Weight Cancer Research Results

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Type:
Weight
Scientific Papers found: Click to Expand⟱
285- ALA,  HCA,    Tolerance of oral lipoid acid and hydroxycitrate combination in cancer patients: first approach of the cancer metabolism research group
- Human, Var, NA
PI3K↝,
AMPK↝,
TumCG↓,
*toxicity↓, No hepatic toxicity found, no weight loss, no hypoglycemia
Weight∅,

1169- Bos,    Boswellic Acid Inhibits Growth and Metastasis of Human Colorectal Cancer in Orthotopic Mouse Model By Downregulating Inflammatory, Proliferative, Invasive, and Angiogenic Biomarkers
- in-vivo, CRC, NA
TumCG↓,
TumVol↓,
Weight∅, without significant decreases in body weight
ascitic↓,
TumMeta↓,
Ki-67↓,
CD31↓,
NF-kB↓,
COX2↓,
Bcl-2↓,
Bcl-xL↓,
IAP1↓,
survivin↓,
cycD1/CCND1↓,
ICAM-1↓,
MMP9↓,
CXCR4↓,
VEGF↓,

2797- CHr,    A flavonoid chrysin suppresses hypoxic survival and metastatic growth of mouse breast cancer cells
- in-vivo, BC, NA - in-vitro, BC, 4T1
tumCV↓, Thai propolis extract and chrysin decreased survival of 4T1 cells after exposure to hypoxia (1% O2), for 2 days.
p‑STAT3↓, chrysin inhibited hypoxia-induced STAT3 phosphorylation without affecting HIF-1α protein level.
VEGF↓, Chrysin also abrogated hypoxia-induced VEGF gene
Weight∅, did not affect body weight of the mice
angioG↓, leading to abrogation of hypoxia-induced angiogenesis

2805- CHr,    Chrysin serves as a novel inhibitor of DGKα/FAK interaction to suppress the malignancy of esophageal squamous cell carcinoma (ESCC)
- in-vitro, ESCC, KYSE150 - in-vivo, ESCC, NA
FAK↓, chrysin significantly disrupted the DGKα/FAK signalosome to inhibit FAK-controlled signaling pathways and the malignant progression of ESCC cells both in vitro and in vivo
GlucoseCon↓, Chrysin significantly reduced the levels of glycolytic indexes, such as glucose uptake
Casp3↑, hrysin dose-dependently increased the apoptotic rate and caspase 3/7 activity in KYSE410, KYSE30, and KYSE150 cells.
Casp7↑,
p‑Akt↓, chrysin dose-dependently inhibited the phosphorylation of AKT
TumCG↓, chrysin dose-dependently reduced the growth of ESCC tumors
Weight∅, difference of body weight between chrysin treatment groups and control group is minimal

1577- Citrate,    Citric acid promotes SPARC release in pancreatic cancer cells and inhibits the progression of pancreatic tumors in mice on a high-fat diet
- in-vivo, PC, NA - in-vitro, PC, PANC1 - in-vitro, PC, PATU-8988 - in-vitro, PC, MIA PaCa-2
Apoptosis↑, citrate treatment demonstrates signifcant effcacy in promoting tumor cell apoptosis, suppressing cell proliferation, and inhibiting tumor growth in vivo
TumCP↓,
TumCG↑,
SPARC↑, citrate treatment reveal decreased glycolysis and oxygen consumption in tumor cells, increased SPARC protein expression, and the promotion of M1 polarization
Glycolysis↓,
OCR↓,
pol-M1↑, repolarizing M2 macrophages into M1 macrophages
pol-M2 MC↓, shift from the M2 phenotype to the M1 phenotype in TAMs following citrate treatment
Weight∅, no signficant changes in body weight observed between the two groups
ATP↓, decreased ATP production of pancreatic tumors in vivo
ECAR↓, signifcantly reduced glycolytic flux, glycolytic reserve, glycolytic capacity, and acidifcation rates
mitResp↓, decreased basal mitochondrial respiration
i-ATP↑, decrease in intracellular ATP levels
p65↓, citrate effectively suppressed the expression of RELA findings collectively underscore the critical role of RELA in mediating citrate's regulation of glycolysis and suppression of pancreatic cancer progression
i-Ca+2↑, inhibition of RELA resulted in a rapid elevation of intracellular calcium levels
eff↓, overexpression of RELA and SPARC knockdown attenuated the therapeutic effects of citrate

1446- Deg,    Efficacy and mechanism of action of Deguelin in suppressing metastasis of 4T1 cells
- in-vitro, BC, 4T1
cMET↓,
p‑ERK↓,
p‑Akt↓,
TumCMig↓,
TumCG↓, vivo
Weight∅, no difference in the body weight as well as liver and spleen weights between vehicle treated control and Deguelin treated animals indicating that Deguelin was nontoxic at the dose used
*toxicity∅, no difference in the body weight as well as liver and spleen weights between vehicle treated control and Deguelin treated animals indicating that Deguelin was nontoxic at the dose used
Hif1a↓, Deguelin inhibits both ERK and p-AKT pathway leading to reduced expression of HIF −1α.
TumMeta↓,

1842- dietFMD,    Safety and Feasibility of Fasting-Mimicking Diet and Effects on Nutritional Status and Circulating Metabolic and Inflammatory Factors in Cancer Patients Undergoing Active Treatment
- Trial, Var, NA
Strength∅, The patients’ weight and handgrip remained stable, the phase angle and fat-free mass increased
Weight∅,
IGF-1↓, FMD reduced the serum c-peptide, IGF1, IGFBP3 and leptin levels
IGFBP3↑,
IGFBP1↑, while increasing IGFBP1
eff↑, these modifications persisted for weeks beyond the FMD period.

1056- EGCG,    EGCG, a major green tea catechin suppresses breast tumor angiogenesis and growth via inhibiting the activation of HIF-1α and NFκB, and VEGF expression
- vitro+vivo, BC, E0771
TumW↓,
VEGF↓,
Weight∅, no effects on the body weight, heart weight, angiogenesis and VEGF expression in the heart and skeletal muscle of mice.
Hif1a↓,
NF-kB↓,

5784- EGCG,    Dietary Epicatechin Promotes Survival of Obese Diabetic Mice and Drosophila melanogaster
- in-vivo, Nor, NA
*OS↑, Dietary intake of epicatechin promoted survival in the diabetic mice (50% mortality in diabetic control group vs. 8.4% in epicatechin group after 15 wk of treatment),
*Inflam↓, reduced systematic inflammation markers and serum LDL cholesterol,
*LDL↓,
*AntiAge↑, epicatechin may be a novel food-derived, antiaging compound.
*GSH↑, In addition, the GSH concentration and total SOD activity in the livers of the db+EC group were significantly greater,
*SOD↑,
*AMPKα↑, Epicatechin improves AMPKα activity in the liver and skeletal muscle of diabetic mice.
*Weight∅, whereas blood pressure, blood glucose, food intake, and body weight gain were not significantly altered.

2903- LT,    Luteolin induces apoptosis by ROS/ER stress and mitochondrial dysfunction in gliomablastoma
- in-vitro, GBM, U251 - in-vitro, GBM, U87MG - in-vivo, NA, NA
ER Stress↑, Luteolin induced a lethal endoplasmic reticulum stress response and mitochondrial dysfunction in glioblastoma cells by increasing intracellular reactive oxygen species (ROS) levels.
ROS↑,
PERK↑, Luteolin induced expression of ER stress-associated proteins, including phosphorylation of PERK, eIF2α, ATF4, CHOP and cleaved-caspase 12.
eIF2α↑,
ATF4↑,
CHOP↑,
Casp12↑,
eff↓, Inhibition of ROS production by anti-oxidant N-acetylcysteine could reverse luteolin-induced ER stress and mitochondrial pathways activation as well as apoptosis.
UPR↑, Researches indicate that abnormalities in ER function can cause ER stress, resulting in unfolded protein response (UPR),
MMP↓, integrity of mitochondrial membranes potential decreased in U87MG cells after treatment of 40 uM luteolin
Cyt‑c↑, release of cytochrome C to cytoplasm was elevated in U251MG cells
Bcl-2↓, significantly decreased the expression of anti-apoptotic protein Bcl-2 and increased the expression of pro-apoptotic protein Bax in U251MG and U87MG glioblastoms cells.
BAX↑,
TumCG↓, Luteolin inhibited tumor growth in a xenograft mouse model
Weight∅, luteolin did not affect body weight, alanine aminotransferase (ALT) or aspartate transaminase (AST)
ALAT∅,
AST∅,

3725- MF,    Short-term effects of extremely low frequency electromagnetic fields exposure on Alzheimer's disease in rats
- in-vivo, AD, NA
*Weight∅, body weight of rats showed no difference compared with the control group.
*memory∅, application of ELF-EMF did not induce any cognitive and memory impairment compared with the sham-exposure group.
*cognitive∅,
*Aβ∅, Aβ showed no significant change between the two groups,

1238- PTS,    Pterostilbene suppresses gastric cancer proliferation and metastasis by inhibiting oncogenic JAK2/STAT3 signaling: In vitro and in vivo therapeutic intervention
- in-vitro, GC, NA - in-vivo, NA, NA
TumCCA↑, significantly induced cell cycle arrest at G0/G1 and S phases
TumCP↓,
TumCMig↓,
TumCI↓,
TumVol↓,
TumW↓,
Weight∅, leaving mouse weight, liver function, and kidney function unaffected
JAK2↓,
STAT3↓,

1483- SFN,    Targeting p62 by sulforaphane promotes autolysosomal degradation of SLC7A11, inducing ferroptosis for osteosarcoma treatment
- in-vitro, OS, 143B - in-vitro, Nor, HEK293 - in-vivo, OS, NA
AntiCan↑, has shown potential anti-cancer effects with negligible toxicity
*toxicity∅, (liver, kidney, heart, spleen, and lung) showed no evidence of toxicity associated with SFN treatment
Ferroptosis↑, results demonstrate the dependency of downregulation of SLC7A11 in SFN-induced ferroptosis in OS cells
ROS↑, elevated ROS levels, lipid peroxidation, and GSH depletion
lipid-P↑,
GSH↓, which was dependent on decreased levels of SLC7A11
p62↑, enhanced p62/SLC7A11 protein-protein interaction, thereby promoting the lysosomal degradation of SLC7A11 and triggering ferroptosis
SLC12A5↓, SFN induces ferroptosis of OS cells through downregulation of SLC7A11
eff↓, ferroptosis inhibitors Fer-1 (ferrostatin-1), DFO (deferoxamine), and Lip-1 (liproxstatin-1) substantially rescued the cells from SFN-induced cell death
GPx4↓, SFN treatment markedly reduced the expression levels of ferroptosis markers GPX4 and SLC7A11 in OS cells
i-Iron↑, validated the intracellular Fe2+ accumulation by SFN
eff↓, SLC7A11 overexpression notably reversed SFN-induced changes in the ROS level, GSH level, and lipid peroxidation
MDA↑, SFN treatment reduced GSH levels and increased MDA production, indicating the induction of ferroptosis
TumVol↓,
TumW↓,
Ki-67↓, subcutaneous tumors revealed significantly lower expression levels of Ki67, SLC7A11, and GPX4, along with upregulated LC3B in the SFN-treated group
LC3B↑,
*Weight∅, no significant difference in body weight was observed between the control and SFN-treated groups

1140- SIL,    Silibinin-mediated metabolic reprogramming attenuates pancreatic cancer-induced cachexia and tumor growth
- in-vitro, PC, AsPC-1 - in-vivo, PC, NA - in-vitro, PC, MIA PaCa-2 - in-vitro, PC, PANC1 - in-vitro, PC, Bxpc-3
TumCG↓,
Glycolysis↓,
cMyc↓,
STAT3↓,
TumCP↓,
Weight∅, prevents the loss of body weight and muscle.
Strength↑,
DNAdam↑,
Casp3↑,
Casp9↑,
GLUT1↓,
HK2↓,
LDHA↓,
GlucoseCon↓, silibinin inhibits glucose uptake and lactate release
lactateProd↓,
PPP↓, significant reduction in pentose phosphate pathway (PPP) metabolites, including 6-phosphogluconate (~50%), erythrose-4-phosphate (~40%), sedoheptulose-7-phosphate and sedoheptulose bis-phosphate (~ 70%)
Ki-67↓, reduced Ki67-positive cells
p‑STAT3↓,
cachexia↓,

1018- SSE,    Selenite-induced autophagy antagonizes apoptosis in colorectal cancer cells in vitro and in vivo
- vitro+vivo, CRC, HCT116 - vitro+vivo, CRC, SW480
TumAuto↑,
LC3s↑, expression of autophagy marker LC3 was increased
TumW↓,
Weight∅, no obvious effect on the body weight of the mice
Beclin-1↑,
p62↓,
ROS↑, concluded that selenite-induced apoptosis and autophagy may be caused by ROS

2132- TQ,    Thymoquinone treatment modulates the Nrf2/HO-1 signaling pathway and abrogates the inflammatory response in an animal model of lung fibrosis
- in-vivo, Nor, NA
*Weight∅, BM administration resulted in a significant weight loss, which was ameliorated by TQ treatment.
*antiOx↑, BMILF was associated with a reduction in the antioxidant mechanisms and increased lipid peroxidation (abnormalities were diminished with TQ treatment)
*lipid-P↓,
*MMP7↓, elevated levels of inflammatory cytokines, MMP-7 expression, apoptotic markers (caspase 3, Bax, and Bcl-2), and fibrotic changes including TGF-β and hydroxyproline levels in lung tissues were evident. These abnormalities were diminished with TQ
*Casp3↓,
*BAX↓,
*TGF-β↓,
*Diff↑, differential cell count in BALF was significantly improved in rats treated with TQ
*NRF2↓, TQ also produced a dose-dependent reduction in the expressions of Nrf2, Ho-1 and TGF-β. (ai:once TQ reduces oxidative damage, the demand for high Nrf2 activity drops)
*HO-1↓,
*NF-kB↓, NF-jB protein expression has been significantly and dose dependently decreased in TQ treated groups (10 and 20 mg/kg bw)
*IκB↑, IkBa has been significantly and dose dependently increase in TQ treated groups (10 and 20 mg/kg bw).


Showing Research Papers: 1 to 16 of 16

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 16

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 1,   i-Iron↑, 1,   lipid-P↑, 1,   MDA↑, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   i-ATP↑, 1,   mitResp↓, 1,   MMP↓, 1,   OCR↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT∅, 1,   AMPK↝, 1,   cMyc↓, 1,   ECAR↓, 1,   GlucoseCon↓, 2,   Glycolysis↓, 2,   HK2↓, 1,   lactateProd↓, 1,   LDHA↓, 1,   PPP↓, 1,  

Cell Death ⓘ

p‑Akt↓, 2,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 2,   Bcl-xL↓, 1,   Casp12↑, 1,   Casp3↑, 2,   Casp7↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   Ferroptosis↑, 1,   IAP1↓, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   eIF2α↑, 1,   ER Stress↑, 1,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3B↑, 1,   LC3s↑, 1,   p62↓, 1,   p62↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

cMET↓, 1,   p‑ERK↓, 1,   IGF-1↓, 1,   IGFBP1↑, 1,   IGFBP3↑, 1,   PI3K↝, 1,   STAT3↓, 2,   p‑STAT3↓, 2,   TumCG↓, 6,   TumCG↑, 1,  

Migration ⓘ

i-Ca+2↑, 1,   CD31↓, 1,   FAK↓, 1,   Ki-67↓, 3,   MMP9↓, 1,   SPARC↑, 1,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 3,   TumMeta↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   ATF4↑, 1,   Hif1a↓, 2,   VEGF↓, 3,  

Barriers & Transport ⓘ

GLUT1↓, 1,   SLC12A5↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CXCR4↓, 1,   ICAM-1↓, 1,   JAK2↓, 1,   pol-M1↑, 1,   pol-M2 MC↓, 1,   NF-kB↓, 2,   p65↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 4,   eff↑, 1,  

Clinical Biomarkers ⓘ

ALAT∅, 1,   ascitic↓, 1,   AST∅, 1,   Ki-67↓, 3,  

Functional Outcomes ⓘ

AntiCan↑, 1,   cachexia↓, 1,   Strength↑, 1,   Strength∅, 1,   TumVol↓, 3,   TumW↓, 4,   Weight∅, 12,  
Total Targets: 97

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GSH↑, 1,   HO-1↓, 1,   lipid-P↓, 1,   NRF2↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

LDL↓, 1,  

Cell Death ⓘ

BAX↓, 1,   Casp3↓, 1,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,  

Migration ⓘ

MMP7↓, 1,   TGF-β↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   IκB↑, 1,   NF-kB↓, 1,  

Protein Aggregation ⓘ

Aβ∅, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   cognitive∅, 1,   memory∅, 1,   OS↑, 1,   toxicity↓, 1,   toxicity∅, 2,   Weight∅, 4,  
Total Targets: 24

Scientific Paper Hit Count for: Weight, Weight
2 Chrysin
2 EGCG (Epigallocatechin Gallate)
1 Alpha-Lipoic-Acid
1 HydroxyCitric Acid
1 Boswellia (frankincense)
1 Citric Acid
1 Deguelin
1 diet FMD Fasting Mimicking Diet
1 Luteolin
1 Magnetic Fields
1 Pterostilbene
1 Sulforaphane (mainly Broccoli)
1 Silymarin (Milk Thistle) silibinin
1 Selenite (Sodium)
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

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