PPARγ Cancer Research Results

PPARγ, Peroxisome proliferator-activated receptor gamma (PPAR-γ or PPARG): Click to Expand ⟱
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Type:
Peroxisome proliferator-activated receptor gamma (PPAR-γ) is a type of nuclear receptor that plays a crucial role in regulating various biological processes, including glucose metabolism, lipid metabolism, and inflammation. It is primarily expressed in adipose tissue, but it is also found in other tissues, including the colon, breast, and prostate.
PPAR-γ has been shown to have both tumor-suppressive and tumor-promoting effects, depending on the type of cancer and the context. In some cancers, activation of PPAR-γ can inhibit cell proliferation and induce apoptosis, while in others, it may promote tumor growth.
PPARγ
– Plays a central role in adipogenesis, lipid storage, and insulin sensitivity.
– Widely expressed in adipose tissue, but also present in colon, breast, and immune cells.
– In addition to metabolic functions, PPARγ regulates cell differentiation, apoptosis, and has anti-inflammatory effects.
– Ligand binding (such as endogenous fatty acids or synthetic agonists like thiazolidinediones) alters transcriptional programs impacting cell cycle and survival.

– In many cases, PPARγ is expressed in tumor cells, and its activation has been linked to induction of differentiation and growth arrest.
– However, expression levels can differ based on tumor subtype, with some studies reporting elevated levels while others note reductions in aggressive tumors.
– Crosstalk with other signaling pathways (e.g., Wnt/β-catenin, MAPK) can alter PPARγ's net effect in cancer cells.
Var, Various Cancer: Click to Expand ⟱
Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.


Scientific Papers found: Click to Expand⟱
3383- ART/DHA,    Dihydroartemisinin: A Potential Natural Anticancer Drug
- Review, Var, NA
TumCP↓, Apoptosis↑, TumMeta↓, angioG↓, TumAuto↑, ER Stress↑, ROS↑, Ca+2↑, p38↑, HSP70/HSPA5↓, PPARγ↑, GLUT1↓, Glycolysis↓, PI3K↓, Akt↓, Hif1a↓, PKM2↓, lactateProd↓, GlucoseCon↓, EMT↓, Slug↓, Zeb1↓, ZEB2↓, Twist↓, Snail?, CAFs/TAFs↓, TGF-β↓, p‑STAT3↓, M2 MC↓, uPA↓, HH↓, AXL↓, VEGFR2↓, JNK↑, Beclin-1↑, GRP78/BiP↑, eff↑, eff↑, eff↑, eff↑, eff↑, eff↑, IL4↓, DR5↑, Cyt‑c↑, Fas↑, FADD↑, cl‑PARP↑, cycE/CCNE↓, CDK2↓, CDK4↓, Mcl-1↓, Ki-67↓, Bcl-2↓, CDK6↓, VEGF↓, COX2↓, MMP9↓,
2615- Ba,    The Multifaceted Role of Baicalein in Cancer Management through Modulation of Cell Signalling Pathways
- Review, Var, NA
*AntiCan↓, *Inflam↓, TumCP↓, NF-kB↓, PPARγ↑, TumCCA↑, JAK2↓, STAT3↓, TumCMig↓, Glycolysis↓, MMP2↓, MMP9↓, selectivity↑, VEGF↓, Hif1a↓, cMyc↓, ChemoSen↑, ROS↑, p‑mTOR↓, PTEN↑,
5859- CAP,    Are We Ready to Recommend Capsaicin for Disorders Other Than Neuropathic Pain?
- Review, Var, NA
*TRPV1↑, *Ca+2↑, *Na+↑, *UCPs↑, *SIRT1↑, *PPARγ↑, *Inflam↓, *lipid-P↑, *IL6↓, *TNF-α↓, *NF-kB↓, *p‑Akt↑, *NRF2↑, *HO-1↑, *ROS↑, *GutMicro↑,
2894- HNK,    Pharmacological features, health benefits and clinical implications of honokiol
- Review, Var, NA - Review, AD, NA
*BioAv↓, *neuroP↑, *BBB↑, *ROS↓, *Keap1↑, *NRF2↑, *Casp3↓, *SIRT3↑, *Rho↓, *ERK↓, *NF-kB↓, angioG↓, RAS↓, PI3K↓, Akt↓, mTOR↓, *memory↑, *Aβ↓, *PPARγ↑, *PGC-1α↑, NF-kB↓, Hif1a↓, VEGF↓, HO-1↓, FOXM1↓, p27↑, P21↑, CDK2↓, CDK4↓, CDK6↓, cycD1/CCND1↓, Twist↓, MMP2↓, Rho↑, ROCK1↑, TumCMig↓, cFLIP↓, BMPs↑, OCR↑, ECAR↓, *AntiAg↑, *cardioP↑, *antiOx↑, *ROS↓, P-gp↓,
3277- Lyco,    Recent trends and advances in the epidemiology, synergism, and delivery system of lycopene as an anti-cancer agent
- Review, Var, NA
antiOx↑, TumCP↓, Apoptosis↑, TumMeta↑, ChemoSen↑, BioAv↓, Dose↝, BioAv↓, BioAv↑, SOD↑, Catalase↑, GPx↑, IL2↑, IL4↑, IL1↑, TNF-α↑, GSH↑, GPx↑, GSTA1↑, GSR↑, PPARγ↑, Casp3↑, NF-kB↓, COX2↓, Bcl-2↑, BAX↓, P53↓, CHK1↓, Chk2↓, γH2AX↓, DNAdam↓, ROS↓, P21↑, PCNA↓, β-catenin/ZEB1↓, PGE2↓, ERK↓, cMyc↓, cycE/CCNE↓, JAK1↓, STAT3↓, SIRT1↑, cl‑PARP↑, cycD1/CCND1↓, TNF-α↓, IL6↓, p65↓, MMP2↓, MMP9↓, Wnt↓,
1708- Lyco,    The Anti-Cancer Activity of Lycopene: A Systematic Review of Human and Animal Studies
- Review, Var, NA
OS↑, ChemoSen↑, QoL↑, PSA∅, eff↑, AntiCan↑, AntiCan↑, angioG↓, VEGF↓, Hif1a↓, SOD↑, Catalase↑, GPx↑, GSH↑, GPx↑, GR↑, MDA↓, NRF2↑, HO-1↑, COX2↓, PGE2↓, NF-kB↓, IL4↑, IL10↑, IL6↓, TNF-α↓, PPARγ↑, TumCCA↑, FOXO3↓, Casp3↑, IGF-1↓, p27↑, STAT3↓, CDK2↓, CDK4↓, P21↑, PCNA↓, MMP7↓, MMP9↓,
4791- Lyco,    Investigating into anti-cancer potential of lycopene: Molecular targets
- Review, Var, NA
*antiOx↑, TumCP↓, TumCCA↓, Apoptosis↑, TumCI↓, angioG↓, TumMeta↓, *Risk↓, cycD1/CCND1↓, CycD3↓, cycE/CCNE↓, CDK2↓, CDK4↓, Bcl-2↓, P21↑, p27↑, P53↑, BAX↑, selectivity↑, MMP↓, Cyt‑c↑, Wnt↓, eff↑, PPARγ↑, LDL↓, Akt↓, PI3K↓, mTOR↓, PDGF↓, NF-kB↓, eff↑,
5252- MAG,    Insights on the Multifunctional Activities of Magnolol
- Review, Var, NA
BioAv↓, *Inflam↓, *Bacteria↓, *antiOx↑, *neuroP↑, *cardioP↑, CYP1A1↓, *PPARγ↑, *NF-kB↓, *COX2↓, *iNOS↓, *ROS↓, Apoptosis↑, TumCCA↑, cycD1/CCND1↓, cycA1/CCNA1↓, CDK2↓, P21↑, TumCG↓, TumCMig↓, TumCI↓, Ki-67↓, PCNA↓, MMP2↓, MMP9↓, MMP7↓, DNAdam↑, MMP↓, TumCP↓, selectivity↑, PI3K↓, Akt↓, H2O2↓, Hif1a↓, *BDNF↑, *NRF2↑, *AChE↑,
4643- OLE,  HT,    Use of Oleuropein and Hydroxytyrosol for Cancer Prevention and Treatment: Considerations about How Bioavailability and Metabolism Impact Their Adoption in Clinical Routine
- Review, Var, NA
TumCCA↑, Apoptosis↑, ER Stress↑, UPR↑, CHOP↑, ROS↑, Bcl-2↓, NOX4↑, Hif1a↓, MMP2↓, MMP↓, VEGF↓, Akt↓, NF-kB↓, p65↓, SIRT3↓, mTOR↓, Catalase↓, SOD2↓, FASN↓, STAT3↓, HDAC2↓, HDAC3↓, BAD↑, BAX↑, Bak↑, Casp3↑, Casp9↑, PARP↑, P53↑, P21↑, p27↑, Half-Life↝, BioAv↓, BioAv↓, selectivity↑, RadioS↑, *ROS↓, *GSH↑, *MDA↓, *SOD↑, *Catalase↑, *NRF2↑, *chemoP↑, *Inflam↓, PPARγ↑,
2124- TQ,    Thymoquinone: an emerging natural drug with a wide range of medical applications
- Review, Var, NA
hepatoP↑, Bax:Bcl2↑, cycD1/CCND1↓, P21↑, TRAIL↑, P53↑, TumCCA↑, hepatoP↑, *ALAT↓, *AST↓, *MDA↓, *GSSG↓, *COX2↓, *lipid-P↓, PPARγ↑, p38↑, ROS↑, ChemoSen↑, selectivity↑, selectivity↑, *MDA↓, *SOD↑,

Showing Research Papers: 1 to 10 of 10

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↓, 1,   Catalase↑, 2,   CYP1A1↓, 1,   GPx↑, 4,   GSH↑, 2,   GSR↑, 1,   GSTA1↑, 1,   H2O2↓, 1,   HO-1↓, 1,   HO-1↑, 1,   MDA↓, 1,   NOX4↑, 1,   NRF2↑, 1,   ROS↓, 1,   ROS↑, 4,   SIRT3↓, 1,   SOD↑, 2,   SOD2↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 3,   OCR↑, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 2,   ECAR↓, 1,   FASN↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 2,   lactateProd↓, 1,   LDL↓, 1,   PKM2↓, 1,   PPARγ↑, 7,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 5,   Apoptosis↑, 5,   BAD↑, 1,   Bak↑, 1,   BAX↓, 1,   BAX↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 3,   Bcl-2↑, 1,   Casp3↑, 3,   Casp9↑, 1,   cFLIP↓, 1,   Chk2↓, 1,   Cyt‑c↑, 2,   DR5↑, 1,   FADD↑, 1,   Fas↑, 1,   JNK↑, 1,   Mcl-1↓, 1,   p27↑, 4,   p38↑, 2,   TRAIL↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 2,   GRP78/BiP↑, 1,   HSP70/HSPA5↓, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   DNAdam↓, 1,   DNAdam↑, 1,   P53↓, 1,   P53↑, 3,   PARP↑, 1,   cl‑PARP↑, 2,   PCNA↓, 3,   γH2AX↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 5,   CDK4↓, 4,   cycA1/CCNA1↓, 1,   cycD1/CCND1↓, 5,   CycD3↓, 1,   cycE/CCNE↓, 3,   P21↑, 7,   TumCCA↓, 1,   TumCCA↑, 5,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   ERK↓, 1,   FOXM1↓, 1,   FOXO3↓, 1,   HDAC2↓, 1,   HDAC3↓, 1,   HH↓, 1,   IGF-1↓, 1,   mTOR↓, 3,   p‑mTOR↓, 1,   PI3K↓, 4,   PTEN↑, 1,   RAS↓, 1,   STAT3↓, 4,   p‑STAT3↓, 1,   TumCG↓, 1,   Wnt↓, 2,  

Migration ⓘ

AXL↓, 1,   Ca+2↑, 1,   CAFs/TAFs↓, 1,   Ki-67↓, 2,   MMP2↓, 5,   MMP7↓, 2,   MMP9↓, 5,   PDGF↓, 1,   Rho↑, 1,   ROCK1↑, 1,   Slug↓, 1,   Snail?, 1,   TGF-β↓, 1,   TumCI↓, 2,   TumCMig↓, 3,   TumCP↓, 5,   TumMeta↓, 2,   TumMeta↑, 1,   Twist↓, 2,   uPA↓, 1,   Zeb1↓, 1,   ZEB2↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 4,   Hif1a↓, 6,   VEGF↓, 5,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   IL1↑, 1,   IL10↑, 1,   IL2↑, 1,   IL4↓, 1,   IL4↑, 2,   IL6↓, 2,   JAK1↓, 1,   JAK2↓, 1,   M2 MC↓, 1,   NF-kB↓, 6,   p65↓, 2,   PGE2↓, 2,   PSA∅, 1,   TNF-α↓, 2,   TNF-α↑, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 2,   GR↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 5,   BioAv↑, 1,   ChemoSen↑, 4,   Dose↝, 1,   eff↑, 9,   Half-Life↝, 1,   RadioS↑, 1,   selectivity↑, 6,  

Clinical Biomarkers ⓘ

BMPs↑, 1,   FOXM1↓, 1,   IL6↓, 2,   Ki-67↓, 2,   PSA∅, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   hepatoP↑, 2,   OS↑, 1,   QoL↑, 1,  
Total Targets: 159

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 3,   Catalase↑, 1,   GSH↑, 1,   GSSG↓, 1,   HO-1↑, 1,   Keap1↑, 1,   lipid-P↓, 1,   lipid-P↑, 1,   MDA↓, 3,   NRF2↑, 4,   ROS↓, 4,   ROS↑, 1,   SIRT3↑, 1,   SOD↑, 2,   UCPs↑, 1,  

Mitochondria & Bioenergetics ⓘ

PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   PPARγ↑, 3,   SIRT1↑, 1,  

Cell Death ⓘ

p‑Akt↑, 1,   Casp3↓, 1,   iNOS↓, 1,   TRPV1↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,  

Migration ⓘ

AntiAg↑, 1,   Ca+2↑, 1,   Na+↑, 1,   Rho↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,   Na+↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   IL6↓, 1,   Inflam↓, 4,   NF-kB↓, 3,   TNF-α↓, 1,  

Synaptic & Neurotransmission ⓘ

AChE↑, 1,   BDNF↑, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↓, 1,   cardioP↑, 2,   chemoP↑, 1,   memory↑, 1,   neuroP↑, 2,   Risk↓, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 50

Scientific Paper Hit Count for: PPARγ, Peroxisome proliferator-activated receptor gamma (PPAR-γ or PPARG)
3 Lycopene
1 Artemisinin
1 Baicalein
1 Capsaicin
1 Honokiol
1 Magnolol
1 Oleuropein
1 HydroxyTyrosol
1 Thymoquinone
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:26  Cells:%  prod#:%  Target#:259  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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