PPARγ Cancer Research Results

PPARγ, Peroxisome proliferator-activated receptor gamma (PPAR-γ or PPARG): Click to Expand ⟱

Source:

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.

Scientific Papers found: Click to Expand⟱

3166-

Ash,

Exploring the Multifaceted Therapeutic Potential of Withaferin A and Its Derivatives

Review,

Var,

*p‑PPARγ↓, preventing the phosphorylation of peroxisome proliferator-activated receptors (PPARγ)
*cardioP↑, cardioprotective activity by AMP-activated protein kinase (AMPK) activation and suppressing mitochondrial apoptosis.
*AMPK↑,
*BioAv↝, The oral bioavailability was found to be 32.4 ± 4.8% after 5 mg/kg intravenous and 10 mg/kg oral WA administration.
*Half-Life↝, The stability studies of WA in gastric fluid, liver microsomes, and intestinal microflora solution showed similar results in male rats and humans with a half-life of 5.6 min.
*Half-Life↝, WA reduced quickly, and 27.1% left within 1 h
*Dose↑, WA showed that formulation at dose 4800 mg having equivalent to 216 mg of WA, was tolerated well without showing any dose-limiting toxicity.
*chemoPv↑, Here, we discuss the chemo-preventive effects of WA on multiple organs.
IL6↓, attenuates IL-6 in inducible (MCF-7 and MDA-MB-231)
STAT3↓, WA displayed downregulation of STAT3 transcriptional activity
ROS↓, associated with reactive oxygen species (ROS) generation, resulted in apoptosis of cells. The WA treatment decreases the oxidative phosphorylation
OXPHOS↓,
PCNA↓, uppresses human breast cells’ proliferation by decreasing the proliferating cell nuclear antigen (PCNA) expression
LDH↓, WA treatment decreases the lactate dehydrogenase (LDH) expression, increases AMP protein kinase activation, and reduces adenosine triphosphate
AMPK↑,
TumCCA↑, (SKOV3 andCaOV3), WA arrest the G2/M phase cell cycle
NOTCH3↓, It downregulated the Notch-3/Akt/Bcl-2 signaling mediated cell survival, thereby causing caspase-3 stimulation, which induces apoptosis.
Akt↓,
Bcl-2↓,
Casp3↑,
Apoptosis↑,
eff↑, Withaferin-A, combined with doxorubicin, and cisplatin at suboptimal dose generates ROS and causes cell death
NF-kB↓, reduces the cytosolic and nuclear levels of NF-κB-related phospho-p65 cytokines in xenografted tumors
CSCs↓, WA can be used as a pharmaceutical agent that effectively kills cancer stem cells (CSCs).
HSP90↓, WA inhibit Hsp90 chaperone activity, disrupting Hsp90 client proteins, thus showing antiproliferative effects
PI3K↓, WA inhibited PI3K/AKT pathway.
FOXO3↑, Par-4 and FOXO3A proapoptotic proteins were increased in Pten-KO mice supplemented with WA.
β-catenin/ZEB1↓, decreased pAKT expression and the β-catenin and N-cadherin epithelial-to-mesenchymal transition markers in WA-treated tumors control
N-cadherin↓,
EMT↓,
FASN↓, WA intraperitoneal administration (0.1 mg) resulted in significant suppression of circulatory free fatty acid and fatty acid synthase expression, ATP citrate lyase,
ACLY↓,
ROS↑, WA generates ROS followed by the activation of Nrf2, HO-1, NQO1 pathways, and upregulating the expression of the c-Jun-N-terminal kinase (JNK)
NRF2↑,
HO-1↑,
NQO1↑,
JNK↑,
mTOR↓, suppressing the mTOR/STAT3 pathway
neuroP↑, neuroprotective ability of WA (50 mg/kg b.w)
*TNF-α↓, WA attenuate the levels of neuroinflammatory mediators (TNF-α, IL-1β, and IL-6)
*IL1β↓,
*IL6↓,
*IL8↓, WA decreases the pro-inflammatory cytokines (IL-6, TNFα, IL-8, IL-18)
*IL18↓,
RadioS↑, radiosensitizing combination effect of WA and hyperthermia (HT) or radiotherapy (RT)
eff↑, WA and cisplatin at suboptimal dose generates ROS and causes cell death [41]. The actions of this combination is attributed by eradicating cells, revealing markers of cancer stem cells like CD34, CD44, Oct4, CD24, and CD117

2617-

Ba,

Potential of baicalein in the prevention and treatment of cancer: A scientometric analyses based review

Review,

Var,

Ca+2↑, MDA-MB-231 ↑Ca2+
MMP2↓, MDA-MB-231 ↓MMP-2/9
MMP9↓,
Vim↓, ↓Vimentin, ↓SNAIL, ↑E-cadherin, ↓Wnt1, ↓β-catenin
Snail↓,
E-cadherin↑,
Wnt↓,
β-catenin/ZEB1↓,
p‑Akt↓, MCF-7 ↓p-Akt, ↓p-mTOR, ↓NF-κB
p‑mTOR↓,
NF-kB↓,
i-ROS↑, MCF-7 ↑Intracellular ROS, ↓Bcl-2, ↑Bax, ↑cytochrome c, ↑caspase-3/9
Bcl-2↓,
BAX↑,
Cyt‑c↑,
Casp3↑,
Casp9↑,
STAT3↓, 4T1, MDA-MB-231 ↓STAT3, ↓ IL-6
IL6↓,
MMP2↓, HeLa ↓MMP-2, ↓MMP-9
MMP9↓,
NOTCH↓, ↓Notch 1
PPARγ↓, ↓PPARγ
p‑NRF2↓, HCT-116 ↓p-Nrf2
HK2↓, ↓HK2, ↓LDH-A, ↓PDK1, ↓glycolysis, PTEN/Akt/HIF-1α regulation
LDHA↓,
PDK1↓,
Glycolysis↓,
PTEN↑, Furthermore, baicalein inhibited hypoxia-induced Akt phosphorylation by promoting PTEN accumulation, thereby attenuating hypoxia-inducible factor-alpha ( HIF-1a) expression in AGS cells.
Akt↓,
Hif1a↓,
MMP↓, SGC-7901 ↓ΔΨm
VEGF↓, ↓VEGF, ↓VEGFR2
VEGFR2↓,
TOP2↓, ↓Topoisomerase II
uPA↓, ↓u-PA, ↓TIMP1, ↓TIMP2
TIMP1↓,
TIMP2↓,
cMyc↓, ↓β-catenin, ↓c-Myc, ↓cyclin D1, ↓Axin-2
TrxR↓, EL4 ↓Thioredoxin reductase, ↑ASK1,
ASK1↑,
Vim↓, ↓vimentin
ZO-1↑, ↑ZO-1
E-cadherin↑, ↑E-cadherin
SOX2↓, PANC-1, BxPC-3, SW1990 ↓Sox-2, ↓Oct-4, ↓SHH, ↓SMO, ↓Gli-2
OCT4↓,
Shh↓,
Smo↓,
Gli1↓,
N-cadherin↓, ↓N-cadherin
XIAP↓, ↓XIAP

2695-

BBR,

The effects of Berberis vulgaris consumption on plasma levels of IGF-1, IGFBPs, PPAR-γ and the expression of angiogenic genes in women with benign breast disease: a randomized controlled clinical trial

Trial,

BC,

85 eligible patients diagnosed with benign breast disease.

IGF-1↓, BV juice intervention over 8 weeks was accompanied by acceptable efficacy and decreased plasma IGF-1, and IGF-1/IGFBP-1 ratio partly could be assigned to enhanced IGFBP-1 level in women with BBD.
PPARγ↓, The intervention caused reductions in the expression levels of PPAR, VEGF, and HIF which are remarkable genomic changes to potentially prevent breast tumorigenesis.
VEGF↓,
Hif1a↓, down-regulating effects of BV juice on PPAR-γ, VEGF, and HIF-1α
angioG↓, berberine can decrease angiogenesis and related biomarkers including VEGF in breast cancer cells

3521-

Bor,

A new hope for obesity management: Boron inhibits adipogenesis in progenitor cells through the Wnt/β-catenin pathway

in-vitro,

Obesity,

3T3

*CEBPA↓, Figure 2
*PPARγ↓,
*FASN↓,
*SREBP1↓,
*FABP4↓,
*GLUT4↓,
*β-catenin/ZEB1↑, Boron Activated the Î²-Catenin Signaling Pathway
*MMP2↓, As shown in Fig. 6, soluble transforming growth factor receptor 1 (sTNFR1) and matrix metalloproteinase 2 (MMP2) protein levels decreased in the presence of boron
*FGF↑, whereas basic fibroblast growth factor expression (bFGF) increased
*Ca+2?, Boric acid has been reported to interact with NAD + and inhibit cyclic ADP ribose-activated Ca 2+ release from ryanodine receptor, leading to decreased endoplasmic reticulum luminal Ca 2+ concentrations

5742-

Buty,

Butyrate: A Double-Edged Sword for Health?

Review,

Var,

HCAR2↑, Another major GPCR activated by butyrate is GPR109A (
Inflam↓, anti-inflammatory properties of butyrate are also achieved through inhibition of the production of proinflammatory enzymes and cytokines
HDAC↓, Butyrate functions as an HDAC inhibitor
*IFN-γ↓, animal studies reported that the proinflammatory cytokines IFN-γ, TNF-α, IL-1β, IL-6, and IL-8 are inhibited, whereas IL-10 and TGF-β are upregulated in response to butyrate
*TNF-α↓,
*IL1β↓,
*IL6↓,
*IL8↓,
*IL10↑,
*TNF-β↑,
*NF-kB↓, butyrate is at least in part due to inhibition of the activation of a transcription factor known as NF-κB (
*ROS↓, by rescuing the redox machinery and controlling reactive oxygen species,
PPARγ↓, Further studies also showed that butyrate is capable of activating PPAR-γ (67), which is a member of the nuclear hormone receptor family and highly expressed in colonic epithelial cells,
Weight↓, although a large body of evidence has suggested the effect of butyrate on alleviating high fat diet–induced obesity and insulin resistance, a few studies showed an opposite effect.

5819-

CBD,

The potential role of cannabidiol (CBD) in lung cancer therapy: a systematic review of preclinical and clinical evidence

Review,

Lung,

Apoptosis↑, Mechanistically, CBD induced apoptosis through pathways such as PPAR-γ activation, mitochondrial dysfunction, and oxidative stress.
PPARγ↓,
mtDam↑,
ROS↑, Induced cell death via apoptosis and increased ROS levels.
EMT↓, It inhibited epithelial-to-mesenchymal transition (EMT), downregulated invasive markers, and modulated the tumor microenvironment by enhancing CD8 + T cell and NK cell activity.
CD8+↑,
NK cell↑,
ChemoSen↑, CBD showed synergistic effects with conventional therapies (e.g., cisplatin, radiotherapy) by increasing drug uptake and overcoming resistance.
ATP↓, CBD decreases intracellular ATP and glucose levels
glucose↓,
Ca+2↑, CBD enhances calcium influx (mediated by TRPV2) and elevates p-ERK expression in CIK cells
TRPV2↑,

4302-

Gins,

Panax ginseng: A modulator of amyloid, tau pathology, and cognitive function in Alzheimer's disease

Review,

AD,

*neuroP↑, highlighting neuroprotective mechanisms, such as the inhibition of Aβ production, enhanced Aβ clearance, and suppression of tau hyperphosphorylation.
*Aβ↓,
*p‑tau↓,
*cognitive↑, Research on P. ginseng and its bioactive ginsenosides has shown potential for improving cognitive function in AD models
*eff↑, particularly pronounced effects in individuals lacking apolipoprotein ε4 allele.
*PKA↑, Upregulates the PKA/CREB signaling pathway
*CREB↑,
*BACE↓, Inhibits BACE1 activity
*ADAM10↑, Enhances the expression of ADAM10 and reduces BACE1 expression through the activation of MAPK/ERK and PI3K/AKT
*MAPK↑,
*ERK↑,
*PI3K↑,
*Akt↑,
*NRF2↑, Activates the Nrf2/Keap1 signaling pathway
*PPARγ↓, Inhibits PPARγ phosphorylation and upregulates the expression of IDE
*IDE↑,
*APP↓, downregulates the expression of BACE1 and APP
*PP2A↑, Ginsenoside Rb1 enhances PP2A levels, thereby facilitating tau dephosphorylation and reducing p-tau levels observed in animal studies
*memory↑, The 400 mg dose of ginseng extract significantly improved “Quality of Memory” and “Secondary Memory” at all post-dose time points,

4780-

Lyco,

Potential inhibitory effect of lycopene on prostate cancer

Review,

Pca,

TumCP↓, Lycopene suppress the progression and proliferation
TumCCA↑, Lycopene has been found to effectively suppress the progression and proliferation, arrest in-cell cycle, and induce apoptosis of prostate cancer cells in both in-vivo and in-vitro conditions.
Apoptosis↑,
*neuroP↑, the neuro-protective effect of lycopene, mediates the signaling pathways, by inhibiting NF-κB (nuclear factor-κB) and JNK protein (c-Jun N-terminal kinase), and activating Nrf2 (Nuclear factor erythroid 2-related factor 2) and BDNF (
*NF-kB↓,
*JNK↓,
*NRF2↑,
*BDNF↑,
*Ca+2↝, as well as keeping homeostasis by restoring intracellular Ca2+
*antiOx↑, most powerful and natural antioxidants, and its role in preventing prostate cancer.
*AntiCan↑,
*Inflam↓, Anti-inflammatory properties of lycopene depends on time, and it has been found to be through the decrease of inflammatory cytokines (i.e. IL1, IL6, IL8 and tumor necrosis factor-α (TNF-α)
*IL1↓,
*IL6↓,
*IL8↓,
*TNF-α↓,
NF-kB↓, lycopene increased the expression of BCO2 enzyme in an androgen-sensitive cell line that prevented cancer cell proliferation and reduced the NF-κB activity
DNAdam↓, 20 and 50 μM doses of lycopene had an effect on PC3 and DU145 cell lines in inducing apoptosis with DNA damages, and preventing cell growth and colony formation
PSA↓, lycopene twice a day for 3 weeks, showed that lycopene decreases the risk and growth of prostate cancer cells, and also a decrease in the level of PSA,
P53↓, down-regulation of p53, Cyclin-D1, and Nrf-2 have occurred after the incubation of prostate cancer cells with the lycopene received patient’s sera in comparison with placebo
cycD1/CCND1↓,
NRF2↓,
Akt2↓, treatment with lycopene in PC3 cancer cell lines was associated with down-regulation of AKT2 [
PPARγ↓, Another anti-proliferative effect of lycopene was done by increasing PPARγ-LXRα-ABCA1signaling molecules in protein and mRNA level

4528-

MAG,

Pharmacology, Toxicity, Bioavailability, and Formulation of Magnolol: An Update

Review,

Nor,

*Inflam↑, already known anti-inflammatory, cardiovascular protection, antiangiogenesis, antidiabetes, hypoglycemic, antioxidation, neuroprotection, gastrointestinal protection, and antibacterial activities of MG.
*cardioP↑,
*angioG↓,
*antiOx↑,
*neuroP↑,
*Bacteria↓,
AntiTum↑, Antitumor Activity
TumCG↓, MG suppressed the growth, migration, and invasion of tumor cells and promoted apoptosis
TumCMig↓,
TumCI↓,
Apoptosis↑,
E-cadherin↑, In MCF-7 cells, MG (20 μM) increased the expression of the tumor suppressor miRNA miR-200c to inhibit zinc finger E-box-binding homeobox 1 and increased the expression of E-cadherin
NF-kB↓, regulated the NF-κB pathway, induced cell cycle arrest, downregulated cyclin D1, and inhibited the expression of proliferating cell nuclear antigen (PCNA), Ki67, matrix metalloproteinase (MMP)-2, MMP-7, and MMP-9
TumCCA↑,
cycD1/CCND1↓,
PCNA↓,
Ki-67↓,
MMP2↓,
MMP7↓,
MMP9↓,
TumCG↓, A549 cells, MG (1–50 μM) showed growth inhibition and autophagy via activating caspase-3 and poly-(ADP)-ribose polymerase cleavage, reducing NF-κB/Rel A and Akt/mTOR pathway expression, dose-dependently blocking mitosis and G2/M progression, and incr
Casp3↑,
NF-kB↓,
Akt↓,
mTOR↓,
LDH↓,
Ca+2↑, MG (20–100 μM) played roles of [Ca2+] increase,
eff↑, cotreatment with MG and honokiol exerted a synergistic antitumor effect to induce cell cycle arrest as well as autophagy and inhibit proliferation by decreasing cyclin A/D1, cyclin-dependent kinase 2, 4, 6, p-PI3K, p-Akt, Ki67, p-p38, and p-JNK and
*toxicity↓, In summary, MG was found to be fairly nontoxic.
*BioAv↝, In recent years, the bioavailability of MG has been significantly improved by various formulations including solid dispersion, phospholipid complex, nanoparticles, emulsion, mixed micelles
*PGE2↓, exert neuroprotective activities by inhibiting the production of PGE2, regulating (GABA)A receptor subtypes
*TLR2↓, MG inhibited TLR2/TLR4/NF-κB/MAPK/PPAR-γ pathways and decreased the expression of inflammatory cytokines to exhibit anti-inflammatory activity.
*TLR4↓,
*MAPK↓,
*PPARγ↓,

218-

MFrot,

MF,

Extremely low frequency magnetic fields inhibit adipogenesis of human mesenchymal stem cells

in-vitro,

Nor,

 7.5 Hz, 0.4 T

human umbilical cord MSCs

*PPARγ↓, PPARg2
*p‑JNK↑, p-JNK
*Wnt↑,
*ALP∅, ELF-MF had no effects on the expression of ALP, COL1a1, Runx2, and OCN
*COL1∅,
*RUNX2∅,
*OCN∅,
*FABP4↓, ELF-MF exposure for 15 days resulted in a decrease in PPARg2 and FABP4
*p‑JNK↑, p-JNK was increased after ELF-MF exposure
*Diff↓, adipogenic differentiation of MSCs could be inhibited by ELF-MF of 7.5 Hz, 0.4 T, suggesting the inhibitory effect of ELF-MF on obesity may be attributed to the inhibition of differentiation of MSCs into adipocytes.

4499-

Se,

Selenium and Selenoproteins in Gut Inflammation—A Review

Review,

IBD,

*Inflam↓, Previous studies have shown the ability of micronutrient selenium (Se) and selenoproteins to impact inflammatory signaling pathways implicated in the pathogenesis of the disease
*IL2↓, decreased pro-inflammatory cytokines such as IL-1β, tumor necrosis factor alpha (TNFα) and interferon gamma (IFNγ
*TNF-α↓,
*IFN-γ↓,
*PPARγ↓, Our laboratory has shown a crucial role for Se in the activation of PPARγ and its ligands, which are derived from the arachidonic acid (AA) pathway of cyclooxygenase metabolism, in macrophages.

2102-

TQ,

A review on therapeutic potential of Nigella sativa: A miracle herb

Review,

Var,

angioG↓, TQ inhibits tumor angiogenesis and tumor growth through suppressing NF-κB and its regulated molecules.
NF-kB↓,
PPARγ↓, TQ was found to increase PPAR-γ activity and down-regulate the expression of the genes for Bcl-2, Bcl-xL and survivin in breast cancer cells.
Bcl-2↓,
Bcl-xL↓,
MUC4↓, TQ down regulated MUC4 expression through the proteasomal pathway and induced apoptosis in pancreatic cancer cells by the activation of c-Jun NH(2)-terminal kinase and p38 mitogen-activated protein kinase pathways
cJun↑,
p38↑,
P21↑, TQ also increased p21 WAF1 expression, inhibited HDAC activity, and induced histone hyperacetylation
HDAC↓,
*radioP↑, N. sativa oil is a promising natural radioprotective agent against immunosuppressive and oxidative effects of ionizing radiation
hepatoP↑, Results suggested that N. sativa treatment protects the rat liver against hepatic ischemia reperfusion injury

3422-

TQ,

Thymoquinone, as a Novel Therapeutic Candidate of Cancers

Review,

Var,

selectivity↑, TQ selectively inhibits the cancer cells’ proliferation in leukemia [9], breast [10], lungs [11], larynx [12], colon [13,14], and osteosarcoma [15]. However, there is no effect against healthy cells
P53↑, It also re-expressed tumor suppressor genes (TSG), such as p53 and Phosphatase and tensin homolog (PTEN) in lung cancer
PTEN↑,
NF-kB↓, antitumor properties by regulating different targets, such as nuclear factor kappa B (NF-Kb), peroxisome proliferator-activated receptor-γ (PPARγ), and c-Myc [1], which resulted in caspases protein activation
PPARγ↓,
cMyc↓,
Casp↑,
*BioAv↓, Due to hydrophobicity, there are limitations in the bioavailability and drug formation of TQ.
BioAv↝, TQ is sensitive to light; a short period of exposure results in severe degradation, regardless of the solution’s acidity and solvent type [27]. It is also unstable in alkaline solutions because TQ’s stability decreases with rising pH
eff↑, Encapsulating TQ with CS improves the uptake and bioavailability of TQ but has low encapsulation efficiency (35%)
survivin↓, TQ showed antiproliferative and pro-apoptotic potency on breast cancer through the suppression of anti-apoptotic proteins, such as survivin, Bcl-xL, and Bcl-2
Bcl-xL↓,
Bcl-2↓,
Akt↓, treating doxorubicin-resistant MCF-7/DOX cells with TQ inhibited Akt and Bcl2 phosphorylation and increased the expression of PTEN and apoptotic regulators such as Bax, cleaved PARP, cleaved caspases, p53, and p21 [
BAX↑,
cl‑PARP↑,
CXCR4↓, inhibited metastasis with significant inhibition of chemokine receptor Type 4 (CXCR4), which is considered a poor prognosis indicator, matrix metallopeptidase 9 (MMP9), vascular endothelial growth factor Receptor 2 (VEGFR2), Ki67, and COX2
MMP9↓,
VEGFR2↓,
Ki-67↓,
COX2↓,
JAK2↓, TQ at 25, 50 and 75 µM inhibited JAK2 and c-Src activity and induced apoptosis by inhibiting the phosphorylation of STAT3 and STAT3 downstream genes, such as Bcl-2, cyclin D, survivin, and VEGF, and upregulating caspases-3, caspases-7, and caspases-9
cSrc↓,
Apoptosis↑,
p‑STAT3↓,
cycD1/CCND1↓,
Casp3↑,
Casp7↑,
Casp9↑,
N-cadherin↓, downregulated the mesenchymal genes expression N-cadherin, vimentin, and TWIST, while upregulating epithelial genes like E-cadherin and cytokeratin-19.
Vim↓,
Twist↓,
E-cadherin↑,
ChemoSen↑, The combined treatment of 5 μM TQ and 2 μg/mL cisplatin was more effective in cancer growth and progression than either agent alone in a xenograft tumor mouse model.
eff↑, TQ–artemisinin hybrid therapy (2.6 μM) showed an enhanced ROS generation level and concomitant DNA damage induction in human colon cancer cells, while not affecting nonmalignant colon epithelial at 100 μM
EMT↓, TQ inhibits the survival signaling pathways to reduce carcinogenesis progress rate, and decreases cancer metastasis through regulation of epithelial to mesenchymal transition (EMT).
ROS↑, Apoptosis is induced by TQ in cancer cells through producing ROS, demethylating and re-expressing the TSG
DNMT1↓, inhibits DNMT1, figure 2
eff↑, TQ–vitamin D3 combination significantly reduced pro-cancerous molecules (Wnt, β-catenin, NF-κB, COX-2, iNOS, VEGF and HSP-90) a
EZH2↓, reduced angiogenesis by downregulating significant angiogenic genes such as versican (VCAN), the growth factor receptor-binding protein 2 (Grb2), and enhancer of zeste homolog 2 (EZH2), which participates in histone methylatio
hepatoP↑, Moreover, TQ improved liver function as well as reduced hepatocellular carcinoma progression
Zeb1↓, TQ decreases the Twist1 and Zeb1 promoter activities,
RadioS↑, TQ combined with radiation inhibited proliferation and induced apoptosis more than a TQ–cisplatin combination against SCC25 and CAL27 cell lines
HDAC↓, TQ has inhibited the histone deacetylase (HDAC) enzyme and reduced its total activity.
HDAC1↓, as well as decreasing the expression of HDAC1, HDAC2, and HDAC3 by 40–60%
HDAC2↓,
HDAC3↓,
*NAD↑, In non-cancer cells, TQ can increase cellular NAD+
*SIRT1↑, An increase in the levels of intracellular NAD+ led to the activation of the SIRT1-dependent metabolic pathways
SIRT1↓, On the other hand, TQ induced apoptosis by downregulating SIRT1 and upregulating p73 in the T cell leukemia Jurkat cell line
*Inflam↓, TQ treatment of male Sprague–Dawley rats has reduced the inflammatory markers (CRP, TNF-α, IL-6, and IL-1β) and anti-inflammatory cytokines (IL-10 and IL-4) triggered by sodium nitrite
*CRP↓,
*TNF-α↓,
*IL6↓,
*IL1β↓,
*eff↑, The TQ–piperin combination has also decreased the oxidative damage triggered by microcystin in liver tissue and reduced malondialdehyde (MDA) and NO, while inducing glutathione (GSH) levels and superoxide dismutase (SOD), catalase (CAT), and glutathi
*MDA↓,
*NO↓,
*GSH↑,
*SOD↑,
*Catalase↑,
*GPx↑,
PI3K↓, repressing the activation of vital pathways, such as JAK/STAT and PI3K/AKT/mTOR.
mTOR↓,

Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

CD8+↑, 1,
Total Targets: 129

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 2, Catalase↑, 1, GPx↑, 1, GSH↑, 1, MDA↓, 1, NRF2↑, 2, ROS↓, 1, SOD↑, 1,

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1, CREB↑, 1, FABP4↓, 2, FASN↓, 1, NAD↑, 1, PPARγ↓, 5, p‑PPARγ↓, 1, SIRT1↑, 1, SREBP1↓, 1,

Cell Death ⓘ

Akt↑, 1, JNK↓, 1, p‑JNK↑, 2, MAPK↓, 1, MAPK↑, 1,

Kinase & Signal Transduction ⓘ

OCN∅, 1,

Proliferation, Differentiation & Cell State ⓘ

CEBPA↓, 1, Diff↓, 1, ERK↑, 1, FGF↑, 1, PI3K↑, 1, RUNX2∅, 1, Wnt↑, 1,

Migration ⓘ

APP↓, 1, Ca+2?, 1, Ca+2↝, 1, COL1∅, 1, MMP2↓, 1, PKA↑, 1, β-catenin/ZEB1↑, 1,

Angiogenesis & Vasculature ⓘ

angioG↓, 1, NO↓, 1,

Barriers & Transport ⓘ

GLUT4↓, 1,

Immune & Inflammatory Signaling ⓘ

CRP↓, 1, IFN-γ↓, 2, IL1↓, 1, IL10↑, 1, IL18↓, 1, IL1β↓, 3, IL2↓, 1, IL6↓, 4, IL8↓, 3, Inflam↓, 3, Inflam↑, 1, NF-kB↓, 2, PGE2↓, 1, TLR2↓, 1, TLR4↓, 1, TNF-α↓, 5, TNF-β↑, 1,

Synaptic & Neurotransmission ⓘ

ADAM10↑, 1, BDNF↑, 1, p‑tau↓, 1,

Protein Aggregation ⓘ

Aβ↓, 1, BACE↓, 1, IDE↑, 1, PP2A↑, 1,

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

ALP∅, 1, CRP↓, 1, IL6↓, 4,

Functional Outcomes ⓘ

AntiCan↑, 1, cardioP↑, 2, chemoPv↑, 1, cognitive↑, 1, memory↑, 1, neuroP↑, 3, radioP↑, 1, toxicity↓, 1,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 81

Scientific Paper Hit Count for: PPARγ, Peroxisome proliferator-activated receptor gamma (PPAR-γ or PPARG)

2 Thymoquinone
1 Ashwagandha(Withaferin A)
1 Baicalein
1 Berberine
1 Boron
1 Butyrate
1 Cannabidiol
1 Ginseng
1 Lycopene
1 Magnolol
1 Magnetic Field Rotating
1 Magnetic Fields
1 Selenium

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#:259  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

PPARγ Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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