Apoptosis Cancer Research Results
Apoptosis, Apoptosis: Click to Expand ⟱
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| Type: type of cell death |
Situation in which a cell actively pursues a course toward death upon receiving certain stimuli.
Cancer is one of the scenarios where too little apoptosis occurs, resulting in malignant cells that will not die.
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Scientific Papers found: Click to Expand⟱
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in-vitro, |
BC, |
MCF-7 |
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in-vitro, |
BC, |
MDA-MB-231 |
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LDH↓, our experimental data show that the inhibition of LDH caused by GF can exert comparable growth inhibitory effects on breast cancer cells
ROS↑, induction of an oxidative stress condition
TumCP↓, Galloflavin (GF), a recently identified lactate dehydrogenase inhibitor, hinders the proliferation of cancer cells by blocking glycolysis and ATP production.
Glycolysis↓,
ATP↓,
ER-α36↓, In MCF-7 cells we observed a down regulation of the ERα-mediated signaling needed for cell survival
Apoptosis?, mechanism of cell death was found to be apoptosis induction
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in-vitro, |
AML, |
HL-60 |
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in-vitro, |
AML, |
K562 |
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in-vitro, |
BC, |
KAIMRC1 |
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ROS↑, Myrrh caused a dose-dependent effect on macrophages to increase the reactive oxygen species (ROS) level
M1↑, promote their polarization to classically activated macrophages (M1) and alternatively activated macrophages (M2) phenotypes, and consequently induce apoptosis
M2 MC↑,
Apoptosis?,
BBB↝, myrrh resin extract, only compounds 3, 4, 5, and 8 are potentially not permeable to the blood-brain barrier (BBB)
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in-vitro, |
OS, |
CAL27 |
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in-vitro, |
Oral, |
HSC3 |
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in-vitro, |
OS, |
SCC4 |
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in-vivo, |
NA, |
NA |
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*NH3↓, Sodium phenylbutyrate (SPB) as a salt of 4-phenylbutyric acid (4-PBA) has been reported to be an ammonia scavenger, histone deacetylase inhibitor, and an endoplasmic reticulum stress inhibitor
*HDAC↓,
*ER Stress↓,
Apoptosis?, SPB could significantly promote cell apoptosis
Bcl-2↓, BCL-2 was downregulated
cl‑Casp3↑, cleavage of caspase-3 was increased
TGF-β↑, transforming growth factor-β (TGFB) related epithelial-mesenchymal transition (EMT) was inhibited by SPB
N-cadherin↓, decreased mesenchymal marker N-cadherin and increased epithelial marker E-cadherin.
E-cadherin↑,
TumVol↓, SPB induced remarkably tumor regression with decreased tumor volume
eff↑, phenylbutyrate improved the sensitivity of cisplatin for cell cycle arrest by inhibiting the FA/BRCA pathway in cancer cells.
ChemoSen↓, 4 human clinical trials that demonstrated the successful use of propolis in alleviating side effects of chemotherapy and radiotherapy while increasing the quality of life of breast cancer patients, with minimal adverse effects.
RadioS↑,
Inflam↓, immunomodulatory, anti-inflammatory, and anti-cancer properties.
AntiCan↑,
Dose∅, Indonesia: IC50 = 4.57 μg/mL and 10.23 μg/mL
mtDam↑, Poland: propolis induced mitochondrial damage and subsequent apoptosis in breast cancer cells.
Apoptosis?,
OCR↓, China: CAPE inhibited mitochondrial oxygen consumption rate (OCR) by reducing basal, maximal, and spare respiration rate and consequently inhibiting ATP production
ATP↓,
ROS↑, Iran: inducing intracellular ROS production, IC50 = 65-96 μg/mL
ROS↑, Propolis induced mitochondrial dysfunction and lactate dehydrogenase release indicating the occurrence of ROS-associated necrosis.
LDH↓,
TP53↓, Interestingly, a reduced expression of apoptosis-related genes such as TP53, CASP3, BAX, and P21)
Casp3↓,
BAX↓,
P21↓,
ROS↑, CAPE: inducing oxidative stress through upregulation of e-NOS and i-NOS levels
eNOS↑,
iNOS↑,
eff↑, The combination of propolis and mangostin significantly reduced the expression of Wnt2, FAK, and HIF-1α, when compared to propolis or mangostin alone
hTERT/TERT↓, downregulation of the mRNA levels of hTERT and cyclin D1
cycD1/CCND1↓,
eff↑, Synergism with bee venom was observed
eff↑, Statistically significant decrease was found in the MCF-7 cell viability 48 h after applying different combinations of cisplatin (3.12 μg/mL) and curcumin (0.31 μg/mL) and propolis (160 μg/mL)
eff↑, Nanoparticles of chrysin had significantly higher cytotoxicity against MCF-7 cells, compared to chrysin
eff↑, Propolis nanoparticles appeared to increase cytotoxicity of propolis against MCF-7 cells
STAT3↓, Chrysin also inhibited the hypoxia-induced STAT3 tyrosine phosphorylation suggesting the mechanism of action was through STAT3 inhibition.
TIMP1↓, Propolis reduced the expression of TIMP-1, IL-4, and IL-10.
IL4↓,
IL10↓,
OS↑, patients supplemented with propolis had significantly longer median disease free survival time (400 mg, 3 times daily for 10 d pre-, during, and post)
Dose∅, 400 mg, 3 times daily for 10 d pre-, during, and post
ER Stress↑, endoplasmic reticulum stress
ROS↑, upregulating the expression of Annexin A7 (ANXA7), reactive oxygen species (ROS) level, and NF-κB p65 level, while simultaneously reducing the mitochondrial membrane potential.
NF-kB↓,
p65↓,
MMP↓,
TumAuto↑, propolis induced autophagy by increasing the expression of LC3-II and reducing the expression of p62 level
LC3II↑,
p62↓,
TLR4↓, propolis downregulates the inflammatory TLR4
mtDam↑, propolis induced mitochondrial dysfunction and lactate dehydrogenase release indicating ROS-associated necrosis in MDA MB-231cancer cells
LDH↓,
ROS↑,
Glycolysis↓, inhibit the proliferation of MDA-MB-231 cells by targeting key enzymes of glycolysis, namely glycolysis-hexokinase 2 (HK2), phosphofructokinase (PFK), pyruvate kinase muscle isozyme M2 (PKM2), and lactate dehydrogenase A (LDHA),
HK2↓,
PFK↓,
PKM2↓,
LDH↓,
IL10↓, propolis significantly reduced the relative number of CD4+, CD25+, FoxP3+ regulatory T cells expressing IL-10
HDAC8↓, Chrysin, a propolis bioactive compound, inhibits HDAC8
eff↑, combination of propolis and mangostin significantly reduced the expression of Wnt2, FAK, and HIF-1α, when compared to propolis or mangostin alone.
eff↑, Propolis also upregulated the expression of catalase, HTRA2/Omi, FADD, and TRAIL-associated DR5 and DR4 which significantly enhanced the cytotoxicity of doxorubicin in MCF-7 cells
P21↑, Chrysin, a propolis bioactive compound, inhibits HDAC8 and significantly increases the expression of p21 (waf1/cip1) in breast cancer cells, leading to apoptosis.
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in-vitro, |
BC, |
MCF-7 |
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
Nor, |
HUVECs |
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Apoptosis?, treatment of EECP for 24 and 48 h induced both cells apoptosis obviously
ANXA7↑, EECP significantly increased ANXA7 expression and ROS level, and NF-κB p65 level
ROS↑,
NF-kB↓, EECP significantly upregulated the expression of ANXA7 and downregulated NF-?B p65 level in a dose-dependent manner
MMP↓, mitochondrial membrane potential were depressed by EECP dramatically
selectivity↑, EECP had little or small cytotoxicity on normal human umbilical vein endothelial cells (HUVECs)
Apoptosis?, shikonin induced apoptosis and autophagy in RA-FLSs by activating the production of reactive oxygen species (ROS) and inhibiting intracellular ATP levels, glycolysis-related proteins, and the PI3K-AKT-mTOR signaling pathway.
TumAuto↑,
ROS↑,
ATP↓,
Glycolysis↓, shikonin can inhibit RA-glycolysis in FLSs
PI3K↓,
Akt↓,
mTOR↓,
*Apoptosis↓, Shikonin can significantly reduce the expression of apoptosis-related proteins, paw swelling in rat arthritic tissues, and the levels of inflammatory factors in peripheral blood, such as TNF-α, IL-6, IL-8, IL-10, IL-17A, and IL-1β while showing less
*Inflam↓,
*TNF-α↓,
*IL6↓,
*IL8↓,
*IL10↓,
*IL17↓,
*hepatoP↑, while showing less toxicity to the liver and kidney.
*RenoP↑,
PKM2↓, The expression of glycogen proteins PKM2, GLUT1, and HK2 decreased with increasing concentrations of shikonin
GLUT1↓,
HK2↓,
Showing Research Papers: 1 to 6 of 6
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
ROS↑, 9,
Mitochondria & Bioenergetics ⓘ
ATP↓, 3, MMP↓, 2, mtDam↑, 2, OCR↓, 1,
Core Metabolism/Glycolysis ⓘ
ANXA7↑, 1, Glycolysis↓, 3, HK2↓, 2, LDH↓, 4, PFK↓, 1, PKM2↓, 2,
Cell Death ⓘ
Akt↓, 1, Apoptosis?, 6, BAX↓, 1, Bcl-2↓, 1, Casp3↓, 1, cl‑Casp3↑, 1, hTERT/TERT↓, 1, iNOS↑, 1,
Protein Folding & ER Stress ⓘ
ER Stress↑, 1,
Autophagy & Lysosomes ⓘ
LC3II↑, 1, p62↓, 1, TumAuto↑, 2,
DNA Damage & Repair ⓘ
TP53↓, 1,
Cell Cycle & Senescence ⓘ
cycD1/CCND1↓, 1, P21↓, 1, P21↑, 1,
Proliferation, Differentiation & Cell State ⓘ
HDAC8↓, 1, mTOR↓, 1, PI3K↓, 1, STAT3↓, 1,
Migration ⓘ
E-cadherin↑, 1, ER-α36↓, 1, N-cadherin↓, 1, TGF-β↑, 1, TIMP1↓, 1, TumCP↓, 1,
Angiogenesis & Vasculature ⓘ
eNOS↑, 1,
Barriers & Transport ⓘ
BBB↝, 1, GLUT1↓, 1,
Immune & Inflammatory Signaling ⓘ
IL10↓, 2, IL4↓, 1, Inflam↓, 1, M1↑, 1, M2 MC↑, 1, NF-kB↓, 2, p65↓, 1, TLR4↓, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↓, 1, Dose∅, 2, eff↑, 8, RadioS↑, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
hTERT/TERT↓, 1, LDH↓, 4, TP53↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, OS↑, 1, TumVol↓, 1,
Total Targets: 59
Pathway results for Effect on Normal Cells:
Core Metabolism/Glycolysis ⓘ
NH3↓, 1,
Cell Death ⓘ
Apoptosis↓, 1,
Protein Folding & ER Stress ⓘ
ER Stress↓, 1,
Proliferation, Differentiation & Cell State ⓘ
HDAC↓, 1,
Immune & Inflammatory Signaling ⓘ
IL10↓, 1, IL17↓, 1, IL6↓, 1, IL8↓, 1, Inflam↓, 1, TNF-α↓, 1,
Clinical Biomarkers ⓘ
IL6↓, 1,
Functional Outcomes ⓘ
hepatoP↑, 1, RenoP↑, 1,
Total Targets: 13
Scientific Paper Hit Count for: Apoptosis, Apoptosis
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#:14 State#:% Dir#:0
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