BAD Cancer Research Results

BAD, BCL2 associated agonist of cell death: Click to Expand ⟱
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BCL2 associated agonist of cell death (BAD) protein is a pro-apoptotic member of the Bcl-2 gene family.
Expression of the BAD is associated with the development and progression of cancer.
Scientific Papers found: Click to Expand⟱
5502- Ba,    An overview of pharmacological activities of baicalin and its aglycone baicalein: New insights into molecular mechanisms and signaling pathways
- Review, Var, NA
*AntiCan↑, antibacterial, antiviral, anticancer, anticonvulsant, anti-oxidant, hepatoprotective, and neuroprotective effects.
*antiOx↑,
*hepatoP↑,
*neuroP↑,
*ROS↓, pharmacological properties of baicalin and baicalein are due to their abilities to scavenge reactive oxygen species (ROS)
Ca+2↑, Baicalein mainly induced apoptosis through Ca+2 influx via Ca2+ release from the reticulum to cytosol dependent on phospholipase C protein
ROS↑, ROS production is associated with baicalein-induced apoptosis via Ca2+-dependent apoptosis in tongue and breast cancer cells (78, 79)
BAX↑, The level of Bax/Bcl-2 increased and caspase-3 and -9 were activated following the release of cytochrome C (80).
Casp3↑,
Casp9↑,
Cyt‑c↑,
MMP↓, In gastric cancer cells, baicalein mediated apoptosis in a dose-dependent manner through disruption of mitochondrial membrane potential
Mcl-1↓, In pancreatic cancer cells, baicalein induced apoptosis via suppression of the Mcl-1 protein.
PI3K↓, In HepG2 cells, baicalin-copper induced apoptosis through down-regulation of phosphoinositide-3 kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway
Akt↓,
mTOR↓,
BAD↓, Studies demonstrated that baicalein treatment suppressed Bad, ERK1/2 phosphorylation, and MEK1 expression both in vitro and in vivo.
ERK↓,
MEK↓,
DR5↑, Baicalein enhanced the activity of death receptor-5 (DR5) in prostate cancer PC3 cells.
Fas↑, baicalin is the active ingredient that acts as Fas ligand and caused up-regulation of Fas protein (89).
TumMeta↓, Baicalin/baicalein not only induced apoptosis in cancer cells but also suppressed metastasis.
EMT↓, both baicalin and baicalein inhibited epithelial-mesenchymal transition (EMT) through the suppression of TGF-β in breast epithelial cells through the NF-κB pathway (92).
SMAD4↓, baicalein suppressed metastasis in gastric cancer through inactivation of the Smad4/TGF-β pathway (93).
TGF-β↓,
MMP9↓, baicalin and baicalein inhibition of the expression level of matrix metalloproteinases (MMP) such as MMP-9 and MMP-2 in liver, breast, lung, ovarian, gastric, and colorectal cancers and glioma
MMP2↓,
HIF-1↓, Baicalin attenuated lung metastasis through inhibition of hypoxia-inducible factor (HIF)
12LOX↓, Baicalein acts as an anticancer agent via inhibiting 12-lipooxygenase (12-LOX),

1145- CHr,    Chrysin inhibits propagation of HeLa cells by attenuating cell survival and inducing apoptotic pathways
- in-vitro, Cerv, HeLa
tumCV↓,
BAX↑,
BID↑,
BOK↑,
APAF1↑,
TNF-α↑,
FasL↑,
Fas↑,
FADD↑,
Casp3↑,
Casp7↑,
Casp8↑,
Casp9↑,
Mcl-1↓,
NAIP↓,
Bcl-2↓,
CDK4↓,
CycB/CCNB1↓,
cycD1/CCND1↓,
cycE1↓,
TRAIL↑,
p‑Akt↓,
Akt↓,
mTOR↓,
PDK1↓,
BAD↓,
GSK‐3β↑,
AMPK↑, AMPKa
p27↑,
P53↑,

3631- Cro,    Investigation of the neuroprotective effects of crocin via antioxidant activities in HT22 cells and in mice with Alzheimer's disease
- in-vitro, AD, HT22 - in-vivo, AD, NA
*ROS↓, suppressed intracellular reactive oxygen species (ROS) accumulation and Ca2+ overload compared with untreated cells.
*Ca+2↓, crocin strongly inhibited the overload of Ca2+ compared with the l-Glu-damaged HT22 cells,
*BAX↓, crocin significantly decreased the expression levels of Bax, Bad and cleaved caspase-3
*BAD↓,
*Casp3↓,
*cognitive↑, crocin substantially improved the cognition and memory abilities of the mice as measured by their coordination of movement in an open field test,
*memory↑,
*Aβ↓, Crocin improved cognitive abilities of AD mice, and reduced Aβ deposition in their brains
*GPx↑, crocin was able to reduce the Aβ1-42 content in the mouse brains, increase the levels of glutathione peroxidase, superoxide dismutase, acetylcholine and choline acetyltransferase,
*SOD↑,
*ChAT↑,
*Ach↑,
*AChE↓, and reduce the levels of ROS and acetylcholinesterase in the serum, cerebral cortex and hypothalamus compared with untreated mice.
*ROS↓,
*p‑Akt↑, crocin upregulated the phosphorylation levels of Akt and mTOR in 24-h l-Glu-exposed cells.
*p‑mTOR↑,
*neuroP↑, crocin-mediated neuroprotection of l-Glu-damaged HT22 cells.

434- CUR,    Curcumin induces apoptosis in lung cancer cells by 14-3-3 protein-mediated activation of Bad
- in-vitro, Lung, A549
14-3-3 proteins↓,
p‑BAD↓, p-Bad
p‑Akt↓,
Akt↓,
cl‑Casp9↑, cleaved
cl‑PARP↑, cleaved

448- CUR,    Heat shock protein 27 influences the anti-cancer effect of curcumin in colon cancer cells through ROS production and autophagy activation
- in-vitro, CRC, HT-29
Apoptosis↑,
TumCCA↑, G2/M cell cycle arrest
p‑Akt↓,
Akt↓,
Bcl-2↓,
p‑BAD↓,
BAD↑,
cl‑PARP↑,
ROS↑,
HSP27↑,
Beclin-1↑,
p62↑,
GPx1↓,
GPx4↓,

1184- DHA,    Syndecan-1-Dependent Suppression of PDK1/Akt/Bad Signaling by Docosahexaenoic Acid Induces Apoptosis in Prostate Cancer
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vivo, NA, NA
SDC1↑,
p‑PCK1↓,
Akt↓,
BAD↓,

26- EGCG,  QC,  docx,    Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapy
- vitro+vivo, Pca, PC3
BAD↓,
cl‑PARP↑,
Casp7↑,
IκB↓,
Ki-67↓,
VEGF↓,
EGFR↓,
FGF↓,
TGF-β↓,
TNF-α↓,
SCF↓,
Bax:Bcl2↑,
NF-kB↓,
chemoP↑, This study provides a novel regimen to enhance the therapeutic effect of Doc in a less-toxic manner and reduce its risk of side effects in treatment of CRPC.
ChemoSen↑, GT and Q with LD Doc significantly enhanced the potency of Doc 2-fold and reduced tumor growth by 62 % compared to LD Doc in 7-weeks intervention.
TumVol↓,

5148- GamB,    Gambogic acid: A shining natural compound to nanomedicine for cancer therapeutics
- Review, Var, NA
AntiCan↑, In this review, we document distinct biological characteristics of GA as a novel anti-cancer agent.
angioG↓, anti-angiogenesis, and chemo-/radiation sensitizer activities
ChemoSen↑, Moreover, GA has shown chemotherapy/radiation sensitization properties in different types of cancers
RadioS↑,
VEGF↓, Figure 2
MMP2↓,
MMP9↓,
Telomerase↓,
TrxR↓,
ERK↓,
HSP90↓,
ROS↑,
SIRT1↑,
survivin↓,
cFLIP↓,
Casp3↑,
Casp8↑,
Casp9↑,
BAD↓,
BID↓,
Bcl-2↓,
BAX↑,
STAT3↓,
hTERT/TERT↓,
NF-kB↓,
Myc↓,
Hif1a↓,
FOXD3↑,
BioAv↓, Unfortunately, the aqueous solubility of GA (0.013 mg/mL) is very low, thus limiting its clinical application.
BioAv↑, For example, GA can be coupled with alkanolamines to improve aqueous solubility and achieve equivalent anti-proliferation effects
P53↑, This inhibition was co-related with increase of p53 levels and reduced bcl-2 levels
eff↓, Such effect was received for GA due to production of ROS which can be removed by N-acetyl-L-cysteine (NAC, a ROS inhibitor)
OCR↓, GA exhibited a dose-dependent generation of intracellular ROS levels and lowered the oxygen consumption rate and the mitochondrial membrane potential.
MMP↓,
PI3K↓, GA happens to promote antimetastasis properties in melanoma cells by active inhibition of PI3K/Akt and ERK signaling pathways
Akt↓,
BBB↑, This study demonstrated successful uptake of GA through blood-brain barrier (BBB)
TumCG↓, GA-based nanomedicine is efficient in targeting tumors, capable to inhibit tumor growth, metastasis, angiogenesis, and reverse drug resistance
TumMeta↓,
BioAv↑, deliver GA using nanoparticles for enhanced solubility, bioavailability, adsorption and tumor imaging and targeting

506- MF,  doxoR,    Pulsed Electromagnetic Field Stimulation Promotes Anti-cell Proliferative Activity in Doxorubicin-treated Mouse Osteosarcoma Cells
- in-vitro, OS, LM8
TumCP↓,
p‑CHK1↓, reducing the increased expression of total IĸB and phosphorylated-CHK1 induced by doxorubicin
Ca+2↑, caused by PEMF alone
Casp3↓, PEMF stimulation significantly reduced the enhancement of caspase 3/7 activity by doxorubicin at 24 h
Casp7↓, PEMF stimulation significantly reduced the enhancement of caspase 3/7 activity by doxorubicin at 24 h
p‑BAD↓,
ChemoSen↑, Our results indicate that combination of PEMF and doxorubicin could be a novel chemotherapeutic strategy.

194- MF,    Electromagnetic Field as a Treatment for Cerebral Ischemic Stroke
- Review, Stroke, NA
*BAD↓,
*BAX↓,
*Casp3↓,
*Bcl-xL↑,
*p‑Akt↑,
*MMP9↓, EMF significantly decreased levels of IL-1β and MMP9 in the peri-infarct area at 24 h and 3rd day of the experiment
*p‑ERK↑, ERK1/2
*HIF-1↓,
*ROS↓, n a similar experiment, ELF-MF (50 Hz/1 mT) increased cell viability and decreased intracellular ROS/RNS in mesenchymal stem cells submitted to OGD conditions and 3 h ELF-MF exposure
*VEGF↑,
*Ca+2↓,
*SOD↑,
*IL2↑,
*p38↑,
*HSP70/HSPA5↑,
*Apoptosis↓, PEMF decreased apoptosis
*ROS↓, Nevertheless, in the presence of ischemia, EMF decreased NO and ROS concentrations.
*NO↓,

71- QC,    Role of Bax in quercetin-induced apoptosis in human prostate cancer cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PrEC - in-vitro, Pca, YPEN-1 - in-vitro, Pca, HCT116
Casp8↑, quercetin inhibits the PI3K/Akt pathway, suppresses phosphorylation of Bad, and subsequently alters interaction between Bcl-xL and Bax in human prostate carcinoma LNCaP cells
Casp9↑,
PARP↑,
BAD↓,
BAX↑,
PI3K/Akt↓, quercetin inhibits the PI3K/Akt pathway, suppresses phosphorylation of Bad, and subsequently alters interaction between Bcl-xL and Bax in human prostate carcinoma LNCaP cells
Cyt‑c↑, accompanied by cytochrome c release, and procaspases-3, -8 and -9 cleavage and increased poly (ADP-ribose) polymerase (PARP) cleavage.
selectivity↑, quercetin treatment did not affect the viability or rate of apoptosis in normal human prostate epithelial cell line (PrEC)

82- QC,  ATG,    Arctigenin in combination with quercetin synergistically enhances the anti-proliferative effect in prostate cancer cells
- in-vitro, Pca, LNCaP
AR↓,
PI3K/Akt↓, The combination treatment significantly inhibited both AR and PI3K/Akt pathways compared to control.
miR-21↓,
STAT3↓,
BAD↓,
PRAS40↓,
GSK‐3β↓,
PSA↓,
NKX3.1↑,
Bax:Bcl2↑, a significantly increased ratio of Bax to Bcl-2 protein expression was observed in LAPC-4 cells by the combination treatment compared to Q alone, and a trend to increase in LNCaP cells
miR-19b↓,
miR-148a↓,
AMPKα↓,
TumCP↓, The anti-proliferative activity of arctigenin was 10-20 fold stronger than quercetin in both cell lines.
chemoPv↑, combination of arctigenin and quercetin, that target similar pathways, at low physiological doses, provides a novel regimen with enhanced chemoprevention in prostate cancer.
TumCMig↓, Enhanced inhibition of cell migration

5080- SSE,    Sodium Selenite Regulates the Proliferation and Apoptosis of Gastric Cancer Cells by Suppressing the Expression of LncRNA HOXB-AS1
- in-vitro, GC, HGC27 - in-vitro, GC, NCI-N87
AntiTum↑, The in vivo antitumor effect of sodium selenite on gastric carcinoma has been demonstrated.
HOXB-AS1↓, Na2SeO3 downregulated the expression of HOXB-AS1 in the human gastric cancer (HGC) cell lines, HGC-27, NCI-N87, and KATO III cells, while inhibiting their proliferation and invasion and inducing apoptosis.
TumCP↓,
TumCI↓,
Apoptosis↑,
BAD↓, the expression of apoptosis-related (Bad, Bcl-2, and cleaved-caspase-3) and invasion-related (MMP2, E-cadherin, and N-cadherin) proteins, indicating increased apoptosis and decreased invasion.
Bcl-2↓, f Bcl-2, MMP2, and N-cadherin proteins was significantly downregulated
cl‑Casp3↑,
MMP2↓,
E-cadherin↑,
N-cadherin↓,
ROS↑, Na2SeO3 can increase ROS levels and inhibit the NF-κB signaling pathway, effectively inhibiting the growth, metastasis, and inducing apoptosis of renal cell carcinoma both in vitro and in vivo [41]
NF-kB↓,


Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GPx1↓, 1,   GPx4↓, 1,   ROS↑, 4,   TrxR↓, 1,  

Mitochondria & Bioenergetics ⓘ

BOK↑, 1,   MEK↓, 1,   MMP↓, 2,   OCR↓, 1,  

Core Metabolism/Glycolysis ⓘ

12LOX↓, 1,   AMPK↑, 1,   p‑PCK1↓, 1,   PDK1↓, 1,   PI3K/Akt↓, 2,   SIRT1↑, 1,  

Cell Death ⓘ

14-3-3 proteins↓, 1,   Akt↓, 6,   p‑Akt↓, 3,   APAF1↑, 1,   Apoptosis↑, 2,   BAD↓, 8,   BAD↑, 1,   p‑BAD↓, 3,   BAX↑, 4,   Bax:Bcl2↑, 2,   Bcl-2↓, 4,   BID↓, 1,   BID↑, 1,   Casp3↓, 1,   Casp3↑, 3,   cl‑Casp3↑, 1,   Casp7↓, 1,   Casp7↑, 2,   Casp8↑, 3,   Casp9↑, 4,   cl‑Casp9↑, 1,   cFLIP↓, 1,   Cyt‑c↑, 2,   DR5↑, 1,   FADD↑, 1,   Fas↑, 2,   FasL↑, 1,   hTERT/TERT↓, 1,   Mcl-1↓, 2,   Myc↓, 1,   NAIP↓, 1,   p27↑, 1,   survivin↓, 1,   Telomerase↓, 1,   TRAIL↑, 1,  

Kinase & Signal Transduction ⓘ

AMPKα↓, 1,   FOXD3↑, 1,  

Transcription & Epigenetics ⓘ

miR-21↓, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

HSP27↑, 1,   HSP90↓, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   p62↑, 1,  

DNA Damage & Repair ⓘ

p‑CHK1↓, 1,   NKX3.1↑, 1,   P53↑, 2,   PARP↑, 1,   cl‑PARP↑, 3,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 1,   cycE1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 1,   ERK↓, 2,   FGF↓, 1,   GSK‐3β↓, 1,   GSK‐3β↑, 1,   HOXB-AS1↓, 1,   mTOR↓, 2,   PI3K↓, 2,   SCF↓, 1,   STAT3↓, 2,   TumCG↓, 1,  

Migration ⓘ

Ca+2↑, 2,   E-cadherin↑, 1,   Ki-67↓, 1,   miR-148a↓, 1,   miR-19b↓, 1,   MMP2↓, 3,   MMP9↓, 2,   N-cadherin↓, 1,   SDC1↑, 1,   SMAD4↓, 1,   TGF-β↓, 2,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 3,   TumMeta↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   HIF-1↓, 1,   Hif1a↓, 1,   VEGF↓, 2,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

IκB↓, 1,   NF-kB↓, 3,   PSA↓, 1,   TNF-α↓, 1,   TNF-α↑, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,   ChemoSen↑, 3,   eff↓, 1,   RadioS↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   EGFR↓, 1,   hTERT/TERT↓, 1,   Ki-67↓, 1,   Myc↓, 1,   PSA↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   chemoP↑, 1,   chemoPv↑, 1,   PRAS40↓, 1,   TumVol↓, 1,  
Total Targets: 123

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GPx↑, 1,   ROS↓, 5,   SOD↑, 2,  

Cell Death ⓘ

p‑Akt↑, 2,   Apoptosis↓, 1,   BAD↓, 2,   BAX↓, 2,   Bcl-xL↑, 1,   Casp3↓, 2,   p38↑, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,  

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↑, 1,   p‑mTOR↑, 1,  

Migration ⓘ

Ca+2↓, 2,   MMP9↓, 1,  

Angiogenesis & Vasculature ⓘ

HIF-1↓, 1,   NO↓, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL2↑, 1,  

Synaptic & Neurotransmission ⓘ

AChE↓, 1,   ChAT↑, 1,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   cognitive↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 2,  
Total Targets: 29

Scientific Paper Hit Count for: BAD, BCL2 associated agonist of cell death
3 Quercetin
2 Curcumin
2 Magnetic Fields
1 Baicalein
1 Chrysin
1 Crocetin
1 Docosahexaenoic Acid
1 EGCG (Epigallocatechin Gallate)
1 Docetaxel
1 Gambogic Acid
1 doxorubicin
1 Arctigenin
1 Selenite (Sodium)
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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