SREBP1/SREBF1 Cancer Research Results

SREBP1/SREBF1, sterol regulatory element-binding protein 1: Click to Expand ⟱
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SREBP1 is a key transcription factor that regulates genes involved in fatty acid and triglyceride synthesis. It primarily governs lipid metabolism by controlling the expression of enzymes required for de novo lipogenesis, such as fatty acid synthase (FASN) and acetyl-CoA carboxylase (ACC), among others.
Two main isoforms—SREBP1a and SREBP1c—with SREBP1c being more involved in the regulation of lipogenesis in metabolic tissues.

Many cancers display elevated levels of SREBP1 activity. Increased expression or activation of SREBP1 supports the metabolic reprogramming that is characteristic of cancer cells, enabling them to meet the enhanced lipid requirements for membrane synthesis and energy storage during rapid cell proliferation.
Elevated SREBP1 activity is often linked to more aggressive cancer phenotypes. High SREBP1 levels can drive rapid proliferation, metastasis, and resistance to certain therapies, thereby correlating with poorer clinical outcomes in several cancers.

SREBF1 - Sterol Regulatory Element-Binding Transcription Factor 1 / SREBP-1

Abbreviation: SREBF1, SREBP-1, SREBP1

Type: Lipogenic transcription factor / basic helix-loop-helix leucine zipper transcription factor

Function: SREBF1 encodes SREBP-1, a master regulator of fatty-acid synthesis, lipid homeostasis, and metabolic gene expression. SREBP-1 is synthesized as an inactive endoplasmic-reticulum membrane precursor and, following SCAP-dependent processing and proteolytic cleavage, its active N-terminal transcription factor enters the nucleus. SREBP-1 regulates genes involved in de novo lipogenesis including FASN, ACACA/ACC, SCD1, and ACLY. The SREBF1 gene produces the SREBP-1a and SREBP-1c isoforms.

Cancer: ↑ Frequently increased or activated in cancer. Elevated SREBP-1 promotes de novo fatty-acid synthesis and metabolic reprogramming required for rapid tumor-cell proliferation. SREBP-1 can also promote survival, epithelial-mesenchymal transition, invasion, metastasis, tumor-microenvironment adaptation, ferroptosis resistance, and resistance to chemotherapy and radiotherapy. Genetic or pharmacological inhibition of SREBP-1 suppresses tumor growth in multiple preclinical cancer models.
Scientific Papers found: Click to Expand⟱
7636- Ins,    Myo-Inositol: Pharmacokinetics, Biological Functions, and Therapeutic Potential in Liver Protection: Insights from Preclinical Models
*glucose↝, Myo-inositol, the most common stereoisomer of inositol, plays an important role in many physiological processes, such as cell signaling, regulation of glucose and lipid metabolism, and protection of cells against oxidative stress.
*lipid-P↓,
*ROS↓,
*BioAv↑, characterized by high oral bioavailability and is primarily eliminated via the kidneys.
*hepatoP↑, Preclinical studies have shown that myo-inositol has hepatoprotective potential, reducing oxidative stress, inflammation, and lipid accumulation in hepatocytes,
*Inflam↓,
*MMP↑, Recent findings suggest that it contributes to the stabilization of mitochondrial membranes and enhances ATP production efficiency,
*ATP↑,
*GutMicro↑, Evidence indicates that myo-inositol may influence intestinal microbiota composition, enhancing populations of beneficial bacterial strains while reducing endotoxemia linked to non-alcoholic fatty liver disease
*Dose↝, a significant portion of the body’s requirement is also supplied by the diet-rich sources, including fruits, whole grains, legumes, and nuts.
*Half-Life↝, Studies on rats has revealed that the highest plasma concentrations were observed within 1–2 h after oral intake, while the half-life ranged from 4 to 8 h.
*BioAv↑, In the case of intravenous administration, higher bioavailability and faster tissue distribution were achieved. intravenous administration of myo-inositol is rare
*eff↑, myo-inositol supplementation may potentially synergize with antioxidants (e.g., vitamin E, curcumin), enhancing their protective effects on the liver and other organs exposed to oxidative stress
*hepatoP↑, Myo-inositol may exert hepatoprotective effects through several biological mechanisms. A key role is played by its involvement in lipid metabolism regulation, modulation of oxidative stress, and influence on insulin signaling.
*SOD↑, Moreover, myo-inositol and its derivatives (including D-chiro-inositol) affect the activation of antioxidant enzymes such as superoxide dismutase (SOD) and catalase, thereby limiting oxidative damage to hepatocytes
*Catalase↑,
*Casp3↓, inhibit the expression of apoptosis markers such as caspase-3,
*ALAT↓, decreased activity of transaminases (ALT, AST).
*AST↓,
*AMPK↑, regulation of lipid metabolism through the activation of AMP-activated protein kinase (AMPK) and downregulation of sterol regulatory element-binding proteins (SREBPs).
*SREBP1/SREBF1↑,
*NA↑,


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:


Total Targets: 0

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

NA↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↑, 1,   lipid-P↓, 1,   ROS↓, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 1,   MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   AMPK↑, 1,   glucose↝, 1,   SREBP1/SREBF1↑, 1,  

Cell Death(tgid=5) ⓘ

Casp3↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 2,   Dose↝, 1,   eff↑, 1,   Half-Life↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   GutMicro↑, 1,  

Functional Outcomes(tgid=23) ⓘ

hepatoP↑, 2,  
Total Targets: 21

Scientific Paper Hit Count for: SREBP1/SREBF1, sterol regulatory element-binding protein 1
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#:1034  State#:%  Dir#:2
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