   selectivity↑, 1,  
Total Targets: 9

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

lipidDe↓, 1,  

Mitochondria & Bioenergetics ⓘ

OCR↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACC↓, 1,   p‑ACC↑, 1,   ACLY∅, 1,   p‑AMPK↑, 1,   ECAR↑, 1,   FAO↑, 1,   Glycolysis↑, 1,   HK2↑, 1,   LDHA↑, 1,   PDKs↓, 1,   PKM2↑, 1,   SREBP1↓, 1,  
Total Targets: 14

Scientific Paper Hit Count for: lipidDe, Lipid Deposition
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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1147  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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