Diff Cancer Research Results

Diff, differentiation: Click to Expand ⟱

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Type:

Differentiation refers to the process by which cells become specialized in structure and function.
-In healthy tissues, cells undergo differentiation to become specialized types (e.g., muscle cells, neurons, blood cells) that perform specific functions. This process is tightly regulated by genetic and epigenetic factors.
-In some cases, cells can lose their specialized characteristics, a process known as dedifferentiation. This is often seen in cancer, where tumor cells revert to a more primitive, less differentiated state.

Scientific Papers found: Click to Expand⟱

7703-

Inositol hexaphosphate-induced cellular response in myeloid leukemia cells is mediated by nicotinamide adenine dinucleotide phosphate oxidase activation

in-vitro,

AML,

PLB-985

TumCG↓, Treatment with 5 and 10 mM IP6 for 24 h was found to suppress the growth of both cell lines, though the effect was more dramatic in PLB-985 cells.
TumCD↑, Inositol hexaphosphate-induced cell death
Diff↑, Inositol hexaphosphate-induced differentiation
NOX2↑, We hypothesized that NADPH oxidase is one of the key components of IP6-induced metabolic disruption.
ROS↑, It is widely accepted that ROS generated by members of the NOX family play important roles in a wide range of signal transduction pathways.

5466-

AF,

Auranofin Inhibition of Thioredoxin Reductase in a Preclinical Model of Small Cell Lung Cancer

in-vivo,

Lung,

AF was administered intraperitoneal, daily or twice daily for 1 to 5 days in mice bearing DMS273 xenografts.

TrxR↓, TrxR is viable target in clinical trials using the anti-rheumatic drug, auranofin (AF).
Dose↝, 4 mg/kg once daily resulting in 18 μM gold in the plasma and 50% inhibition of TrxR activity in DMS273 SCLC tumors.
RadioS↑, effective inhibitor of TrxR and suggest that AF could be used as an adjuvant in radio-chemotherapy protocols to enhance therapeutic efficacy.
ChemoSen↑,
ROS↑, We also demonstrated the suppressing TrxR with AF can sensitize breast cancer stem cells to ROS induced differentiation and cytotoxicity.16
Diff↑,
toxicity↓, These results suggest that this dosing regimen is nontoxic to kidneys, liver, and bone marrow as well as demonstrating a trend toward a survival advantage in tumor bearing animals.

4365-

AgNPs,

Biomedical Applications of Silver Nanoparticles: An Up-to-Date Overview

Review,

Var,

ROS↑, the most remarkable mechanistic mode of AgNP-based antimicrobial effects is represented by their adhesion to microbial cells, ROS and free-radical generation, microbial wall piercing and penetration inside cells, and modulation and modification of mi
*toxicity↓, high intrinsic antimicrobial efficiency and non-toxic nature
*Bacteria↓,
*Inf↓, silver-based compounds and materials were used for the unconventional and effective control of distinctive infections
*Diff↑, Previous studies reported that AgNPs naturally improve the differentiation process of MC3T3-1 pre-osteoblast cells and subsequent bone-like tissue mineralization,
*eff↑, studies showed that AgNP-implanted titanium displayed improved antibacterial ability,
RadioS↑, making them suitable candidates for detection and dose-enhancement purposes in X-ray irradiation applications
selectivity↑, selective uptake into cancerous cells, AgNP-derived scattered light can be used for imaging purposes, whereas absorbed light can be used for selective hyperthermia

3396-

ART/DHA,

Progress on the study of the anticancer effects of artesunate

Review,

Var,

TumCP↓, reported inhibitory effects on cancer cell proliferation, invasion and migration.
TumCI↓,
TumCMig↓,
Apoptosis↑, ART has been reported to induce apoptosis, differentiation and autophagy in colorectal cancer cells by impairing angiogenesis
Diff↑,
TumAuto↑,
angioG↓,
TumCCA↑, inducing cell cycle arrest (11), upregulating ROS levels, regulating signal transduction [for example, activating the AMPK-mTOR-Unc-51-like autophagy activating kinase (ULK1) pathway in human bladder cancer cells]
ROS↑,
AMPK↑,
mTOR↑,
ChemoSen↑, ART has been shown to restore the sensitivity of a number of cancer types to chemotherapeutic drugs by modulating various signaling pathways
Tf↑, ART could upregulate the mRNA levels of transferrin receptor (a positive regulator of ferroptosis), thus inducing apoptosis and ferroptosis in A549 non-small cell lung cancer (NSCLC) cells.
Ferroptosis↑,
Ferritin↓, ferritin degradation, lipid peroxidation and ferroptosis
lipid-P↑,
CDK1↑, Cyclin-dependent kinase 1, 2, 4 and 6
CDK2↑,
CDK4↑,
CDK6↑,
SIRT1↑, Sirt1 levels
COX2/PTGS2↓,
IL1β↓, IL-1? ?
survivin↓, ART can selectively downregulate the expression of survivin and induce the DNA damage response in glial cells to increase cell apoptosis and cell cycle arrest, resulting in increased sensitivity to radiotherapy
DNAdam↑,
RadioS↑,

4992-

ART/DHA,

Dihydroartemisinin Increases the Sensitivity of Acute Myeloid Leukemia Cells to Cytarabine via the Nrf2/HO-1 Anti-Oxidant Signaling Pathway

in-vitro,

AML,

HL-60

Apoptosis↑, The combination of Ara-C and DHA synergistically promoted the apoptosis and differentiation of HL-60 cells
Diff↑,
ROS↓, Mechanistically, synergistic cytotoxic effects of Ara-C/DHA on HL-60 cells may be mediated by decreasing intracellular ROS levels
HO-1↓, However, DHA only caused the down-regulation of HO-1, whereas the expression level of nuclear Nrf2 was unaffected.
NRF2∅,

7183-

CHA,

The SUV39H1 inhibitor chaetocin induces differentiation and shows synergistic cytotoxicity with other epigenetic drugs in acute myeloid leukemia cells

in-vitro,

AML,

HL-60

in-vitro,

AML,

KG-1

in-vitro,

lymphoma,

U937

TumCD↓, The SUV39H1 inhibitor (chaetocin) and the G9a inhibitor (UNC0638) caused cell death in AML cells at high concentrations.
SUV39H↓,
CD11b↑, only chaetocin-induced CD11b expression and differentiation of AML cells at non-cytotoxic concentration.
Diff↑,
H3K9↓, Long-term incubation of chaetocin led to downregulation of SUV39H1 and reduction of H3K9 tri-methylation in HL-60 and KG-1a cells.
eff↑, Combination of chaetocin with suberoylanilide hydroxamic acid (SAHA, a histone deacetylase inhibitor) or JQ (a BET (bromodomain extra terminal) bromodomain inhibitor) showed synergistic cytotoxicity.

2798-

CHr,

Chrysin: a histone deacetylase 8 inhibitor with anticancer activity and a suitable candidate for the standardization of Chinese propolis

in-vitro,

BC,

MDA-MB-231

in-vivo,

NA,

90 mg/kg/day

xenograft animal model

HDAC↓, chrysin is a histone deacetylase inhibitor (HDACi) and that it markedly inhibited HDAC8 enzymatic activity
HDAC8↓,
TumCG↓, chrysin significantly suppressed cell growth and induced differentiation in MDA-MB-231 cells
Diff↑,

6294-

Cro,

Crocetin and Crocin from Saffron in Cancer Chemotherapy and Chemoprevention

Review,

Var,

*chemoPv↑, there are evidences that saffron and its carotenoids exert chemopreventive activity through anti-oxidant activity, cancer cells apoptosis, inhibition of cell proliferation, enhancement of cell differentiation, modulation of cell cycle progression and
*antiOx↑,
Apoptosis↑,
TumCP↓,
Diff↑,
TumCCA↑,
TumCG↓,
TOP2↓, (iv) direct or indirect regulation of topoisomerase II activity
hTERT/TERT↓, (vi) down-regulation of hTERT (human Telomerase Catalytic Subunit Expression
Inflam↓, crocetin has shown an anti-inflammatory effect, in vivo and in vitro, in terms of reduction of the activity of IL-1beta, TNF-alpha
IL1β↓,
TNF-α↓,
Casp8↑, elevated levels of caspase-8 activated, BAX protein and release of cytochrome C by mitochondria
BAX↑,
Cyt‑c↑,
ChemoSen↑, Synergistic effects of crocin with paclitaxel (PTX) and radiation (RT) have also been demonstrated in MCF-7 cells
RadioS↑,
Apoptosis↑, authors show a p53-dependent induction of apoptosis, inhibition of cell cycle progression, and down regulation of cyclin D1 and p21Cip1 expression
cycD1/CCND1↓,
P21↑, crocin upregulated CDK inhibitors (p21 and p27) and induced apoptosis up regulating Bax and downregulating of Bcl-2 with decreased Bcl-2/Bax ratio and activation of caspase 9
p27/CDKN1B↑,
Bcl-2↓,
Bax:Bcl2↑,
Casp9↑,
EMT↓, crocetin reversion of the Epithelial to Mesenchymal Trans-differentiation (EMT) phenotype with increased epithelial (E-cadherin) and decreased mesenchymal (Beta-catenin and N-cadherin)
E-cadherin↑,
β-catenin/ZEB1↓,
N-cadherin↓,

6317-

DRE,

The efficacy of dandelion root extract in inducing apoptosis in drug-resistant human melanoma cells

in-vitro,

Melanoma,

A375

Apoptosis↑, we show that dandelion root extract (DRE) specifically and effectively induces apoptosis in human melanoma cells without inducing toxicity in noncancerous cells.
selectivity↑,
Casp8↑, DRE-induced apoptosis activates caspase-8 in A375 cells early on, demonstrating employment of an extrinsic apoptotic pathway to kill A375 cells
mt-ROS↑, Reactive Oxygen Species (ROS) generated from DRE-treated isolated mitochondria indicates that natural compounds in DRE can also directly target mitochondria.
eff↑, Interestingly, the relatively resistant G361 human melanoma cell line responded to DRE when combined with the metabolism interfering antitype II diabetic drug metformin.
*toxicity↓, without toxicity to healthy cells. This triterpene is regarded as cytostatic and not cytotoxic.
Diff↑, Taraxacum Officinale was an effective inducer of differentiation in mouse melanoma cells.
TumCP↓, up-regulated melanogenesis and decreased cell proliferation in mouse melanoma [7].
chemoPv↑, taraxasterol (a triterpenoid), is a worthy chemopreventative agent
*ROS↓, ethanolic Taraxacum Officinale extracts and derivative forms thereof reduce levels of reactive oxygen species (ROS) and nitric oxide production (NO) and inhibit COX-2 expression or its antioxidant activity,
*NO↓, Dandelion flower extracts (DFE) were tested on RAW264.7 cells (mouse macrophages) and exhibited inhibition of NO production in these noncancerous cells.
*COX2/PTGS2↓,
*RNS↓, The inhibition of reactive nitrogen species (RNS) as well as ROS by DFE was attributed to its phenolic components
TumCI↓, Inhibition of cell invasion was corroborated by reduced matrix metalloproteinase activity of MMP-2 and -9, as well as reduced phosphorylation levels of src and FAK [2]
MMP2↓,
MMP9↓,
p‑Src↓,
p‑FAK↓,

6365-

DRE,

AN OVERVIEW OF THERAPEUTIC POTENTIALS OF TARAXACUM OFFICINALE (DANDELION): A TRADITIONALLY VALUABLE HERB WITH A REACH HISTORICAL BACKGROUND

Review,

Var,

*Inflam↓, including anti-inflammatory, anti-tumor, immunostimulatory, anti-microbial, anti-viral, anti-oxidant, anti-diabetic, geno-protective, diuretic and kidney-protective, hepato-protective, neuro-protective
*AntiTum↑,
*Imm↑,
*antiOx↑,
*AntiDiabetic↑,
*diuretic↑,
*RenoP↑,
*hepatoP↑,
*neuroP↑,
AntiTum↑, In 1981, for the first time, it was shown that the hot water extract of dandelion possessed anti-tumor activity
TNF-α↑, It induces apoptotic cell death by raising the production of tumor necrosis factor (TNF)-α and interleukin (IL)-1α
IL1β↑,
Apoptosis↑, The TNF-α and IL-1α are two potent inducers of cancer cell apoptosis
MMP2↓, dampening the activities of matrix metallopro- teinases (MMPs) such as MMP-2 and MMP-9
MMP9↑,
eff↑, Combination treatment with TRAIL targeting and dandelion resulted in TRAIL-induced apoptosis mediated through inhibition of the MKK7-TIPRL interaction and subsequent ac- tivation of MKK7-JNK phosphorylation.
Diff↑, The differentiation-inducing effects of dandelion on the human leukemia cell line (HL60) and a B16 mouse melanoma-derived sub-clone with high differentiation capability (B16 2F2) were investigated
*ROS↓, Both cell viability and ROS assays confirmed that extract effectively attenuated glutamate-induced cytotoxicity and ROS generation.
*HO-1↑, Moreover, extract increased the expression of HO-1 and promoted the nuclear translocation of nuclear factor erythroid 2-relat- ed factor-2 (Nrf2).
*NRF2↑,
*lipid-P↓, andelion can improve lipid metabolism and is advantageous in preventing diabetic complica- tions from lipid peroxidation and free radicals in diabetic rats124

6835-

EMD,

Suppressed transformation and induced differentiation of HER-2/neu-overexpressing breast cancer cells by emodin

in-vitro,

BC,

HER2/EBBR2↓, our results indicate that emodin inhibits HER-2/neu tyrosine kinase activity and preferentially suppresses growth and induces differentiation of HER-2/neu-overexpressing cancer cells.
TumCG↓,
Diff↑,

5520-

EP,

Nanosecond Pulsed Electric Field (nsPEF): Opening the Biotechnological Pandora’s Box

Review,

Var,

Ca+2↑, leading to an incremental increase in cytoplasmic Ca2+ concentration,
Apoptosis↑, from apoptosis up to cell differentiation and proliferation.
Diff↑,
TumCP↓,
Wound Healing↑, sterilization in the food industry, seed germination, anti-parasitic effects, wound healing, increased immune response
CellMemb↑, available evidence suggest that the increase in cytoplasmic Ca2+ concentration produced by the application of nsPEF could be due to the formation of membrane nanopores.
VGCC↑, most probable cause should be the increase of intracellular Ca2+ concentration via VGCC activation [185].
VGSC↑, findings relating VGNC activation by nsPEF are exciting and deserve more attention.
DNAdam↑, Stacey et al. in 2002 demonstrated that exposing cancer cells to nsPEF with 60 kV/cm could induce DNA damage [243]
selectivity↑, More importantly for nsPEF as cancer treatment, tumor cells are more sensitive to nsPEF than normal cells [246].

7011-

Fuc,

ATO,

VitA,RetA,

Fucoidan enhances the therapeutic potential of arsenic trioxide and all-trans retinoic acid in acute promyelocytic leukemia, in vitro and in vivo

NA,

APL,

APL NB4

vitro+vivo,

NA,

TumCCA↑, ATO and ATRA at therapeutic and sub-therapeutic doses, there was an increase in sub-G0/G1 cells, annexin V/PI-positive-apoptotic cells and DNA fragmentation.
DNAdam↑,
TumCP↓, this reduction in proliferation and increase in apoptosis was accompanied by enhanced myeloid differentiation as indicated by an increased expression of CD11b.
Apoptosis↑,
Diff↑,
CD11b↑,
eff↑, Fucoidan synergizes ATO-mediated apoptosis in APL cells
Dose↝, Decreased proliferation was observed at both low (0.25, 0.5 μM) and clinical doses of ATO (1 μM).

2511-

H2,

Molecular hydrogen suppresses glioblastoma growth via inducing the glioma stem-like cell differentiation

in-vivo,

GBM,

U87MG

mice

TumCG↓, hydrogen inhalation could effectively suppress GBM tumor growth and prolong the survival of mice with GBM
OS↑,
CD133↓, hydrogen treatment markedly downregulated the expression of markers involved in stemness (CD133, Nestin), proliferation (ki67), and angiogenesis (CD34) and also upregulated GFAP expression, a marker of differentiation.
Ki-67↓,
angioG↓,
Diff↑, pregulated GFAP expression, a marker of differentiation
TumCMig↓, Moreover, hydrogen treatment also suppressed the migration, invasion
TumCI↓,
Dose↝, AMS-H-3 hydrogen-oxygen nebulizer machine (Asclepius Meditec Inc., Shanghai, China), which produces 67% H2 and 33% O. inhaled the mixed air for 1 h two times per day
BBB↑, hydrogen gas can easily cross the BBB.
mt-ROS↑, Intriguingly, molecular hydrogen has also been reported to act as a mitohormetic effector by mildly inducing mitochondrial superoxide production [28]. Perhaps hydrogen-induced ROS promoted the differentiation and downregulation of stemness in GSCs.

7385-

IBC,

Fighting cancer by triggering non-canonical mitochondrial permeability transition-driven necrosis through reactive oxygen species induction

vitro+vivo,

Lung,

A549

in-vitro,

BC,

4T1

Apoptosis↑, Previous reports demonstrated that isobavachalcone (IBC), a natural chalcone, has anticancer effect by apoptosis induction
necrosis↑, Here, we found that IBC induced regulated necrosis in cancer cells
ROS↑, IBC triggered non-apoptotic cell death in lung and breast cancer cells mediated by reactive oxygen species (ROS)
mtDam↑, IBC caused mitochondrial injury and dysfunction as evidenced by mitochondrial Ca2+ overload, the opening of MPT pore, mitochondrial membrane potential collapse, and structural damages
Ca+2↑,
MPT↑,
MMP↓,
AntiCan↑, In addition, IBC showed an anticancer effect in a 4T1 breast cancer cell-derived allograft mouse model
*AntiBio↑, Isobavachalcone (IBC), a natural chalcone, has anticancer, antimicrobial, anti-inflammatory, antioxidative, and neuroprotective activities
*Inflam↓,
*antiOx↓,
*neuroP↑,
p‑Akt↓, IBC potentially inhibits Akt by reducing Akt phosphorylation in lung cancer cells
DHODH↓, in acute myeloid leukemia cells, IBC directly targets dihydroorotate dehydrogenase (DHODH) to induce apoptosis and differentiation . BC is a potent inhibitor of Akt and DHODH [24,25] and actively regulates MAPKs
Diff↑,
MAPK↑, robust MAPK activation by IBC

7772-

IBC,

Isobavachalcone inhibits acute myeloid leukemia: Potential role for ROS-dependent mitochondrial apoptosis and differentiation

vitro+vivo,

AML,

NOD/SCID mice

Apoptosis↑, Isobavachalcone (IBC) has been shown to induce apoptosis and differentiation of acute myeloid leukemia (AML) cells.
Diff↑,
tumCV↓, Herein, IBC exhibited significant inhibition on the cell viability, proliferation, and the colony formation ability of AML cells.
TumCP↓,
MMP↓, IBC induced mitochondrial apoptosis evidenced by reduced mitochondrial membrane potential, increased Bax level, decreased Bcl-2, Bcl-xL, and Mcl-1 levels, elevated cytochrome c level in the cytosol and increased cleavage of caspase-9, caspase-3, and
BAX↑,
Bcl-2↓,
Bcl-xL↓,
Mcl-1↓,
Cyt‑c↑,
cl‑Casp3↑,
cl‑Casp9↑,
cl‑PARP↑,
p‑MEK↑, increase of the phosphorylation of MEK and ERK and the C/EBPα expression as well as the C/EBPβ LAP/LIP isoform ratio, which was significantly reversed by U0126, a specific inhibitor of MEK
p‑ERK↑,
ROS↑, Notably, IBC enhanced the intracellular ROS level.
eff↓, More importantly, IBC-induced apoptosis and differentiation of HL-60 cells were significantly mitigated by NAC.

7722-

IP6,

Cancer inhibition by inositol hexaphosphate (IP6) and inositol: from laboratory to clinic

Review,

Var,

eff↑, The most consistent and best anticancer results were obtained from the combination of IP6 plus inositol.
TumCP↓, In addition to reducing cell proliferation, IP6 increases differentiation of malignant cells, often resulting in a reversion to normal phenotype.
Diff↑,
TumCCA↑, Exogenously administered IP6 is rapidly taken into the cells and dephosphorylated to lower-phosphate inositol phosphates, which further interfere with signal transduction pathways and cell cycle arrest.
Imm↑, Enhanced immunity and antioxidant properties can also contribute to tumor cell destruction.
antiOx↑,
BioAv↑, Because it is abundantly present in regular diet, efficiently absorbed from the gastrointestinal tract, and safe, IP6 holds great promise in our strategies for the prevention and treatment of cancer.
toxicity↓,
ChemoSen↑, IP6 plus inositol enhances the anticancer effect of conventional chemotherapy, controls cancer metastases, and improves the quality of life, as shown in a pilot clinical trial.
TumMeta↓,
QoL↑,

7725-

IP6,

Inositol hexaphosphate inhibits growth and induces differentiation of PC-3 human prostate cancer cells

in-vitro,

Pca,

PC3

TumCG↓, A significant dose- and time-dependent growth inhibition was observed as tested by the MTT-incorporation assay (P < 0.05 at 1 mM InsP6 after 24 h treatment, P < 0.01 at 0.1 mM after 3 days).
HLA-I/II↑, A 9- to 10-fold increase (P < 0.01) in expression of HLA class I molecule associated with tumor immunosurveillance and cell differentiation was induced by InsP6.
Diff↑,

7645-

IP6,

Ins,

Anticancer Properties of Inositol Hexaphosphate and Inositol: An Overview

AntiCan↑, A consistent and reproducible anticancer action of IP6 has been demonstrated in various experimental models.
TumCP↓, IP6 reduces cell proliferation, induces apoptosis and differentiation of malignant cells via PI3K, MAPK, PKC, AP-1 and NF-kappaB.
Apoptosis↑,
Diff↑,
p27/CDKN1B↓, down-regulates p27, inhibits pRB phosphorylation and cell cycle (23), reduces PI3K and consequently counteracts the activation of PKC/RAS/ERK pathway (23), downregulates Akt and ERK, leading to reduction of NF-kappaB and inhibition of inflammation.
pRB↓,
PI3K↓,
RAS↓,
ERK↓,
Akt↓,
NF-kB↓,
Inflam↓,
AntiTum↓, Studies demonstrated that continuous administration of 2% IP 6 in the drinking water, beginning 24 h after implantation of DU-145 prostate cancer cells, resulted in a 64% decrease in tumor burden

7646-

IP6,

Ins,

Protection against cancer by dietary IP6 and inositol

Review,

Var,

*antiOx↑, For a long time IP(6) has been recognized as a natural antioxidant.
TumCG↓, Recently IP(6) has received much attention for its role in cancer prevention and control of experimental tumor growth, progression, and metastasis.
TumMeta↓,
Imm↑, ability to enhance immune system, prevent pathological calcification and kidney stone formation, lower elevated serum cholesterol, and reduce pathological platelet activity.
kidSt↓,
LDL↓,
TumCCA↑, Exogenously administered IP(6) is rapidly taken up into cells and dephosphorylated to lower inositol phosphates, which further affect signal transduction pathways resulting in cell cycle arrest.
TumCP↓, In addition to reducing cell proliferation, IP(6) also induces differentiation of malignant cells.
Diff↑,
ChemoSen↑, Preliminary studies in humans show that IP(6) and inositol, the precursor molecule of IP(6), appear to enhance the anticancer effect of conventional chemotherapy, control cancer metastases, and improve quality of life.
QoL↑,

7690-

IP6,

Ins,

Inositol Hexaphosphate (IP6) and Colon Cancer: From Concepts and First Experiments to Clinical Application

Review,

Colon,

AntiCan↑, the striking and broad-spectrum anticancer activity of IP6, consistently demonstrated in different experimental models, has been in a spotlight of the scientific community dealing with the nutrition and cancer during the last several decades
Imm↑, Enhanced immunity and antioxidant properties also contribute to the tumor cell destruction.
antiOx↑,
TumCP↓, Along with this reduction in cell proliferation, rather normalization, IP6 induces differentiation and maturation of malignant cells,
Diff↑,
TumCG↓, Also, IP6 administered in drinking water was a potent inhibitor of in vivo growth of human prostate cancer xenografts in nude mice
eff↑, Synergistic cancer inhibition by IP6 when combined with inositol was observed in colon cancer
P21↓, IP6 downregulates p21 and p27, inhibits pRB phosphorylation and cell cycle progression [72], targets PI3K/Akt pathway and counteracts the activation of PKC/RAS/ERK pathway
p27/CDKN1B↓,
pRB↓,
TumCCA↑,
PI3K↓,
Akt↓,
PKCδ↓,
RAS↓,
ERK↓,
NF-kB↓, IP6 reduces NF-kappaB and inhibits inflammation
Inflam↓,
MMP9↓, IP6 and Ins were shown to inhibit the MMP-9
IronCh↑, Additionally, IP6 can remove the excess iron, which may facilitate and augment colorectal cancer IP6
NK cell↑, IP6 was shown to augment the activity of natural killer (NK) cells in vitro, and in vivo
selectivity↑, IP6 was shown that while it can sensitize cancer cells for treatment, at the same time can offer a protection to normal tissues.
ChemoSen↑, Furthermore, IP6 was shown to acts synergistically with standard chemotherapeutics. Cancer therapy recognizes the importance of using combination therapy with rationale to increase efficacy and decrease side-effects of conventional chemotherapy.
chemoP↑, when IP6 + Ins was given in combination with chemotherapy, side effects of chemotherapy, such as drop in leukocyte and platelet counts, nausea, vomiting, alopecia, were diminished and patients were able to perform their daily activities, shown mostly
toxicity↓, In a phase I clinical trial Ins was shown to be safe and well-tolerated
Remission↑, A patient with metastatic melanoma declined traditional therapy and opted to try the IP6 + Ins supplement only. He received a complete remission and remained in remission 3 years later.

7699-

IP6,

IP6: From Seeds to Science—A Natural Compound’s Path to Clinical Promise

Review,

Var,

*Iron∅, Early reports fueled concerns that high dietary phytate intake could contribute to mineral deficiencies, albeit without direct scientific evidence, particularly in populations lacking dietary diversity
ChemoSen↑, Preclinical and clinical research indicate that IP6, alone or in tandem with inositol (Ins), selectively targets cancer cells and enhances chemotherapy efficacy.
*cardioP↑, Growing evidence also suggests that IP6 plays a protective role in cardiovascular health, neurodegenerative disorders, and metabolic diseases
neuroP↑,
IronCh∅, confirmed that life-time consumption of IP6±Inositol did not cause any reduction in Ca, Mg, Fe, or Zn levels in the blood or bones of rats and mice
P21↓, IP6 downregulates cell cycle regulators such as p21 and p27, inhibits phosphorylation of retinoblastoma protein (pRB), and suppresses PI3K/protein kinase B (PI3K/Akt)
p27/CDKN1B↓,
p‑pRB↓,
PI3K↓,
Akt↓,
NF-kB↓, decreased NF-kB activity and inflammatory responses
Inflam↓,
TumW↓, After 12 days of treatment, IP6-treated mice exhibited a 3.4-fold lesser tumor weight as compared to controls
TumCI↓, figure 3
TumMeta↓,
Imm↑,
Diff↑,
selectivity↑, the growth of non-cancerous MCF-10A epithelial breast cells remained unaffected, further illustrating IP6’s capacity to differentiate between cancerous and normal cells
toxicity↓, Importantly, no adverse effects have been reported in studies administering IP6 or Ins to humans or animal models, even at high doses
RenoP↑, Plant-based food diets are often recommended to individuals with chronic kidney disease, where the protective effects of the diet are ascribed to IP6
QoL↑, Clinical trials, though still sparse, have yielded encouraging results regarding IP6’s synergistic enhancement of chemotherapy efficacy and improvement of patients’ quality of life.

7838-

ISQ,

Protective effects of isoquercitrin on streptozotocin‐induced neurotoxicity

in-vivo,

AD,

rats

*Apoptosis↓, isoquercitrin (ISO) display the most effective anti‐cytotoxic activities via inhibiting STZ‐induced apoptosis, mitochondria dysfunction and oxidative stress.
*mtDam↓,
*ROS↓,
*Diff↑, ISO largely rescues STZ‐induced differentiation inhibition and enhances neurite outgrowth of Neuro2a (N2a) cells in vitro.
*cognitive↑, oral administration of ISO protects hippocampal neurons from STZ‐induced neurotoxicity and significantly improves the cognitive and behavioural impairment in STZ‐induced AD rats.

4233-

LEC,

Lecithinized brain-derived neurotrophic factor promotes the differentiation of embryonic stem cells in vitro and in vivo

in-vitro,

Nor,

embryonic stem cells

*BDNF↑, In the current study, we show that lecithinized BDNF (PC-BDNF) has a higher affinity than BDNF for neural precursor cells.
*motorD↑, PC-BDNF-treated cells was more effective than BDNF-treated cells at improving impaired motor function caused by spinal cord injury.
*Diff↑, PC-BDNF has a better potential than BDNF for promoting neural differentiation, partly due to a higher cellular affinity.

2242-

MF,

Electromagnetic stimulation increases mitochondrial function in osteogenic cells and promotes bone fracture repair

in-vitro,

Nor,

2.5G, 5G, 10G, 15G, and 20G

*MMP↑, we show that application of a low intensity constant EM field source on osteogenic cells in vitro resulted in increased mitochondrial membrane potential and respiratory complex I activity and induced osteogenic differentiation.
*Diff↑,
*OXPHOS↑, effect was mediated via increased OxPhos activity
*BMD↑, EM field source enhanced fracture repair via improved biomechanical properties and increased callus bone mineralization
ATP∅, higher mitochondrial OxPhos activity leads to higher ATP production, increased cellular activity leads to increased ATP consumption.

2243-

MF,

Pulsed electromagnetic fields increase osteogenetic commitment of MSCs via the mTOR pathway in TNF-α mediated inflammatory conditions: an in-vitro study

in-vitro,

Nor,

mesenchymal stem cells (MSCs)

*eff↑, PEMF exposure increased cell proliferation and adhesion
*mTOR↑, PEMFs contribute to activation of the mTOR pathway via upregulation of the proteins AKT, MAPP kinase, and RRAGA, suggesting that activation of the mTOR pathway is required for PEMF-stimulated osteogenic differentiation.
*Akt↑,
*PKA↑, PEMFs increase the activity of certain kinases belonging to known intracellular signaling pathways, such as the protein kinase A (PKA) and the MAPK ERK1/2
*MAPK↑,
*ERK↑,
*BMP2↑, PEMFs stimulation also upregulates BMP2 expression in association with increased differentiation in mesenchymal stem cells (MSCs
*Diff↑,
*PKCδ↓, Decrease in PKC protein (involved on Adipogenesis)
*VEGF↑, Increase on VEGF (involved on angiogenesis)
*IL10↑, PEMF induced a significant increase of in vitro expression of IL-10 (that exerts anti-inflammatory activity)

2240-

MF,

Pulsed electromagnetic field induces Ca2+-dependent osteoblastogenesis in C3H10T1/2 mesenchymal cells through the Wnt-Ca2+/Wnt-β-catenin signaling pathway

in-vitro,

Nor,

C3H10T1/2

30 Hz, 1 mT, 2 h/day

PEMF output waveform consisted of a 400 kV/m pulsed burst (pulse width 0.2 m s; pulse wait 0.02 m s; burst width 5 m s; burst wait 60 m s; pulse rise 0.3 m s; pulse fall 2.0 m s) repeated at 30 Hz.

*Ca+2↑, intracellular [Ca2+]i in C3H10T1/2 cells can be upregulated upon exposure to PEMF
*Diff↑, PEMF-induced C3H10T1/2 cell differentiation was Ca2+-dependent.
*BMD↑, pro-osteogenic effect of PEMF on Ca2+-dependent osteoblast differentiation
*Wnt↑, PEMF promoted the gene expression and protein synthesis of the Wnt/β-catenin pathway.
*β-catenin/ZEB1↑, PEMF activates the Wnt/b-catenin signaling pathway in C3H10T1/2 cells
*eff↝, These data indicated that increased intranuclear [Ca2+]i resulted in altered electrical activity in the nucleus.

2255-

MF,

Pulsed Electromagnetic Fields Induce Skeletal Muscle Cell Repair by Sustaining the Expression of Proteins Involved in the Response to Cellular Damage and Oxidative Stress

in-vitro,

Nor,

SkMC

1.5 mT PEMF for four hours repeated for two days

*HSP70/HSPA5↑, HSP70), which can promote muscle recovery, inhibits apoptosis and decreases inflammation in skeletal muscle, together with thioredoxin, paraoxonase, and superoxide dismutase (SOD2), which can also promote skeletal muscle regeneration following injury
*Apoptosis↓,
*Inflam↓,
*Trx↓,
*PONs↓, Paraoxonase 2 (PON2, Paraoxonase 3 (PON3) (+19% vs. controls)
*SOD2↓,
*TumCG↑, PEMF treatment enhanced muscle cell proliferation by approximately 20% both in cells grown in complete medium
*Diff↑, suggest the potential role of PEMF in the induction of muscle differentiation
*HIF2a↑, hypoxia-inducible transcription factor 2a (HIF-2a) (+40% vs. controls),
*Cyt‑c↑, Cytochrome c (+39% vs. controls)
P21↑, p21/CIP1 (+27% vs. controls)

4356-

MF,

Pulsed electromagnetic fields synergize with graphene to enhance dental pulp stem cell-derived neurogenesis by selectively targeting TRPC1 channels

in-vitro,

Nor,

(10 min) and low amplitude (2 mT) PEMF

human dental pulp stem cells (hDPSCs)

*Diff↑, brief PEMF exposure promotes in vitro differentiation by activating a TRPC1-mitochondrial axis
*TRPC1↑,
*ROS↑, PEMF-stimulated neurogenic induction of hDPSCs through their mutual capacity to activate TRPC1with subsequent ROS production.

530-

MF,

Low frequency sinusoidal electromagnetic fields promote the osteogenic differentiation of rat bone marrow mesenchymal stem cells by modulating miR-34b-5p/STAC2

in-vivo,

Nor,

15 Hz, 0.4 -1 mT

rat bone marrow mesenchymal stem cells

*miR-34b-5p↓, expression of miR-34b-5p decreased under SEMF stimulation,
*ALP↑, significant upregulation in the relative expression levels of osteogenic markers (ALP, RUNX2, BMP2, OCN, and OPN)
*RUNX2↑,
*BMP2↑,
*OCN↑,
*OPN↑,
*β-catenin/ZEB1↑, protein expression levels of osteogenic makers, including Active-β-catenin, RUNX2, and ALP, were elevated upon SEMFs exposure at 0.4 mT, 0.7 mT, and 1 mT
*STAC2↑, subsequently increasing STAC2 level.
*Diff↑, electromagnetic fields promote the osteogenic differentiation
*BMD↑, low-frequency SEMFs promote osteogenesis

3536-

MF,

Targeting Mesenchymal Stromal Cells/Pericytes (MSCs) With Pulsed Electromagnetic Field (PEMF) Has the Potential to Treat Rheumatoid Arthritis

Review,

Arthritis,

Review,

Stroke,

*Inflam↓, (PEMF), a biophysical form of stimulation, has an anti-inflammatory effect by causing differentiation of MSCs.
*Diff↑,
*toxicity∅, PEMF have been reported to last up to 3 months or longer in human patients with chronic inflammatory/autoimmune disorders (38) with no evidence of adverse effects (39).
*other↑, MSCs to promote immunomodulation and improve cartilage and bone regeneration in vitro (10) and in vivo (73).
*SOX9↑, enhanced chondrogenic gene expression in SOX-9, COL II, and aggrecan in MSCs
*COL2A1↑,
*NO↓, Prevented increases in NO
*PGE2↓, Exposure to PEMF induces early upregulation of adenosine receptors A2A and A3 that reduce PGE2 and pro-inflammatory cytokines such as TNF-α, which combine to inhibit the activation of transcription factor NF-kB
*NF-kB↓,
*TNF-α↓, 1 h exposure to PEMF has been shown to down-regulate both NF-kB and TNF-α in murine macrophages
*IL1β↓, By inhibiting NF-kB activation (94), exposure to PEMF led to decreased production of TNF-α, IL-1β, IL-6, and PGE2 in human chondrocytes, osteoblasts, and synovial fibroblasts
*IL6↓,
*IL10↑, Inhibited release of PGE2, and IL-1β and IL-6 production, while stimulating release of IL-10 in synovial fibroblasts
*angioG↑, progenitor cells (EPCs) to an RA injury site is important for repair of vasculature and angiogenesis. PEMF has also been reported to increase the number and function of circulating EPCs in treating myocardial ischemia/reperfusion (I/R) injury in rat
*MSCs↑, Since PEMF have been shown to stimulate the production of MSCs
*VEGF↑, promoting the expression of growth factors such as VEGF and TGF-β
*TGF-β↑,
*angioG↝, modulate the aberrant angiogenesis present in RA: reported to significantly reduce activation levels of VEGF (15), to inhibit the proliferative ability of HUVECs, and to reduce the extent of vascularization in diseased tissue
*VEGF↓, diseased tissue
Ca+2↝, By restoring normal Ca2+ ion flux and Na+/K+ balance, the cell can begin the process of down-regulating inflammatory cytokines, HSPs, and proangiogenic molecules such as VEGF, making it possible for the body to commence rebuilding healthy cartilage.

3464-

MF,

Progressive Study on the Non-thermal Effects of Magnetic Field Therapy in Oncology

Review,

Var,

AntiTum↑, frequency below 300 Hz) exert anti-tumor function, independent of thermal effects
TumCG↓, Magnetic fields (MFs) could inhibit cell growth and proliferation; induce cell cycle arrest, apoptosis, autophagy, and differentiation; regulate the immune system; and suppress angiogenesis and metastasis via various signaling pathways
TumCCA↑,
Apoptosis↑,
TumAuto↑,
Diff↑,
angioG↓,
TumMeta↓,
EPR↑, MFs not only promote the absorption of chemotherapy drugs by producing small holes on the surface of cell membrane
ChemoSen↑,
ROS↑, MF treatment has been shown to promote the generation of ROS in many studies (31, 71, 72), with exposure within a 60 Hz sinusoidal MF for 48 h in induced human prostate cancer for DU145, PC3, and LNCaP apoptoses
DNAdam↑, Repetitive exposure to LF-MFs induced DNA damage and accumulation of DSBs and triggered apoptosis in Hela and MCF7 cell lines
P53↑, PMFs could trigger apoptosis cell death by upregulating the p53 level and through the mitochondrial-dependent pathway
Akt↓, LF-MFs (300 mT, 6 Hz, 24 h) also induced apoptosis by suppressing protein kinase B (Akt) signaling, activating p38 mitogen-activated protein kinase (MAPK) signaling, and caspase-9, which is the executor of the mitochondrial apoptosis pathway
MAPK↑,
Casp9↑,
VEGFR2/KDR/Flk1↓, reducing the expression and activation levels of VEGFR2
P-gp/ABCB1↓, A combination with the SMF (8.8 m T, 12 h) decreased the expression of P-glycoprotein (P-gp) in K562 cancer cells, while adriamycin itself induced an increase

3535-

MFrot,

MF,

Pulsed Electromagnetic Field Stimulation in Osteogenesis and Chondrogenesis: Signaling Pathways and Therapeutic Implications

Review,

Nor,

*eff↑, Pulsed electromagnetic fields (PEMFs) are currently used as a safe and non-invasive treatment to enhance bone healing and to provide joint protection.
*COL2A1↑, exposure to PEMFs induced increased collagen type II (Col2) expression and glycosaminoglycan (GAG) content
*SOX9↑, PEMFs significantly increased the expression of chondrogenic genes (SOX9, collagen type II, and aggrecan) and the deposition of cartilaginous matrix (sulphated GAG)
*Ca+2↑, Intracellular Ca2+ increase
*FAK↑, FAK activation
*F-actin↑, increased F-actin network formation
*Inflam↓, anti-inflammatory effect of PEMFs exposure has been extensively described above
*other↑, PEMFs exert a strong anti-inflammatory effect protecting cartilage tissue from the catabolic activity of pro-inflammatory cytokines.
*Diff↑, commonly recognized that PEMFs exposure induces osteogenic differentiation of MSCs
*BMD↑, Emerging evidence shows that PEMFs stimulation represents a safe non-invasive approach to favor bone repair and optimize bone tissue engineering

2311-

MFrot,

MF,

Magnetic fields as a potential therapy for diabetic wounds based on animal experiments and clinical trials

in-vivo,

Nor,

HaCaT

diabetic wounds based on animal experiments

*COX2/PTGS2↓, ELF‐EMF exposure enhances the proliferation of keratinocyte HaCaT cells and improves early NOS activity, while decreases cyclooxygenase 2 (COX‐2) which indicates its role in accelerating the transition from inflammation phase to remodelling phase.
*Inflam↓,
*MMP9↑, Exposure to ELF‐EMF with frequency of 50 Hz and intensity of 1 mT increases cytokine release and activates the expression of MMP‐9 in human immortalized keratinocytes
*GPx↑, On the contrary, ELF‐EMF activates glutathione peroxidase with decrease in malondialdehyde in the live tissue of rats during wound healing process
*Diff↑, ELF‐EMF promotes the proliferation and differentiation of transplanted epidermal stem cells in the full‐thickness defect nude mice

5254-

NCL,

The magic bullet: Niclosamide

Review,

Var,

Wnt↓, In particular, niclosamide inhibits multiple oncogenic pathways such as Wnt/β-catenin, Ras, Stat3, Notch, E2F-Myc, NF-κB, and mTOR and activates tumor suppressor signaling pathways such as p53, PP2A, and AMPK.
β-catenin/ZEB1↓,
RAS↓,
STAT3↓,
NOTCH↓,
E2Fs↓,
mTOR↓,
eff↑, Moreover, niclosamide potentially improves immunotherapy by modulating pathways such as PD-1/PDL-1.
PD-1↓,
PD-L1↓, primarily through PD-L1 ligand downregulation in cancer cells.
BioAv↝, The original pharmacokinetics study showed that the maximal serum concentration can reach 0.25-6.0ug/ml (0.76-18.34 µM) following administration of a single 2g dose (11).
toxicity↓, a strong safety profile and tolerability in humans.
BioAv↑, A potential solution to the aforementioned challenge is niclosamide ethanolamine (NEN), a salt form of niclosamide that also functions as a mitochondrial uncoupler with a superior safety profile and enhanced bioavailability
ETC↑, NEN activates the ETC to boost NADH oxidation, thereby leading to an increased intracellular NAD+/NADH ratio and driving the TCA cycle forward.
NADH:NAD↓,
TCA↑,
Warburg↓, leading to a reversal of the Warburg effect and the induction of cellular differentiation
Diff↑,
AMPK↑, figure 3
P53↑,
PP2A↑,
HIF-1↓,
KRAS↓,
Myc↓,
RadioS↑, leading to a reversal of the Warburg effect and the induction of cellular differentiation
ChemoSen↑, Niclosamide has shown synergistic anti-tumor effects with a broad spectrum of chemotherapy drugs.
Dose↝, In this trial, either 500mg or 1000mg niclosamide was given three times daily to patients. However, the maximal plasma concentration ranged from 35.7–82 ng/mL (0.1µM-0.25 µM), a range that failed to be consistently above the minimum effective concent
Dose↑, In contrast, the ongoing clinical trial NCT02807805 is administering 1200 mg of reformulated orally bioavailable niclosamide orally (PO) three times daily to patients, resulting in 0.21µM-0.723 plasma niclosamide concentrations exceeding the therape

2055-

PB,

The Effects of Butyric Acid on the Differentiation, Proliferation, Apoptosis, and Autophagy of IPEC-J2 Cells

in-vitro,

Nor,

IPEC-J2

0.2-0.4 mM BT

also  (0.5 mM or higher)

*Diff↑, 0.2-0.4 mM BT promoted the differentiation of procine jejunal epithelial (IPEC-J2) cells
*TumCP↓, BT at high concentrations inhibited the IPEC-J2 cell proliferation and induced cell cycle arrest in the G2/M phase.
*TumCCA↑,
*ROS↑, BT triggered IPEC-J2 cell apoptosis via the caspase8-caspase3 pathway accompanied by excess reactive oxygen species (ROS) and TNF-α production (0.5 mM or higher)
*Casp3↑,
*TNF-α↑,

2064-

PB,

Rad,

Phenylbutyrate Attenuates the Expression of Bcl-XL, DNA-PK, Caveolin-1, and VEGF in Prostate Cancer Cells

in-vitro,

Pca,

PC3

2 or 5 mM PB

in-vitro,

Pca,

DU145

in-vitro,

Pca,

LNCaP

Bcl-xL↓, PB attenuates the expression of the apoptosis antagonist Bcl-XL, the double-strand break repair protein DNA-dependent protein kinase, the prostate progression marker caveolin -1, and the pro-angiogenic vascular endothelial growth factor
Cav1↓, PB Inhibits the Protein Expression of DNA-PK and Caveolin-1 in Prostate Cancer Cells
VEGF↓, Secretion of VEGF from Prostate Cancer Cells is Attenuated by PB
RadioS↑, PB was found to act in synergy with ionizing radiation to induce apoptosis in prostate cancer cells
chemoP↑, Moreover, butyrate may act as a chemopreventive agent against colon cancer [22]
HDAC↓, mechanism of action of butyrate and butyrate derivatives involves inhibition of the histone deacetylase activity in cells
*toxicity↓, Due to its low toxicity in vivo
Diff↑, differentiation-inducing activity towards cancer cells, PB and other butyrate derivatives have been considered as potential anticancer agents
Prot↓, Thus, our results show that PB can, like butyrate, attenuate the protein levels of Bcl-XL in prostate cancer cells.

2036-

PB,

Phenylbutyrate induces apoptosis in human prostate cancer and is more potent than phenylacetate

in-vitro,

Pca,

in-vivo,

NA,

Copenhagen rats

TumCG↓, PB is 1.5-2.5 times more active at inhibiting growth and inducing programmed cell death than PA at clinically achievable doses against each human prostate cancer line studied.
eff↑, Prostate cancer cell lines overexpressing P-glycoprotein or possessing heterogeneous molecular alterations, including p53 mutations, are also sensitive to the effects of PB.
Diff↑, PB is equipotent to sodium butyrate, which induces apoptosis and differentiation through multiple mechanisms.

2040-

SAHA,

The histone deacetylase inhibitor SAHA arrests cancer cell growth, up-regulates thioredoxin-binding protein-2, and down-regulates thioredoxin

in-vitro,

Pca,

LNCaP

7.5 μM

in-vitro,

CRC,

T24/HTB-9

in-vitro,

BC,

MCF7

HDAC↓, SAHA) is a potent inhibitor of histone deacetylases (HDACs) that causes growth arrest, differentiation, and/or apoptosis of many tumor types in vitro and in vivo.
TumCG↓,
Diff↑,
Apoptosis↑,
TXNIP↑, SAHA induces the expression of vitamin D-up-regulated protein 1/thioredoxin-binding protein-2 (TBP-2) in transformed cells

5004-

Sal,

Targeting Telomerase Enhances Cytotoxicity of Salinomycin in Cancer Cells

in-vitro,

BC,

MCF7

in-vitro,

BC,

MDA-MB-231

eff↑, Herein, we improve the toxicity of salinomycin against cancer cells by telomerase inhibition BIBR1532 (BIBR), which binds to the active site of telomerase reverse transcriptase.
AntiCan↑, targeting telomerase improves anti-cancer effects of salinomycin.
CSCs↑, Until 2009, Weinberg group reported that salinomycin possessed anti-cancer effects, especially anti-cancer stem-like cell activities
Wnt↓, inhibition of the Wnt/β-catenin signaling pathway, induction differentiation, and overproduction of reactive oxygen species (ROS).
β-catenin/ZEB1↓,
Diff↑,
ROS↑,
toxicity↝, has been reported that salinomycin in high dose exhibits severe systemic adverse reactions in mammals, which hinders its application as a drug for human diseases.
selectivity↝, Therefore, it is urgent to find more effective methods for increasing salinomycin’s toxicity to cancer cells with little effects on normal cells.
eff↑, BIBR improves salinomycin’s toxicity partially through enhancing ROS generation.

4905-

Sal,

Salinomycin as a drug for targeting human cancer stem cells

Review,

Var,

CSCs↓, Salinomycin, a polyether ionophore antibiotic isolated from Streptomyces albus, has been shown to kill CSCs in different types of human cancers,
selectivity↑, Salinomycin has been shown to induce massive apoptosis in acute T-cell leukemia cells [125] and chronic lymphocytic leukemia cells [126] isolated from leukemia patients but failed to induce apoptosis in normal human T cells
Apoptosis↑, salinomycin induces apoptosis in CSCs of different origin
Casp3↑, salinomycin has been shown to activate the mitochondrial pathway of apoptosis and the caspase-3-mediated cleavage of PARP in human PC-3 prostate cancer cells
ROS↑, Salinomycin is able to generate reactive oxygen species (ROS) in prostate cancer cells
Wnt↓, downregulating the expression of the Wnt target genes LEF1, cyclin D1, and fibronectin, finally leading to apoptosis
cycD1/CCND1↓,
Fibronectin↓,
OXPHOS↓, salinomycin is known to inhibit oxidative phosphorylation in mitochondria [144] that may contribute to the elimination of CSCs by salinomycin.
Diff↑, salinomycin is able to promote differentiation of CSCs
Dose↝, the patient received 12 intravenous administrations of 200 μg·kg−1 salinomycin every second day.

5122-

Sal,

Identification of selective inhibitors of cancer stem cells by high-throughput screening

in-vivo,

BC,

SUM159

NA,

4T1

CSCs↓, In functional assays, one compound (salinomycin) reduced the proportion of CSCs by >100-fold relative to paclitaxel, a commonly used breast cancer chemotherapeutic drug
TumCG↓, Treatment of mice with salinomycin inhibits mammary tumor growth in vivo and induces increased epithelial differentiation of tumor cells.
Diff↑,
selectivity↑, Salinomycin selectively kills breast CSCs
CD44↓, Salinomycin treatment decreased the proportion of CD44high/CD24low breast cancer cells by 20-fold relative to vehicle-treated controls
CD24↓,
TumVol↓, Subsequent tumor size in salinomycin-treated animals was reduced relative to tumors in vehicle-treated animals

5045-

SAS,

Sulfasalazine, a potent cystine-glutamate transporter inhibitor, enhances osteogenic differentiation of canine adipose-derived stem cells

in-vivo,

Var,

50 µM and 100 µM

xCT/SLC7A11↓, Sulfasalazine (SSZ), a drug used to treat rheumatoid arthritis, suppresses xCT expression in cancer cells.
GSH↓, this treatment decreased the intracellular glutathione concentration.
BMPs↑, significantly increased alizarin red staining and its quantification, as well as the concentration-dependent osteogenic differentiation markers (BMP1 and SPP) mRNA expression.
Diff↑, SSZ treatment of CADSCs increased the efficiency of osteogenic differentiation induction in vitro.

2212-

SK,

Shikonin Exerts an Antileukemia Effect against FLT3-ITD Mutated Acute Myeloid Leukemia Cells via Targeting FLT3 and Its Downstream Pathways

in-vitro,

AML,

FLT3↓, SHK suppresses the expression and phosphorylation of FLT3 receptors and their downstream molecules
NF-kB↓, Inhibition of the NF-κB/miR-155 pathway is an important mechanism through which SHK kills FLT3-AML cells
miR-155↓,
Diff↑, Moreover, a low concentration of SHK promotes the differentiation of AML cells with FLT3-ITD mutations.
TumCG↓, Finally, SHK could significantly inhibit the growth of MV4-11 cells in leukemia bearing mice.

1345-

SK,

The Critical Role of Redox Homeostasis in Shikonin-Induced HL-60 Cell Differentiation via Unique Modulation of the Nrf2/ARE Pathway

in-vitro,

AML,

HL-60

100 ng/mL

CD14↑,
CD11b↑,
ROS↑, Shikonin result in the predominance of cell death because the oxidative stress is more severe and overcome the antioxidative capacity of Nrf2/ARE pathway, resulting in cell death.
GSH↓,
GSH/GSSG↓,
GPx↑, mRNA expression levels of GPX and CAT were markedly upregulated by Shikonin in a dose-dependent manner
Catalase↓, Shikonin causes apoptosis in human glioma cells by interrupting intracellular redox homeostasis, which included CAT downregulation
Diff↑, Shikonin-induced HL-60 cell differentiation

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,

10 and 20 mg/kg p.o.) for 28 days

Lung fibrosis was induced in rats

*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).

5019-

UA,

Ursolic acid in colorectal cancer: mechanisms, current status, challenges, and future research directions

Review,

Var,

TumCP↓, Multiple studies have confirmed that UA inhibits tumor cell proliferation, induces differentiation and apoptosis, suppresses invasion, and impedes tumor angiogenesis via diverse mechanisms.
Diff↑,
Apoptosis↑,
TumCI↓,
angioG↓,

Showing Research Papers: 1 to 47 of 47

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 47

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1, diuretic↑, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1, antiOx↑, 4, GPx↑, 1, HO-1↓, 1, HO-1↑, 1, Iron∅, 1, lipid-P↓, 2, NRF2↓, 1, NRF2↑, 1, OXPHOS↑, 1, RNS↓, 1, ROS↓, 3, ROS↑, 2, SOD2↓, 1, Trx↓, 1,

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↑, 1, mtDam↓, 1,

Core Metabolism/Glycolysis(tgid=4) ⓘ

PONs↓, 1,

Cell Death(tgid=5) ⓘ

Akt↑, 1, Apoptosis↓, 2, BAX↓, 1, BMP2↑, 2, Casp3↓, 1, Casp3↑, 1, Cyt‑c↑, 1, MAPK↑, 1,

Kinase & Signal Transduction(tgid=6) ⓘ

OCN↑, 1, SOX9↑, 2,

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 2,

Protein Folding & ER Stress(tgid=8) ⓘ

HSP70/HSPA5↑, 1,

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Diff↑, 14, ERK↑, 1, MSCs↑, 1, mTOR↑, 1, RUNX2↑, 1, TumCG↑, 1, Wnt↑, 1,

Migration(tgid=13) ⓘ

Ca+2↑, 2, COL2A1↑, 2, F-actin↑, 1, FAK↑, 1, MMP7↓, 1, MMP9↑, 1, OPN↑, 1, PKA↑, 1, PKCδ↓, 1, STAC2↑, 1, TGF-β↓, 1, TGF-β↑, 1, TRPC1↑, 1, TumCP↓, 1, β-catenin/ZEB1↑, 2,

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 1, angioG↝, 1, HIF2a↑, 1, miR-34b-5p↓, 1, NO↓, 2, VEGF↓, 1, VEGF↑, 2,

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 2, IL10↑, 2, IL1β↓, 1, IL6↓, 1, Imm↑, 1, Inflam↓, 6, IκB↑, 1, NF-kB↓, 2, PGE2↓, 1, TNF-α↓, 1, TNF-α↑, 1,

Synaptic & Neurotransmission(tgid=18) ⓘ

BDNF↑, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 3, eff↝, 1,

Clinical Biomarkers(tgid=22) ⓘ

ALP↑, 1, BMD↑, 4, IL6↓, 1,

Functional Outcomes(tgid=23) ⓘ

AntiDiabetic↑, 1, AntiTum↑, 1, cardioP↑, 1, chemoPv↑, 1, cognitive↑, 1, hepatoP↑, 1, motorD↑, 1, neuroP↑, 2, RenoP↑, 1, toxicity↓, 3, toxicity∅, 1, Weight∅, 1,

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1, Inf↓, 1,
Total Targets: 93

Scientific Paper Hit Count for: Diff, differentiation

10 Magnetic Fields
6 IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)
3 Inositol
3 Phenylbutyrate
3 salinomycin
2 Artemisinin
2 Dandelion Root
2 Isobavachalcone
2 Magnetic Field Rotating
2 Shikonin
1 Auranofin
1 Silver-NanoParticles
1 chaetocin
1 Chrysin
1 Crocetin
1 Emodin
1 Electrical Pulses
1 Fucoidan
1 Arsenic trioxide
1 Vitamin A, Retinoic Acid
1 Hydrogen Gas
1 isoquercitrin
1 Lecithin
1 Niclosamide (Niclocide)
1 Radiotherapy/Radiation
1 Vorinostat
1 Sulfasalazine
1 Thymoquinone
1 Ursolic acid

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#:1235  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

Diff Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Metal & Cofactor Biology(tgid=2) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Protein Aggregation(tgid=19) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Synaptic & Neurotransmission(tgid=18) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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