IGF-1 Cancer Research Results
IGF-1, insulin-like growth factor-1: Click to Expand ⟱
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Higher blood levels of IGF-1, a growth factor, are linked to increased risk of several types of cancer, including thyroid, melanoma and myeloma. IGF-1 is what some call "a growth-promoter" because it has been shown to promote the growth of cancer cells.
The IGF-1 signaling pathway promotes cancer progression; its downregulation is associated with lowered risk.
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Scientific Papers found: Click to Expand⟱
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*memory↑, a number of preclinical studies showing beneficial effects of LA in memory functioning, and pointing to its neuroprotective potential effect
*neuroP↑,
*motorD↑, Improved motor dysfunction
*VitC↑, elevates the activities of antioxidants such as ascorbate (vitamin C), α-tocoferol (vitamin E) (Arivazhagan and Panneerselvam, 2000), glutathione (GSH)
*VitE↑,
*GSH↑,
*SOD↑, superoxide dismutase (SOD) activity (Arivazhagan et al., 2002; Cui et al., 2006; Militao et al., 2010), catalase (CAT) (Arivazhagan et al., 2002; Militao et al., 2010), glutathione peroxidase (GSH-Px)
*Catalase↑,
*GPx↑,
*5HT↑, ↑levels of neurotransmitters (dopamine, serotonin and norepinephrine) in various brain regions
*lipid-P↓, ↓ level of lipid peroxidation,
*IronCh↑, ↓cerebral iron levels,
*AChE↓, ↓ AChE activity, ↓ inflammation
*Inflam↓,
*GlucoseCon↑, ↑brain glucose uptake; ↑ in the total GLUT3 and GLUT4 in the old mice;
*GLUT3↑,
*GLUT4↑,
NF-kB↓, authors showed that LA inhibited the stimulation of nuclear factor-κB (NF-κB)
*IGF-1↑, LA restored the parameters of total homocysteine (tHcy), insulin, insulin like growth factor-1 (IGF-1), interlukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). Mahboob et al. (2016), analyzed the effects of LA in AlCl3- model of neurodegeneration,
*IL1β↓,
*TNF-α↓, Suppression of NF-κβ p65 translocation and production of proinflammatory cytokines (IL-6 and TNF-α) followed inhibition of cleaved caspase-3
*cognitive↑, demonstrating its capacity in ameliorating cognitive functions and enhancing cholinergic system functions
*ChAT↑, LA treatment increased the expression of muscarinic receptor genes M1, M2 and choline acetyltransferase (ChaT) relative to AlCl3-treated group.
*HO-1↑, R-LA and S-LA also enhanced expression of genes related to anti-oxidative response such as heme oxygenase-1 (HO-1) and phase II detoxification enzymes such as NAD(P)H:Quinone Oxidoreductase 1 (NQO1).
*NQO1↑,
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*AntiAge↑, supplementation positively affects mitochondrial deficiency syndrome and the symptoms of aging based mainly on improvements in bioenergetics.
*cardioP↑, Cardiovascular disease and inflammation are alleviated by the antioxidant effect of CoQ10
*Inflam↓, Administration of CoQ10 in doses ranging from 60 to 500 mg/day for a 1-week to 4-month intervention period significantly decreased production of inflammatory cytokines
*antiOx↑,
*lipid-P↓, The concentrations of CoQ10 in the plasma of elderly people are positively correlated with levels of physical activity and cholesterol concentrations (Del Pozo-Cruz et al., 2014a,b), as well as with lower lipid oxidative damage.
*QoL↑, Older individuals given a combination of selenium and CoQ10 over a 4-year period reported an improvement in vitality, physical performance, and quality of life
*neuroP↑, health benefits in elderly people by preventing chronic oxidative stress associated with cardiovascular and neurodegenerative diseases
*Dose↝, the highest dose for CoQ10 supplementation is 1200 mg daily according to well-designed randomized, controlled human trials, although doses as high as 3000 mg/day have been used in shorter clinical trials
*BP↓, These authors interpreted the results to indicate a significant reduction in systolic blood pressure without improvements in other CVD risk factors, such as diastolic blood pressure, total cholesterol, LDL- and high-density lipoprotein (HDL)-choleste
*IGF-1↑, elderly healthy participants who received selenium and CoQ10 supplementation for over 4 years, an increase in insulin-like growth factor 1 (IGF-1) and postprandial insulin-like growth factor-binding protein 1 (IGFBP-1) levels
*IGFBP1↑,
*eff↑, A combination of CoQ10 with red yeast rice, berberina, policosanol, astaxanthin, and folic acid significantly decreased total cholesterol, LDL-cholesterol, triglycerides, and glucose in the blood while increasing HDL-cholesterol levels
*LDL↓,
*HDL↑,
*eff↑, 60 patients suffering from statin-associated myopathy were enrolled in a 3-month study to test for efficacy of CoQ10 and selenium treatment. A consistent reduction in their symptoms, including muscle pain, weakness, cramps, and fatigue was observed
*other↑, Because of its capacity to reduce the side-effects of statins, CoQ10 has been proposed to prevent and/or slow the progression of frailty and sarcopenia in the elderly chronically treated with statins.
*RenoP↑, experiments performed on rats showed a promising protective effect of ubiquinol in the kidneys
*ROS↓, 65 patients undergoing hemodialysis, supplementation with high amounts of CoQ10 (1200 mg/day) lowered F2-isoprostane plasma levels indicative of a reduction in oxidative stress
*TNF-α↓, low grade inflammation, respond well to CoQ10 supplementation with significant decrease in TNF-α plasma levels without having an effect on C-reactive protein and IL-6 production
*IL6↓, Another study reported that CoQ10 therapy in doses ranging from 60 to 300 mg/day caused no significant decrease in C-reactive protein while eliciting a significant reduction in IL-6 levels
*other↝, Preclinical studies demonstrated that CoQ can preserve mitochondrial function and reduce the loss of dopaminergic neurons in the case of Parkinson's disease
*other∅, There was no improvement observed in oxidative stress or neurodegeneration markers in a randomized clinical trial in Alzheimer's Disease patients with CoQ10 supplementation at a dose of 400 mg/day for 16 weeks
*toxicity∅, Data suggest overall good compliance, no malnutrition, minimal side effects. No significant changes were identified to suggest increased harm.
QoL∅, unchanged quality of life (QOL),
eff↑, improved endocrine parameters
eff↝, mixed results for cancer outcomes
ChemoSideEff↓, decreasing chemotherapy-related side effects
TumCG↓, limiting tumor growth
Dose↑, When fasting is used as an adjunct to chemotherapy, a minimum fasting period of at least 48 hours is currently recommended for nutritional interventions in order to achieve a measurable metabolic response at the cellular level
toxicity↝, The increased risk for poor outcomes associated with malnutrition, weight loss, and cachexia poses an obvious safety concern for patients with cancer who participate in calorie-restricted fasting
eff↑, short-term fasting involving water-only or limited daily calorie consumption for less than a week has the potential to achieve positive metabolic changes while avoiding malnutrition and significant weight loss
IGF-1↑, statistically significant decrease in IGF-1 among participants compliant with fasting compared with regular diet during the middle of therapy
*OXPHOS↑, Healthy cells also use mitochondrial oxidative phosphorylation for metabolism while cancer cells use aerobic glycolysis, also known as the Warburg effect
BG↓, statistically significant decrease in glucose among participants compliant with fasting compared with controls
Insulin↓, statistically significant decrease in insulin among participants compliant with fasting compared with regular diet before the first cycle of chemotherapy (p = .001), as well as during the middle of therapy
RadioS↑, A complete or partial radiographic response was also noted more often among fasting participants compared with normal diet participants
*IGF-1↑, Fitness correlates positively with the growth hormone–insulin-like growth factor-1 (GH–IGF-1) axis activity, and physical training may increase levels of GH and IGF-1 in healthy adults
*IGF-1↑, Three of the studies showed an exercise-induced increase in IGF-1; three found stable IGF-1 levels and one found a reduction in IGF-1; with and without improvement in cognition.
*IGF-1↑, Meta-analysis revealed that exercise interventions significantly increased serum IGF-1 levels in older adults with frailty and/or sarcopenia
*IGF-1↑, Based on the results of this systemic investigation, exercise has been shown to increase IGF-1 levels, a hormone that promotes growth. Physical exercise as a therapeutic effort and a means of improving public health.
IGF-1↑, 13 weeks of resistance training significantly reduced serum IGF1 by 13.1% (P ≤ 0.05) in prostate cancer patients
*IGF-1↑, Exercise significantly increased IGF-1 in healthy individuals (WMD=21.41, 95% CI 8.01–34.81) and in those with obesity
IGF-1↓, In contrast, exercise significantly reduced IGF-1 in cancer patients or survivors
IGFBP3↑, In studies reporting both IGF-1 and IGF-binding protein 3 (IGFBP-3), exercise increased IGFBP-3 in healthy and cancer populations, suggesting a modulatory role of IGFBP-3 in IGF-1 regulation, particularly in cancer.
*GH↑, Exercise, sleep, food intake, stress, and body composition are all stimuli and inhibitors that affect the hypothalamic components that govern GH production
*IGF-1↑, eight weeks of supervised aerobic exercise instruction resulted in a considerable rise in insulin-like growth factor
*IGF-1↑, resistance exercise significantly increases insulin-like growth factor 1 in subjects older than 60 years, both males and females, and subjects performing resistance exercise for all any period
*IGF-1↓, resistance exercise significantly decreases insulin-like growth factor 1 in subjects younger than 60 years.
*IGF-1↑, resistance training was associated with an increased IGF-1 level among those who received the training for ≤16 weeks, among participants older than 60 years old, and among women
*IGF-1↑, Exercise-induced increases in IGF-1 were large (11.3 ± 12.9 ng/mL) and similar across participants regardless of depression severity, antidepressant usage/type, and chronic physical activity differences.
Dose↝, Acute exercise increases peripheral IGF-1 briefly, and in response to repeated exercise bouts, the IGF-1 system could normalize over time.
cachexia↓, We showed that magnolol significantly attenuated the body weight and the muscle loss induced by cisplatin injection.
*IGF-1↑, magnolol increased insulin-like growth factor (IGF)-1 expression
chemoP↑, magnolol may be a promising chemoprotective agent for the prevention of muscle atrophy through the upregulating M2c macrophages, which are a major source of IGF-1.
*M2 MC↑,
*PDGFR-BB↑, The highest concentration of PDGF-BB was observed in the samples placed in RMF for 1 h at 25 Hz
*TGF-β↑, For TGF-β1, the highest concentrations were obtained in the samples exposed to RMF for 3 h at 25 Hz and 1 h at 50 Hz.
*IGF-1↑, highest concentrations of IGF-1 and FGF-1 were shown in plasma placed in RMF for 3 h at 25 Hz.
*FGF↑,
*angioG↑, Magnetic fields have been shown to have a beneficial effect on vasodilation, angiogenesis, accelerating repair, regeneration, and healing of soft tissues, nervous tissues and bones, analgesic aspects, anti-swelling, reducing inflammation and pain, an
*Inflam↓,
*ROS↓, RMF exposure can increase resistance to heat stress, reduce levels of ROS, affect intracellular calcium ion concentrations, and contribute to cell aging deceleration
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*BioAv↑, It has increased bioavailability in comparison to other stilbene compounds. pterostilbene was shown to have 80% bioavailability compared to 20% for resveratrol making it potentially advantageous as a therapeutic agent
*antiOx↑, Multiple studies have demonstrated the antioxidant activity of pterostilbene in both in vitro and in vivo models illustrating both preventative and therapeutic benefits.
*neuroP↑, anticarcinogenesis, modulation of neurological disease, anti-inflammation, attenuation of vascular disease, and amelioration of diabetes.
*Inflam↓,
*ROS↓, pterostilbene reduces oxidative stress (OS) and production of reactive oxygen species (ROS), such as hydrogen peroxide (H2O2) and superoxide anion (O2 −), which are implicated in the initiation and pathogenesis of several disease processes
*H2O2↓,
*GSH↑, pterostilbene have shown increased expression of the antioxidants catalase, total glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), and superoxide dismutase (SOD).
*GPx↑,
*GSR↑,
*SOD↑,
TumCG↓, pterostilbene inhibit breast cancer in vitro and in vivo
PTEN↑, rats fed the blueberry diet exhibited higher mammary branching, increased nuclear immunoreactivity of tumor suppressor phosphatase and tensin homolog deleted in chromosome 10 (PTEN)
HGF/c-Met↓, blueberry extract significantly decreased human-growth-factor (HGF-) induced activation of the PI3 K/AkT/NK-κB pathway, which is implicated in breast carcinogenesis
PI3K↓,
Akt↓,
NF-kB↓,
TumMeta↓, inhibited the metastatic potential of breast cancer cells in vitro by inhibiting HGF-induced cell migration and matrix metalloproteinase-(MMP-) 2 and MMP-9 activity.
MMP2↓,
MMP9↓,
Ki-67↓, blueberry extract produced smaller tumors with decreased expression of Ki-67, a marker of cell proliferation, and increased expression of caspase-3, an apoptosis marker
Casp3↑,
MMP↓, increased mitochondrial depolarization,
H2O2↑, pterostilbene treatment increased GPx antioxidant activity and the production of H2O2 and singlet oxygen indicating a mechanism of ROS-induced apoptosis
ROS↑,
ChemoSen↑, pterostilbene treatment produced a synergistic inhibitory effect when combined with the chemotherapy drug Tamoxifen, demonstrating clinical potential in the treatment of breast cancer
*cardioP↑, blueberries, and pterostilbene alike, exhibit protective effects against cardiovascular disease possibly due to induction of antioxidant enzymes.
*CDK2↓, Pterostilbene also produced downregulation of the cell-cycle mediators, cyclin-dependent kinase (CDK)-2, CDK-4, cyclin E, cyclin D1, retinoblastoma (Rb), and proliferative cell nuclear antigen (PCNA), all of which promote unchecked VSMC proliferation
*CDK4↓,
*cycE/CCNE↓,
*cycD1/CCND1↓,
*RB1↓,
*PCNA↓,
*CREB↑, The authors found that treatment with blueberry extract decreased dopamine- (DA-) induced upregulation of the oxidative mediators, CREB and pPKCγ, indicating a significant antioxidant effect
*GABA↑, blueberry-fed aged rats had significant improvements in GABA potentiation and increased GSH compared to aged controls
*memory↑, 1- or 2-month blueberry diet showed significantly higher object memory recognition compared to control rats
*IGF-1↑, supplementation with blueberry extract was shown to enhance hippocampal plasticity and increase levels of insulin-like growth factor (IGF-) 1, IGF-2, and ERK resulting in improved spatial memory
*ERK↑,
TIMP1↑, increased endogenous tissue inhibitors of metalloproteinases (TIMPs)
BAX↑, ↑Bax, ↑cytochrome C, ↑Smac/Diablo, ↑MnSOD
Cyt‑c↑,
Diablo↑,
SOD2↑,
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*Aβ↓, It was found that rosemary could reversed Aβ25–35 induced damage to mouse hippocampal neuron HT22 cells,
*Apoptosis↓, significantly improved the viability of damaged cells, and reduced apoptosis
*antiOx↑, main antioxidant compound in rosemary, carnosic acid, also has neuroprotective effects.
*neuroP↑,
*eff↑, main active carnosic acid, carnosol, rosmarinol, rosmadial, genkwanin, cirsimaritin, rosmarinic acid and caffeic acid in Rosmarinus officinalis L,
*IGF-1↑, rosemary could elevated expression of IGF1, MMP9 and decreased mRNA levels of SRC, MAPK14, compared with the control group.
*MMP9↑,
*Src↓,
*MAPK↓,
*MMP↑, Rosemary reduced Aβ-induced HT22 cell damage in AD models to enhance the mitochondrial membrane potential levels
*OS↑, Silymarin treatment improved survival in both ischemic groups (non-diet control: 95.7%, HFD: 78.3%).
*BDNF↑, Silymarin raised cortical TNFα, IL4, IL10, IGF1, BDNF, and CX3CL1 levels in the HFD group with stroke, while the striatum did not present relevant differences.
*IGF-1↑,
Showing Research Papers: 1 to 18 of 18
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 18
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
H2O2↑, 1, ROS↑, 1, SOD2↑, 1,
Mitochondria & Bioenergetics ⓘ
Insulin↓, 1, MMP↓, 1,
Cell Death ⓘ
Akt↓, 1, BAX↑, 1, Casp3↑, 1, Cyt‑c↑, 1, Diablo↑, 1, HGF/c-Met↓, 1,
Proliferation, Differentiation & Cell State ⓘ
IGF-1↓, 1, IGF-1↑, 2, IGFBP3↑, 1, PI3K↓, 1, PTEN↑, 1, TumCG↓, 2,
Migration ⓘ
Ki-67↓, 1, MMP2↓, 1, MMP9↓, 1, TIMP1↑, 1, TumMeta↓, 1,
Immune & Inflammatory Signaling ⓘ
NF-kB↓, 2,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 1, Dose↑, 1, Dose↝, 1, eff↑, 2, eff↝, 1, RadioS↑, 1,
Clinical Biomarkers ⓘ
BG↓, 1, Ki-67↓, 1,
Functional Outcomes ⓘ
cachexia↓, 1, chemoP↑, 1, ChemoSideEff↓, 1, QoL∅, 1, toxicity↝, 1,
Total Targets: 36
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 3, Catalase↑, 1, GPx↑, 2, GSH↑, 2, GSR↑, 1, H2O2↓, 1, HDL↑, 1, HO-1↑, 1, lipid-P↓, 2, NQO1↑, 1, OXPHOS↑, 1, ROS↓, 3, SOD↑, 2, VitC↑, 1, VitE↑, 1,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Mitochondria & Bioenergetics ⓘ
MMP↑, 1,
Core Metabolism/Glycolysis ⓘ
CREB↑, 1, GlucoseCon↑, 1, LDL↓, 1,
Cell Death ⓘ
Apoptosis↓, 1, MAPK↓, 1,
Transcription & Epigenetics ⓘ
other↑, 1, other↝, 1, other∅, 1,
DNA Damage & Repair ⓘ
PCNA↓, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, CDK4↓, 1, cycD1/CCND1↓, 1, cycE/CCNE↓, 1, RB1↓, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↑, 1, FGF↑, 1, GH↑, 1, IGF-1↓, 1, IGF-1↑, 16, IGFBP1↑, 1, Src↓, 1,
Migration ⓘ
MMP9↑, 1, TGF-β↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↑, 1, PDGFR-BB↑, 1,
Barriers & Transport ⓘ
GLUT3↑, 1, GLUT4↑, 1,
Immune & Inflammatory Signaling ⓘ
IL1β↓, 1, IL6↓, 1, Inflam↓, 4, M2 MC↑, 1, TNF-α↓, 2,
Synaptic & Neurotransmission ⓘ
5HT↑, 1, AChE↓, 1, BDNF↑, 1, ChAT↑, 1, GABA↑, 1,
Protein Aggregation ⓘ
Aβ↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, Dose↝, 1, eff↑, 3,
Clinical Biomarkers ⓘ
BP↓, 1, IL6↓, 1,
Functional Outcomes ⓘ
AntiAge↑, 1, cardioP↑, 2, cognitive↑, 1, memory↑, 2, motorD↑, 1, neuroP↑, 4, OS↑, 1, QoL↑, 1, RenoP↑, 1, toxicity∅, 1,
Total Targets: 70
Scientific Paper Hit Count for: IGF-1, insulin-like growth factor-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
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