CD24 Cancer Research Results

CD24, CD24: Click to Expand ⟱

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CD24 is a cell surface protein that plays a role in cell adhesion and signaling. In the context of cancer, CD24 has been found to be overexpressed in many types of cancer, including breast, ovarian, and pancreatic cancer.
CD24− refers to cells that do not express CD24.
CD24− cells in cancer are often more resistant to chemotherapy and radiation therapy, and may be more likely to metastasize (spread) to other parts of the body.
CD24− cells have been found to be more likely to be cancer stem cells, which are thought to be responsible for the initiation and progression of cancer.

Scientific Papers found: Click to Expand⟱

3454-

ALA,

Lipoic acid blocks autophagic flux and impairs cellular bioenergetics in breast cancer and reduces stemness

in-vitro,

BC,

MCF-7

(0.5 mM, 1 mM, 2.5 mM, and 5 mM)

in-vitro,

BC,

MDA-MB-231

TumCG↑, Lipoic acid inhibits breast cancer cell growth via accumulation of autophagosomes.
Glycolysis↓, Lipoic acid inhibits glycolysis in breast cancer cells.
ROS↑, Lipoic acid induces ROS production in breast cancer cells/BCSC.
CSCs↓, Here, we demonstrate that LA inhibits mammosphere formation and subpopulation of BCSCs
selectivity↑, In contrast, LA at similar doses. had no significant effect on the cell viability of the human embryonic kidney cell line (HEK-293)
LC3B-II↑, LA treatment (0.5 mM and 1.0 mM) increased the expression level of LC3B-I to LC3B-II in both MCF-7 and MDA-MB231cells at 48 h
MMP↓, LA induced mitochondrial ROS levels, decreased mitochondria complex I activity, and MMP in both MCF-7 and MDA-MB231 cells
mitResp↓, In MCF-7 cells, we found a substantial reduction in maximal respiration and ATP production at 0.5 mM and 1 mM of LA treatment after 48 h
ATP↓,
OCR↓, LA at 2.5 mM decreased OCR
NAD↓, we found that LA (0.5 mM and 1 mM) significantly reduced ATP production and NAD levels in MCF-7 and MDA-MB231 cells
p‑AMPK↑, LA treatment (0.5 mM and 1.0 mM) increased p-AMPK levels;
GlucoseCon↓, LA (0.5 mM and 1 mM) significantly decreased glucose uptake and lactate production in MCF-7, whereas LA at 1 mM significantly reduced glucose uptake and lactate production in MDA-MB231 cells but it had no effect at 0.5 mM
lactateProd↓,
HK2↓, LA reduced hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase M2 (PKM2), and lactate dehydrogenase A (LDHA) expression in MCF-7 and MDA-MB231 cells
PFK↓,
LDHA↓,
eff↓, Moreover, we found that LA-mediated inhibition of cellular bioenergetics including OCR (maximal respiration and ATP production) and glycolysis were restored by NAC treatment (Fig. 6E and F) which indicates that LA-induced ROS production is responsibl
mTOR↓, LA inhibits mTOR signaling and thereby decreased the p-TFEB levels in breast cancer cells
ECAR↓, LA also inhibits glycolysis as evidenced by decreased glucose uptake, lactate production, and ECAR.
ALDH↓, LA decreased ALDH1 activity, CD44+/CD24-subpopulation, and increased accumulation of autophagosomes possibly due to inhibition of autophagic flux of breast cancer.
CD44↓,
CD24↓,

2606-

Ba,

Baicalein: A review of its anti-cancer effects and mechanisms in Hepatocellular Carcinoma

Review,

HCC,

ChemoSen↑, In addition, the combination of baicalein and silymarin eradicates HepG2 cells efficiently superior to baicalein or silymarin alone
TumCP↓, Cell viability assays have demonstrated that baicalein is significantly cytotoxic against several HCC cell lines and can inhibit the proliferation of HCC cells through arresting the cell cycle.
TumCCA↑,
TumCMig↓, Baicalein has been proved to inhibit migration and invasion of human HCC cells by reducing the expression and their proteinase activity of matrix metalloproteinases (MMPs),
TumCI↓,
MMPs↓,
MAPK↓, A large number of studies found that baicalein could inhibit migration and invasion of cancer cells by targeting the MAPK, TGF-b/Smad4, GPR30 pathway and molecules such as, ezrin, zinc-finger protein X-linked (ZFX),
TGF-β↓,
ZFX↓,
p‑MEK↓, Baicalein could inhibited the phosphorylation of MEK1 and ERK1/2, leading to decreased expression and proteinase activity of MMP-2/9 and urokinase-type plasminogen activator (u-PA),
ERK↓,
MMP2↓,
MMP9↓,
uPA↓,
TIMP1↓, as well as increased expression of TIMP-1 and TIMP-2
TIMP2↓,
NF-kB↓, Additionally, the nuclear translocation of NF-kB/p50 and p65/RelA and the phosphorylation of I-kappa-B (IKB)-b could be down-regulated by baicalein
p65↓,
p‑IKKα↓,
Fas↑, Hep3 B cells via activating Fas, Caspase -2, -3, -8, -9, down-regulating Bcl-xL, and upregulating Bax [
Casp2↑,
Casp3↑,
Casp8↑,
Casp9↑,
Bcl-xL↓,
BAX↑,
ER Stress↑, baicalein could induced apoptosis via endoplasmic reticulum (ER) stress in SMMC-7721 and Bel-7402
Ca+2↑, increasing intracellular calcium(Ca2+ ), and activating JNK pathwa
JNK↑,
P53↑, selectively induce apoptosis in HCC J5 cells via upregulation of p53
ROS↑, baicalein could induced cell apoptosis through regulating ROS via increasing intracellular H2O 2 level [
H2O2↑,
cMyc↓, baicalein could promote apoptosis in HepG2 and Bel-7402 cells through inhibiting c-Myc and CD24 expression
CD24↓,
12LOX↓, baicalein could induced cell apoptosis in SMMC-7721 and HepG2 cells by specifically inhibiting expression of 12-lipoxygenase(12-LOX), a critical anti-apoptotic genes

420-

CUR,

Anti-metastasis activity of curcumin against breast cancer via the inhibition of stem cell-like properties and EMT

in-vitro,

BC,

MCF-7

10, 15, 20, 25, 30, 35 and 40 µM, 24 and 48 h

in-vitro,

BC,

MDA-MB-231

Vim↓,
Fibronectin↓,
β-catenin/ZEB1↓,
E-cadherin↓,
CD44↑, The CD44+CD24-/low subpopulation was larger in mammospheres when MCF-7 and MDA-MB-231 adherent cells were cultured with SFM.
CD24↓,
OCT4↓,
Nanog↓,
SOX2↓,

2974-

CUR,

Curcumin Suppresses Metastasis via Sp-1, FAK Inhibition, and E-Cadherin Upregulation in Colorectal Cancer

in-vitro,

CRC,

HCT116

0, 5, 10, and 20 μM

in-vitro,

CRC,

HT29

in-vitro,

CRC,

HCT15

in-vitro,

CRC,

COLO205

in-vitro,

CRC,

SW-620

in-vivo,

NA,

1 g/kg once daily for 30 days

mice

TumCMig↓, Curcumin significantly inhibits cell migration, invasion, and colony formation in vitro and reduces tumor growth and liver metastasis in vivo.
TumCI↓,
TumCG↓,
TumMeta↓,
Sp1/3/4↓, curcumin suppresses Sp-1 transcriptional activity and Sp-1 regulated genes including ADEM10, calmodulin, EPHB2, HDAC4, and SEPP1 in CRC cells.
HDAC4↓,
FAK↓, Curcumin inhibits focal adhesion kinase (FAK) phosphorylation
CD24↓, Curcumin reduces CD24 expression in a dose-dependent manner in CRC cells
E-cadherin↑, E-cadherin expression is upregulated by curcumin and serves as an inhibitor of EMT.
EMT↓,
TumCP↓,
NF-kB↓, CUR prevents cancer cells migration, invasion, and metastasis through inhibition of PKC, FAK, NF-κB, p65, RhoA, MMP-2, and MMP-7 gene expressions
AP-1↝,
STAT3↓, downregulation of CD24 reduces STAT and FAK activity, decreases cell proliferation, metastasis in human tumor
P53?,
β-catenin/ZEB1↓, CUR could activate protein kinase D1 (PKD1) suggesting that suppressing of β-catenin transcriptional activity prevents growth of prostate cancer
NOTCH1↝,
Hif1a↝,
PPARα↝,
Rho↓, CUR prevents cancer cells migration, invasion, and metastasis through inhibition of PKC, FAK, NF-κB, p65, RhoA, MMP-2, and MMP-7 gene expressions
MMP2↓,
MMP9↓,

3244-

EGCG,

Novel epigallocatechin gallate (EGCG) analogs activate AMP-activated protein kinase pathway and target cancer stem cells

AMPK↑, In this study we demonstrated that synthetic EGCG analogs 4 and 6 were more potent AMPK activators than metformin and EGCG.
TumCP↓, EGCG analogs resulted in inhibition of cell proliferation, up-regulation of the cyclin-dependent kinase inhibitor p21, down-regulation of mTOR pathway, and suppression of stem cell population in human breast cancer cells.
P21↑,
mTOR↓,
CSCs↓,
CD44↓, Both EGCG analogs 4 and 6 significantly decreased the CD44+high/CD24-low population in breast cancer cells
CD24↓,

4957-

PEITC,

Phenethyl Isothiocyanate (PEITC) from Cruciferous Vegetables Targets Human Cancer Stem-Like Cells

vitro+vivo,

Cerv,

HeLa

10 µM PEITC-

 human cervical HeLa CSC (hCSC) in vitro and on attenuation of tumorigenicity in hCSC-transplanted mice.

CSCs↓, PEITC attenuated proliferation of sphere-culture-enriched (ANOVA, p蠄 0.001), aldehyde dehydrogenase (ALDH1)bright, CD44high⁄+/CD24low⁄–, Hoechst 33342-excluded hCSC in a concentration- and time-dependent manner.
ALDH↓,
CD44↓,
CD24↓,
cl‑PARP↑, PEITC up-regulated cleaved poly (ADP-ribose) polymerase (p蠄 0.05) and induced death receptors, DR4 (p蠄 0.01) and DR5 (p蠄 0.001), of tumor necrotic factor-related apoptosis-inducing ligand signaling.
DR4↑,
DR5↑,

4960-

PEITC,

Phenethyl isothiocyanate upregulates death receptors 4 and 5 and inhibits proliferation in human cancer stem-like cells

in-vivo,

Cerv,

HeLa

mouse model

CD44↓, PEITC attenuated proliferation of CD44high/+/CD24low/–, stem-like, sphere-forming subpopulations of hCSCs in a concentration- and time-dependent manner that was comparable to the CSC antagonist salinomycin
CD24↓,
CSCs↓,
cl‑PARP↑, PEITC exposure-associated up-regulation of cPARP (apoptosis-associated cleaved poly [ADP-ribose] polymerase) levels and induction of DR4 and DR5 (death receptor 4 and 5) of TRAIL signaling were observed.
DR4↑,
DR5↑,
TumCP↓, PEITC also significantly reduced proliferation of both HeLa cells and hCSCs in a concentration-dependent manner after 24- and 48-hour exposures, which was a pattern comparable to the effects of salinomycin.

4690-

PTS,

immuno,

Pterostilbene: Mechanisms of its action as oncostatic agent in cell models and in vivo studies

Review,

Var,

eff↑, Due to the better lipophilic and oral absorption, higher cellular uptake and a longer half-life than resveratrol, pterostilbene may have a good prospect in the future clinic application.
Half-Life↑,
TumCG↓, Special focus is placed on the oncostatic effects of pterostilbene, including inhibition of tumor growth, metastasis, angiogenesis and cancer stem cells, activation of apoptosis, and enhancement of immunotherapy.
TumMeta↓,
angioG↓,
CSCs↓, There is solid evidence that pterostilbene inhibited multiple CSCs, including breast CSCs [18,20,41,68,[110], [111], [112]], glioma CSCs [42], and lung CSCs [22]
Apoptosis↑,
eff↑, enhancement of immunotherapy
CD44↓, Pterostilbene selectively repressed CD44+/CD24− CSCs in MCF-7 cells
CD24↓,

59-

QC,

Quercetin Inhibits Breast Cancer Stem Cells via Downregulation of Aldehyde Dehydrogenase 1A1 (ALDH1A1), Chemokine Receptor Type 4 (CXCR4), Mucin 1 (MUC1), and Epithelial Cell Adhesion Molecule (EpCAM)

in-vitro,

BC,

MDA-MB-231

 50 uM

 BCSC

ALDH1A1↓, lowered the expression levels of proteins related to tumorigenesis and cancer progression, such as aldehyde dehydrogenase 1A1, C-X-C chemokine receptor type 4, mucin 1, and epithelial cell adhesion molecules.
CXCR4↓,
MUC1↓,
EpCAM↓,
CSCs↓, quercetin suppressed breast cancer stem cell proliferation, self-renewal, and invasiveness
TumCP↓,
TumCI↓,
CD44↓, High doses of quercetin inhibit proliferation of MDA-MB-231 cells and CD44+/CD24− CSCs
CD24↓,
Apoptosis↑, Quercetin induces apoptosis of MDA-MB-231 cells
TumCCA↑, These results indicate that quercetin alters the MDA-MB-231 cell cycle

3353-

QC,

Quercetin triggers cell apoptosis-associated ROS-mediated cell death and induces S and G2/M-phase cell cycle arrest in KON oral cancer cells

in-vitro,

Oral,

KON

 0, 1.5625, 3.125, 6.25, 12.5, 25, 50, 100, and 400 µg/mL

50ug/L @ 72h

in-vitro,

Nor,

MRC-5

tumCV↓, reduced the vitality of KON cells and had minimal effect on MRC cells.
selectivity↑, Owing to the appropriate dosages of quercetin needed to treat these diseases, normal cells do not exhibit any overtly harmful side effects.
TumCCA↑, quercetin increased the percentage of dead cells and cell cycle arrests in the S and G2/M phases.
TumCMig↓, quercetin inhibited KON cells’ capacity for migration and invasion in addition to their effects on cell stability and structure
TumCI↓,
Apoptosis↑, inducing apoptosis and preventing metastasis, quercetin was found to downregulate the expression of BCL-2/BCL-XL while increasing the expression of BAX.
TumMeta↓,
Bcl-2↓,
BAX↑,
TIMP1↑, TIMP-1 expression was upregulated while MMP-2 and MMP-9 were downregulated.
MMP2↓,
MMP9↓,
*Inflam↓, anti-inflammatory, anti-cancer, antibacterial, antifungal, anti-diabetic, antimalarial, neuroprotective, and cardioprotective properties.
*neuroP↑,
*cardioP↑,
p38↓, MCF-7 cells, quercetin successfully decreased the expression of phosphor p38MAPK, Twist, p21, and Cyclin D1
MAPK↓,
Twist↓,
P21↓,
cycD1/CCND1↓,
Casp3↑, directly aided by the significant increase in caspase-3 and − 9 levels and activities
Casp9↑,
p‑Akt↓, High quercetin concentrations also caused an inhibition of Akt and ERK phosphorylation
p‑ERK↓,
CD44↓, reduced cell division and triggered apoptosis, albeit to a lesser degree in CD44+/CD24− cells.
CD24↓,
ChemoSen↑, combination of quercetin and doxorubicin caused G2/M arrest in T47D cells, and to a lesser amount in cancer stem cells (CSCs) that were isolate
MMP↓, (lower levels of ΔΨ m), which is followed by the release of Cyto C, AIF, and Endo G from mitochondria, which causes apoptosis and ultimately leads to cell death.
Cyt‑c↑,
AIF↑,
ROS↑, Compared to the control group, quercetin administration significantly raised ROS levels at 25, 50, 100, 200, and 400 µg/mL.
Ca+2↑, increased production of reactive oxygen species and Ca2+, decreased levels of mitochondrial membrane potential (ΔΨ m),
Hif1a↓, Quercetin treatment resulted in a considerable downregulation of HIF-1α, VEGF, MMP2, and MMP9 mRNA and protein expression levels in HOS cells.
VEGF↓,

3094-

RES,

Resveratrol suppresses growth of cancer stem-like cells by inhibiting fatty acid synthase

in-vitro,

BC,

MCF-7

in-vitro,

BC,

MDA-MB-231

CSCs↓, resveratrol significantly reduced the cell viability and mammosphere formation followed by inducing apoptosis in cancer stem-like cells
tumCV↓,
FASN↑, This inhibitory effect of resveratrol is accompanied by a significant reduction in lipid synthesis which is caused by the down-regulation of the fatty acid synthase (FAS) gene
BNIP3↑, followed by up-regulation of pro-apoptotic genes, DAPK2 and BNIP3.
*cardioP↑, cardio-protective effect of resveratrol has been extensively studied in various pre-clinical models, and it has been shown that the strong anti-oxidant activity of resveratrol
*antiOx↑,
NF-kB↓, down-regulation of NF-kappaB, COX and matrix metalloprotease-9 (MMP9) expression
COX2↓,
MMP9↓,
IGF-1↓, resveratrol as diet significantly reduced the onset of prostate cancer and exhibited a decrease in IGF1 (insulin-like growth factor 1) and phosphorylated-ERK1 (extracellular regulating kinase 1)
ERK↓,
lipid-P↓, resveratrol is indeed capable of suppressing lipid metabolism by blocking the FAS expression followed by induction of apoptosis in cancer stem-like cells
CD24↓, Resveratrol induces apoptosis in tumor stem-like cells by suppressing FAS (we first isolated cancer stem-like cells (CD24-/CD44+/ESA+) from MDA-MB231)

4997-

Sal,

Salinomycin Treatment Specifically Inhibits Cell Proliferation of Cancer Stem Cells Revealed by Longitudinal Single Cell Tracking in Combination with Fluorescence Microscopy

in-vitro,

BC,

CD24↓, we show that salinomycin specifically targeted the CD24− subpopulation, i.e., the CSCs, by inhibiting cell proliferation, which was evident already after 24 h of drug treatment.
TumCP↓,
CSCs↓,

4996-

Sal,

The Molecular Basis for Inhibition of Stemlike Cancer Cells by Salinomycin

CSCs↓, The natural product salinomycin, a K+ -selective ionophore, was recently found to exert selectivity against such cancer stem cells.
selectivity↑,
Wnt↓, This selective effect is thought to be due to inhibition of the Wnt signaling pathway, but the mechanistic basis remains unclear.
ERStress↑, accumulation in the endoplasmic reticulum (ER).
Ca+2↓, This localization is connected to induction of Ca2+ release from the ER into the cytosol.
UPR↑, Depletion of Ca 2+ from the ER induces the unfolded protein response a
CHOP↑, salinomycin-induced ER Ca2+ depletion up-regulates C/EBP homologous protein (CHOP), which inhibits Wnt signaling by down-regulating β-catenin.
β-catenin/ZEB1↓,
CD44↓, alinomycin efficiently and selectively reduced the proportion of breast cancer CD44 + /CD24− cells, a phenotype associated with enhanced tumorigenic capacity.
CD24↓,
PKCδ↑, Salinomycin Induces ER Ca2+ Release, ER Stress, and PKC Activation

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

Showing Research Papers: 1 to 14 of 14

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Pathway results for Effect on Cancer / Diseased Cells:

Functional Outcomes ⓘ

TumVol↓, 1,
Total Targets: 117

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1,

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,

Functional Outcomes ⓘ

cardioP↑, 2, neuroP↑, 1,
Total Targets: 4

Scientific Paper Hit Count for: CD24, CD24

3 salinomycin
2 Curcumin
2 Phenethyl isothiocyanate
2 Quercetin
1 Alpha-Lipoic-Acid
1 Baicalein
1 EGCG (Epigallocatechin Gallate)
1 Pterostilbene
1 immunotherapy
1 Resveratrol

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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CD24 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 ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Immune & Inflammatory Signaling ⓘ

Functional Outcomes ⓘ

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