BID Cancer Research Results

BID, BH3 interacting-domain death agonist: Click to Expand ⟱

Source:

Type: pro-apoptotic protein

Bid is an abundant pro-apoptotic protein of the Bcl-2 family that is crucial for death receptor-mediated apoptosis in many cell systems.
The expression of BID can serve as a prognostic marker in several cancers. Higher levels of BID are often associated with increased apoptosis and better treatment responses, while lower levels may indicate resistance to therapy and poorer outcomes.

Generation of Truncated Bid (tBid):
• When apoptosis is signaled, specific proteases (such as caspase-8) cleave full-length Bid into its truncated form, tBid.
• tBid is the active form that translocates to mitochondria.

So "the truncation of Bid" means that the protein has been converted into an active form (tBid) that supports apoptosis.

Scientific Papers found: Click to Expand⟱

4427-

AgNPs,

Silver nanoparticles induce apoptosis and G2/M arrest via PKCζ-dependent signaling in A549 lung cells

in-vitro,

Lung,

A549

tumCV↓, Ag NPs reduced cell viability, increased LDH release, and modulated cell cycle distribution through the accumulation of cells at G2/M and sub-G1 phases (cell death)
LDH↑,
TumCCA↑, G2/M and sub-G1 phases (
BAX↑, Ag NP treatment increased Bax and Bid mRNA levels and downregulated Bcl-2 and Bcl-w mRNAs in a dose-dependent manner.
BID↑,
Bcl-2↓,
PKCδ↓, Ag NPs induce strong toxicity and G2/M cell cycle arrest by a mechanism involving PKCζ downregulation in A549 cells.

324-

AgNPs,

CPT,

Silver Nanoparticles Potentiates Cytotoxicity and Apoptotic Potential of Camptothecin in Human Cervical Cancer Cells

in-vitro,

Cerv,

HeLa

ROS↑,
Casp3↑,
Casp9↑,
Casp6↑,
GSH↓,
SOD↓,
GPx↓,
MMP↓, loss of
P53↑,
P21↑,
Cyt‑c↑,
BID↑,
BAX↑,
Bcl-2↓,
Bcl-xL↓,
Akt↓,
Raf↓,
ERK↓,
MAP2K1/MEK1↓,
JNK↑,
p38↑,

2634-

Api,

Apigenin induces both intrinsic and extrinsic pathways of apoptosis in human colon carcinoma HCT-116 cells

in-vitro,

CRC,

HCT116

TumCG↓, Apigenin exerted cytotoxic effect on the cells via inhibiting cell growth in a dose-time-dependent manner and causing morphological changes, arrested cell cycle progression at G0/G1 phase
TumCCA↑,
MMP↓, decreased mitochondrial membrane potential of the treated cells
ROS↑, Apigenin increased respective ROS generation and Ca2+ release and thereby, caused ER stress in the treated cells.
Ca+2↑,
ER Stress↑,
mtDam↑, together with damaged mitochondrial membrane, and upregulated protein expression of CHOP, DR5, cleaved BID, Bax, cytochrome c, cleaved caspase-3, cleaved caspase-8 and cleaved caspase-9, which triggered apoptosis of the cells.
CHOP↑,
DR5↑,
cl‑BID↑,
BAX↑,
Cyt‑c↑,
cl‑Casp3↑,
cl‑Casp8↑,
cl‑Casp9↑,
Apoptosis↑,

1526-

Ba,

Baicalein induces apoptosis through ROS-mediated mitochondrial dysfunction pathway in HL-60 cells

in-vitro,

AML,

HL-60

25uM

Apoptosis↑, 100 microM for 6 h
cl‑PARP↑,
DNAdam↑, DNA fragmentation.
cl‑BID↑,
Cyt‑c↑, cytochrome c release from mitochondria into cytosol
Casp3↑,
Casp8↑,
Casp9?,
H2O2↑, baicalein caused elevation of intracellular hydrogen peroxide level
ROS↑, apoptotic death program through reactive oxygen species (ROS)-mediated mitochondrial dysfunction pathway

1524-

Ba,

Baicalein Induces Caspase‐dependent Apoptosis Associated with the Generation of ROS and the Activation of AMPK in Human Lung Carcinoma A549 Cells

in-vitro,

Lung,

A549

25–125 uM, 24hr

100uM

DR5↑, Baicalein stimulated the expression of DR5, FasL, and FADD, and activated caspase‐8
FADD↑,
FasL↑,
Casp8↑,
cFLIP↓, reducing the levels of FLIPs
Casp3↑, activation of caspase‐9 and −3, and cleavage of poly(ADP‐ribose) polymerase
Casp9↑,
cl‑PARP↑,
MMP↓, baicalein caused a mitochondrial membrane potential (MMP),
BID↑, the truncation of Bid (means that the protein has been converted into an active form (tBid) that supports apoptosis.)
Cyt‑c↑, inducing the release of cytochrome c into the cytosol
ROS↑, baicalein increased the generation of reactive oxygen species (ROS)
eff↓, however, an ROS scavenger, N‐acetylcysteine, notably attenuated baicalein‐mediated loss of MMP and activation of caspases
AMPK↑,
Apoptosis↑,
TumCCA↑, sub-G1 phase
DR5↑, baicalein increased the expression of DR5 and FasL in a concentration-dependent manner, whereas the levels of DR4
FasL↑,
DR4∅,
cFLIP↓, baicalein reduced both FLIP(L) and FLIP(S) protein levels
FADD↑, increased FADD expression
MMPs↓, baicalein treatment reduced MMP levels in a concentrationdependent manner

1521-

Ba,

Baicalein induces apoptosis via ROS-dependent activation of caspases in human bladder cancer 5637 cells

in-vitro,

Bladder,

5637

0,50,150,250 uM

TumCG↓,
Apoptosis↑,
IAP1↓, downregulation of members of the inhibitor of apoptosis protein (IAP) family, including cIAP-1 and cIAP-2,
IAP2↓,
Casp3↑, activation of caspase-9 and -3
Casp9↑,
BAX↑,
Bcl-2↓,
MMP↓, dose-dependent loss of MMP
Casp8↑,
BID↑,
ROS?, baicalein can induce the production of reactive oxygen species (ROS) hese findings suggest that an increase in ROS is required for the occurrence of baicalein- induced apoptosis in 5637 cells.
eff↓, pretreatment with the antioxidant N-acetyl-L-cysteine significantly attenuates the baicalein effects on the loss of MMP and activation of caspase
DR4↑, baicalein considerably increased the levels of DR4, DR5, FasL, and TRAIL.
DR5↑,
FasL↑,
TRAIL↑,

2476-

Ba,

Baicalein Induces Caspase-dependent Apoptosis Associated with the Generation of ROS and the Activation of AMPK in Human Lung Carcinoma A549 Cells

in-vitro,

Lung,

A549

0-125uM

TumCG↓, baicalein-induced growth inhibition was associated with the induction of apoptosis in human lung carcinoma A549 cells.
Apoptosis↑,
DR5↑, Baicalein stimulated the expression of DR5, FasL, and FADD, and activated caspase-8 by reducing the levels of FLIPs (FLICE-inhibitory proteins).
FasL↑,
FADD↑,
Casp8↑,
cFLIP↓,
Casp9↑, activation of caspase-9 and -3, and cleavage of poly(ADP-ribose) polymerase
Casp3↑,
cl‑PARP↑,
MMP↓, Additionally, baicalein caused a mitochondrial membrane potential (MMP), the truncation of Bid, and the translocation of pro-apoptotic Bax to the mitochondria, thereby inducing the release of cytochrome c into the cytosol.
BID↑,
BAX↑,
Cyt‑c↑,
ROS↑, In turn, baicalein increased the generation of reactive oxygen species (ROS)
eff↓, however, an ROS scavenger, N-acetylcysteine, notably attenuated baicalein-mediated loss of MMP and activation of caspases.
AMPK↑, connected with ROS generation and AMPK activation.

726-

Bor,

Redox Mechanisms Underlying the Cytostatic Effects of Boric Acid on Cancer Cells—An Issue Still Open

Review,

NA,

NAD↝, high affinity for the ribose moieties of NAD+
SAM-e↝, high affinity for S-adenosylmethione
PSA↓,
IGF-1↓,
Cyc↓, reduction in cyclins A–E
P21↓,
p‑MEK↓,
p‑ERK↓, ERK (P-ERK1/2)
ROS↑, induce oxidative stress by decreasing superoxide dismutase (SOD) and catalase (CAT)
SOD↓,
Catalase↓,
MDA↑,
GSH↓,
IL1↓, IL-1α
IL6↓,
TNF-α↓,
BRAF↝,
MAPK↝,
PTEN↝,
PI3K/Akt↝,
eIF2α↑,
ATF4↑,
ATF6↑,
NRF2↑,
BAX↑,
BID↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
Bcl-xL↓,

1652-

CA,

Caffeic Acid and Diseases—Mechanisms of Action

Review,

Var,

Dose∅, Black chokeberries seem to be the most potent source of caffeic acid (645 mg/100 g of dry weight)
ROS⇅, Therefore, we will mention the antioxidant (and prooxidant) effects of caffeic acid only briefly
NF-kB↓, In HepG2 cells, caffeic acid (100 µM) inhibited the activity of NF-κB/IL-6/STAT3 signaling, which decreased the expression of VEGF
STAT3↓,
VEGF↓,
MMP9↓, inhibited another downstream product of NF-κB: matrix metalloproteinase 9 (MM-9), which promotes tumor invasiveness and metastases
HSP70/HSPA5↑, caffeic acid (20 μM) also decreased the expression of mortalin(mitochondrial 70 kDa heat shock protein),
AST↝, normalized levels of alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bile acid, total cholesterol, HDL and LD
ALAT↝,
ALP↝,
Hif1a↓,
IL6↓,
IGF-1R↓,
P21↑,
iNOS↓,
ERK↓,
Snail↓,
BID↑,
BAX↑,
Casp3↑,
Casp7↑,
Casp9↑,
cycD1/CCND1↓,
Vim↓,
β-catenin/ZEB1↓,
COX2↓,
ROS↑, the chelating ability of caffeic acid is also responsible for its occasional pro-oxidant ability. After chelating Cu2+, the Cu2+ can be reduced to Cu+. combination of caffeic acid and endogenous copper ions can result in oxidative damage

5914-

Cats,

Induction of apoptosis by Uncaria tomentosa through reactive oxygen species production, cytochrome c release, and caspases activation in human leukemia cells

in-vitro,

AML,

HL-60

*Inflam↓, Recently, it has been found to possess potent anti-inflammation activities.
eff↑, CC-EA induced DNA fragmentation in HL-60 cells in a clearly more a concentration- and time-dependent manner than the other extracts.
DNAdam↑,
Cyt‑c↑, CC-EA underwent a rapid loss of mitochondrial transmembrane (DeltaPsi(m)) potential, stimulation of phosphatidylserine flip-flop, release of mitochondrial cytochrome c into cytosol,
Casp3↑, induction of caspase-3 activity in a time-dependent manner, and induced the cleavage of DNA fragmentation
PARP↑, nd PARP poly-(ADP-ribose) polymerase (PARP).
Fas↑, CC-EA promoted the up-regulation of Fas before the processing and activation of procaspase-8 and cleavage of Bid.
proCasp8↑,
cl‑BID↑,
BAX↑, apoptosis induced by CC-EA was accompanied by up-regulation of Bax, down-regulation of Bcl-X(L) and cleavage of Mcl-1,
Bcl-xL↑,
cl‑Mcl-1↑,

5959-

CEL,

Celecoxib induces apoptosis in cervical cancer cells independent of cyclooxygenase using NF-κB as a possible target

in-vitro,

Cerv,

HeLa

Apoptosis↑, Celecoxib induced apoptosis independent of COX-2 activity.
Casp8↑, This event accompanied the activation of caspase-8 and -9 with Bid cleavage and the loss of mitochondrial membrane potential.
Casp9↑,
cl‑BID↑,
MMP↓,
NF-kB↑, Celecoxib-induced apoptosis is associated with NF-κB activation.
Dose⇅, The chemopreventive effect of celecoxib was also achieved only at relatively high doses (400–800 mg daily) in a human clinical trial, but not at a therapeutic daily dose of 200 mg
chemoPv⇅,
COX2↓, less than 10 μM of celecoxib is needed to inhibit the COX activity, while the concentrations required to inhibit tumor cell growth range from 30 μM to 100 μM

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↑,

136-

CUR,

docx,

Combinatorial effect of curcumin with docetaxel modulates apoptotic and cell survival molecules in prostate cancer

in-vitro,

Pca,

DU145

 5-50uM

 19.2 nM(docx), 32.3 μM(CUR)

20 μM curcumin and 10 nM docetaxel significantly decrease (2.7 fold) the proliferation

in-vitro,

Pca,

PC3

 46 nM(docx), 36.1 μM(CUR)

combined treatment decrease (3.2 fold)

Bcl-2↓, combined treatment with curcumin with docetaxel down-regulates the expression of the anti-apoptotic proteins BCL-2, BCL-XL and MCL-1 in DU145 and PC3 cells
Bcl-xL↓,
Mcl-1↓,
BAX↑, Whereas, the expression of the pro-apoptotic markers BAK and BID were significantly up-regulated in curcumin with docetaxel treated group compared to curcumin and docetaxel-treated group alone
BID↑,
PARP↑, combined treatment with curcumin and docetaxel in DU145 and PC3 cells enhanced proteolysis of PARP compared
NF-kB↓, Curcumin blocks NF-κB activation in docetaxel-treated PCa cells
CDK1↓, treatment of curcumin and docetaxel significantly reduced the expression of the proliferation marker CDK-1 and inflammatory marker COX-2
COX2↓,
RTK-RAS↓,
PI3K/Akt↓, combined treatment of curcumin and docetaxel reduced the expression of PI3K, phospho-AKT, EGFR and HER2 in both DU145 and PC3 cells
EGFR↓,
HER2/EBBR2↓, docetaxel in combination with curcumin down-regulates the expression of HER2 and EGFR resulting inhibition of the expression of PI3K kinase and phospho-AKT
P53↑,
ChemoSen↑, The combined treatment of curcumin and docetaxel inhibited the proliferation and induced apoptosis significantly higher than the curcumin and docetaxel-treated group alone.

1155-

The anti-cancer effects of fucoidan: a review of both in vivo and in vitro investigations

Review,

NA,

100 μg/mL

*toxicity↓, Sprague–Dawley rats, researchers didn’t observe significant side effects when taking 0–1000 mg/kg fucoidan orally for 28 days.
Casp3↑,
Casp7↑,
Casp8↑,
Casp9↑,
VEGF↓,
angioG↓,
PI3K↓,
Akt↓,
PARP↑,
Bak↑,
BID↑,
Fas↑,
Mcl-1↓,
survivin↓,
XIAP↓,
ERK↓,
EMT↓, Fucoidan can reverse the EMT effectively
EM↑,
IM↓,
Snail↓,
Slug↓,
Twist↓,

2832-

FIS,

Fisetin's Promising Antitumor Effects: Uncovering Mechanisms and Targeting for Future Therapies

Review,

Var,

MMP↓, fraction of cells with reduced mitochondrial membrane potential also increased, indicating that fisetin-induced apoptosis also destroys mitochondria.
mtDam↑,
Cyt‑c↑, Cytochrome c and Smac/DIABLO levels are also released when the mitochondrial membrane potential changes, and this results in the activation of the caspase cascade and the cleavage of poly [ADP-ribose] polymerase (PARP)
Diablo↑,
Casp↑,
cl‑PARP↑,
Bak↑, Fisetin induced apoptosis in HCT-116 human colon cancer cells by upregulating proapoptotic proteins Bak and BIM and downregulating antiapoptotic proteins B cell lymphoma (BCL)-XL and -2.
BIM↑,
Bcl-xL↓,
Bcl-2↓,
P53↑, fisetin through the activation of p53
ROS↑, over generation of ROS, which is also directly initiated by fisetin, the stimulation of AMPK
AMPK↑,
Casp9↑, activating caspase-9 collectively, then activating caspase-3, leading to apopotosis
Casp3↑,
BID↑, Bid, AIF and the increase of the ratio of Bax to Bcl-2, causing the activation of caspase 3–9
AIF↑,
Akt↓, The inhibition of the Akt/mTOR/MAPK/
mTOR↓,
MAPK↓,
Wnt↓, Fisetin has been shown to degrade the Wnt/β/β-catenin signal
β-catenin/ZEB1↓,
TumCCA↑, fisetin triggered G1 phase arrest in LNCaP cells by activating WAF1/p21 and kip1/p27, followed by a reduction in cyclin D1, D2, and E as well as CDKs 2, 4, and 6
P21↑,
p27↑,
cycD1/CCND1↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,
CDK6↓,
TumMeta↓, reduces PC-3 cells' capacity for metastasis
uPA↓, fisetin decreased MMP-2 protein, messenger RNA (mRNA), and uPA levels through an ERK-dependent route
E-cadherin↑, Fisetin can upregulate the epithelial marker E-cadherin, downregulate the mesenchymal marker vimentin, and drastically lower the EMT regulator twist protein level at noncytotoxic dosages, studies have revealed.
Vim↓,
EMT↓,
Twist↓,
DNAdam↑, Fisetin induces apoptosis in the human nonsmall lung cancer cell line NCI-H460, which causes DNA breakage, the growth of sub-G1 cells, depolarization of the mitochondrial membrane, and activation of caspases 9, 3, which are involved in prod of iROS
ROS↓, fisetin therapy has been linked to a reduction in ROS, according to other research.
COX2↓, Fisetin lowered the expression of COX-1 protein, downregulated COX-2, and decreased PGE2 production
PGE2↓,
HSF1↓, Fisetin is a strong HSF1 inhibitor that blocks HSF1 from binding to the hsp70 gene promoter.
cFos↓, NF-κB, c-Fos, c-Jun, and AP-1 nuclear levels were also lowered by fisetin treatment
cJun↓,
AP-1↓,
Mcl-1↓, inhibition of Bcl-2 and Mcl-1 all contribute to an increase in apoptosis
NF-kB↓, Fisetin's ability to prevent NF-κB activation in LNCaP cells
IRE1↑, fisetin (20–80 µM) was accompanied by brief autophagy and the production of ER stress, which was shown by elevated levels of IRE1 α, XBP1s, ATF4, and GRP78 in A375 and 451Lu cells
ER Stress↑,
ATF4↑,
GRP78/BiP↑,
MMP2↓, lowering MMP-2 and MMP-9 proteins in melanoma cell xenografts
MMP9↓,
TCF-4↓, fisetin therapy reduced levels of β-catenin, TCF-4, cyclin D1, and MMP-7,
MMP7↓,
RadioS↑, fisetin treatment could radiosensitize human colorectal cancer cells that are resistant to radiotherapy.
TOP1↓, fisetin blocks DNA topoisomerases I and II in leukemia cells.
TOP2↓,

2912-

LT,

Luteolin: a flavonoid with a multifaceted anticancer potential

Review,

Var,

ROS↑, induction of oxidative stress, cell cycle arrest, upregulation of apoptotic genes, and inhibition of cell proliferation and angiogenesis in cancer cells.
TumCCA↑,
TumCP↓,
angioG↓,
ER Stress↑, Luteolin induces mitochondrial dysfunction and activates the endoplasmic reticulum stress response in glioblastoma cells, which triggers the generation of intracellular reactive oxygen species (ROS)
mtDam↑,
PERK↑, activate the expression of stress-related proteins by mediating the phosphorylation of PERK, ATF4, eIF2α, and cleaved-caspase 12.
ATF4↑,
eIF2α↑,
cl‑Casp12↑,
EMT↓, Luteolin is known to reverse epithelial-to-mesenchymal transition (EMT), which is associated with the cancer cell progression and metastasis.
E-cadherin↑, upregulating the biomarker E-cadherin expression, followed by a significant downregulation of the N-cadherin and vimentin expression
N-cadherin↓,
Vim↓,
*neuroP↑, Furthermore, luteolin holds potential to improve the spinal damage and brain trauma caused by 1-methyl-4-phenylpyridinium due to its excellent neuroprotective properties.
NF-kB↓, downregulation and suppression of cellular pathways such as nuclear factor kappa B (NF-kB), phosphatidylinositol 3’-kinase (PI3K)/Akt, and X-linked inhibitor of apoptosis protein (XIAP)
PI3K↓,
Akt↑,
XIAP↓,
MMP↓, Furthermore, the membrane action potential of mitochondria depletes in the presence of luteolin, Ca2+ levels and Bax expression upregulate, the levels of caspase-3 and caspase-9 increase, while the downregulation of Bcl-2
Ca+2↑,
BAX↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
Cyt‑c↑, cause the cytosolic release of cytochrome c from mitochondria
IronCh↑, Luteolin serves as a good metal-chelating agent owing to the presence of dihydroxyl substituents on the aromatic ring framework
SOD↓, luteolin further triggered an early phase accumulation of ROS due to the suppression of the activity of cellular superoxide dismutase.
*ROS↓, Luteolin reportedly demonstrated an optimal 43.7% inhibition of the accumulation of ROS, 24.5% decrease in malondialdehyde levels, and 38.7% lowering of lactate dehydrogenase levels at a concentration of 30 µM
*LDHA↑,
*SOD↑, expression of superoxide dismutase ameliorated by 73.7%, while the activity of glutathione improved by 72.3% at the same concentration of luteolin
*GSH↑,
*BioAv↓, Poor bioavailability of luteolin limits its optimal therapeutic efficacy and bioactivity
Telomerase↓, MDA-MB-231 cells with luteolin led to dose dependent arrest of cell cycle in S phase by reducing the levels of telomerase and by inhibiting the phosphorylation of NF-kB inhibitor α along with its target gene c-Myc
cMyc↓,
hTERT/TERT↓, These events led to the suppression of the expression of human telomerase reverse transcriptase (hTERT) encoding for the catalytic subunit of telomerase
DR5↑, luteolin upregulated the expression of caspase cascades and death receptors, including DR5
Fas↑, expression of proapoptotic genes such as FAS, FADD, BAX, BAD, BOK, BID, TRADD upregulates, while the anti-apoptotic genes NAIP, BCL-2, and MCL-1 experience downregulation.
FADD↑,
BAD↑,
BOK↑,
BID↑,
NAIP↓,
Mcl-1↓,
CDK2↓, expression of cell cycle regulatory genes CDK2, CDKN2B, CCNE2, CDKN1A, and CDK4 decreased on incubation with luteolin
CDK4↓,
MAPK↓, expression of MAPK1, MAPK3, MAP3K5, MAPK14, PIK3C2A, PIK3C2B, AKT1, AKT2, and ELK1 downregulated
AKT1↓,
Akt2↓,
*Beclin-1↓, luteolin led to downregulation of the expression of hypoxia-inducible factor-1α and autophagy-associated proteins, Beclin 1, and LC3
Hif1a↓,
LC3II↑, LC3-II is upregulated following the luteolin treatment in p53 wild type HepG2 cells i
Beclin-1↑, Luteolin treatment reportedly increased the number of intracellular autophagosomes, as indicated by an increased expression of Beclin 1, and conversion of LC3B-I to LC3B-II in hepatocellular carcinoma SMMC-7721 cells.

150-

NRF,

CUR,

docx,

Subverting ER-Stress towards Apoptosis by Nelfinavir and Curcumin Coexposure Augments Docetaxel Efficacy in Castration Resistant Prostate Cancer Cells

in-vitro,

Pca,

C4-2B

 NFR (5 µM), CUR (5 µM),DTX 10nM

 CRPC

p‑Akt↓,
p‑eIF2α↑, phosphorylated
ER Stress↑, Acute exposure (3–9 hrs) to this 3-drug combination intensified ER-stress induced pro-apoptotic markers, i.e. ATF4, CHOP, and TRIB3.
ATF4↑, 3-drug combination rapidly enhances ER-stress associated death sensors, CHOP, ATF-4 and TRIB3 in C4-2B cells
CHOP↑,
TRIB3↑,
ChemoSen↑, subverting ER-stress towards apoptosis using adjuvant therapy with NFR and CUR can chemosensitize the CRPC cells to DTX therapy.
Casp3↑, NFR or CUR alone could increase Caspase-3 activity in DTX exposed cells
cl‑PARP↑, PARP cleavage assays further confirmed this differential effect of drug combination on apoptotic cell death. In C4-2B cells, a 9-fold increase was observed
BID↑, 3-drug combination rapidly increases ER-stress transducers, BiP, eIF2µ and Xbp-1 in C4-2B cells
XBP-1↑,

2076-

PB,

Sodium Butyrate Induces Endoplasmic Reticulum Stress and Autophagy in Colorectal Cells: Implications for Apoptosis

in-vitro,

CRC,

HCT116

0-5mM

in-vitro,

CRC,

HT29

TumCP↓, Sodium butyrate suppressed colorectal cancer cell proliferation, induced autophagy, and resulted in apoptotic cell death
TumAuto↑,
Apoptosis↑,
ER Stress↑, sodium butyrate treatment markedly enhanced the expression of endoplasmic reticulum stress-associated proteins, including BIP, CHOP, PDI, and IRE-1a.
BID↑,
CHOP↑,
PDI↑,
IRE1↓,
LC3‑Ⅱ/LC3‑Ⅰ↑, A marked conversion of free LC3-I to heavier lipid bound LC3-II was detected after exposing HCT-116 (Fig 3A) and HT-29 (Fig 3B) cells to 2mM sodium butyrate for 24 h
LC3B↑, mRNA levels of Beclin 1 and LC3B, but not ATG3, significantly increased with increasing doses of NaBu
Beclin-1↑,
other↝, These results strongly suggested that NaB induced autophagy was mediated by ER stress in CRC cells.
other↝, Inhibition of autophagy enhanced NaB-induced apoptotic cell death

4947-

PEITC,

Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G0/G1 Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death

in-vitro,

Oral,

HSC3

AntiCan↑, Phenethyl isothiocyanate (PEITC), an effective anticancer and chemopreventive agent, has been reported to inhibit cancer cell growth through cell-cycle arrest and induction of apoptotic events in various human cancer cells models.
chemoPv↑,
TumCG↓,
Apoptosis↑,
TumCCA↑, PEITC effectively inhibited the HSC-3 cells’ growth and caused apoptosis. PEITC induced G0/G1 phase arrest through the effects of associated protein such as p53, p21, p17, CDK2 and cyclin E,
P53↑,
P21↑,
BAX↑, triggered apoptosis through promotion of Bax and Bid expression and reduction of Bcl-2, leading to decrease the levels of mitochondrial membrane potential (ΔΨm), and followed the releases of cytochrome c, AIF and Endo G then for causing apoptosis in
BID↑,
Bcl-2↓,
MMP↓,
Cyt‑c↑,
AIF↑,
ROS↑, PEITC promoted the production of ROS (Figure 4(a)) and Ca2+ (Figure 4(c)) but decreased the levels of ΔΨm
Ca+2↑,

4923-

PEITC,

Quantitative chemical proteomics reveals that phenethyl isothiocyanate covalently targets BID to promote apoptosis

Study,

Var,

cl‑BID↑, We show that BID, an apoptosis regulator of the Bcl-2 family, is covalently modified by ITCs on its N-terminal cysteines. PEITC promotes the cleavage and mitochondrial translocation of BID
Apoptosis↑, leading to a strong induction of apoptosis.
Bcl-xL↓, this exposure allows BID to bind anti-apoptotic proteins such as Bcl-xL, thereby suppressing their anti-apoptotic activity.
Casp8↑, Meanwhile, caspase-8 is activated shortly after PEITC treatment [12], leading to the cleavage of PEITC-modified full-length BID.
Cyt‑c↑, induce cytochrome c release

4940-

PEITC,

Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G 0/G 1 Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death

in-vitro,

Oral,

HSC3

TumCCA↑, reported to inhibit cancer cell growth through cell-cycle arrest and induction of apoptotic events in various human cancer cells models
Apoptosis↑, PEITC induced cytotoxic effects on HSC-3 cells through the induction of apoptosis, and it also related to the involvement of ROS via mitochondria-dependent signal pathways.
BAX↑, it triggered apoptosis through promotion of Bax and Bid expression and reduction of Bcl-2, leading to decrease the levels of mitochondrial membrane potential (ΔΨm)
BID↑,
Bcl-2↓,
MMP↓,
Cyt‑c↑, and followed the releases of cytochrome c, AIF and Endo G then for causing apoptosis in HSC-3 cells.
AIF↑,
tumCV↓, PEITC Induced Cell-Morphological Changes and Decreased the Percentage of Viable Cells
ROS↑, We confirmed that whether PEITC-induced apoptosis is accompanied by the production of ROS and Ca2+ . PEITC promoted the production of ROS (Figure 4(a)) and Ca2+
Ca+2↑,
CDC25↓, PEITC decreased expression of cdc25A, CDK6 and cyclin D (Figure 5(a)), CDK2 and cyclin E (Figure 5(b)) proteins but increased the levels of p15
CDK6↓,
cycD1/CCND1↓,
CDK2↓,
cycE/CCNE↓,
P53↑, but increased the levels of p15 (Figure 5(a)), p53, p27, and p21 (Figure 5(b)) that led to G 0/G 1 phase arrest in HSC-3 cells.
p27↑,
P21↑,
Casp9↑, Here, we found that PEITC promoted ROS production and decreased the levels of ΔΨm and cytochrome c release, the activation of caspase-9 and caspase-3
Casp3↑,
GRP78/BiP↑, promotion of ROS and Ca2+ production that caused ER stress which based on increasing the GRP78 and ROS,

4942-

PEITC,

Phenethyl Isothiocyanate (PEITC) Inhibits the Growth of Human Oral Squamous Carcinoma HSC-3 Cells through G(0)/G(1) Phase Arrest and Mitochondria-Mediated Apoptotic Cell Death

in-vitro,

Oral,

HSC3

0.5, 1, 2, 2.5, and 5 μM) for 24, 48, or 72 h.

chemoPv↑, Phenethyl isothiocyanate (PEITC), an effective anticancer and chemopreventive agent, has been reported to inhibit cancer cell growth through cell-cycle arrest and induction of apoptotic events in various human cancer cells models
TumCG↓,
TumCCA↑,
Apoptosis↑, PEITC effectively inhibited the HSC-3 cells' growth and caused apoptosis.
BAX↑, triggered apoptosis through promotion of Bax and Bid expression and reduction of Bcl-2, leading to decrease the levels of mitochondrial membrane potential (ΔΨm),
BID↑,
Bcl-2↓,
MMP↓,
Cyt‑c↑, and followed the releases of cytochrome c, AIF and Endo G then for causing apoptosis in HSC-3 cells
AIF↑,
ROS↑, PEITC promoted the production of ROS (Figure 4(a)) and Ca2+
Ca+2↑,

3192-

SFN,

Transcriptome analysis reveals a dynamic and differential transcriptional response to sulforaphane in normal and prostate cancer cells and suggests a role for Sp1 in chemoprevention

in-vitro,

Pca,

PC3

15 μM SFN

Sp1/3/4↓, Sp1 protein was significantly decreased by SFN treatment in prostate cancer cells . Because SFN decreased the expression of Sp1, and to a lesser extent Sp3
selectivity↑, SFN alters gene expression differentially in normal and cancer cells with key targets in chemopreventive processes, making it a promising dietary anti-cancer agent.
NRF2↑, through the induction of phase 2 enzymes via Keap1-Nrf2 signaling
HDAC↓, SFN also inhibits the activity and/or expression of genes that regulate epigenetic mechanisms including histone deactylases (HDACs) and DNA methyltransferases (DNMTs) in cancer cells
DNMTs↓,
TumCCA↑, 15 μM SFN treatment induces cell cycle arrest at the G1 phase and only modestly increases apoptosis
selectivity↑, Normal prostate epithelial cells (PREC) do not undergo cell cycle arrest or apoptosis in response to this SFN treatment
HO-1↑, In all cell lines and time points, HO1 and NQO1 were identified as significantly upregulated by SFN
NQO1↑,
CDK2↓, MX non-receptor tyrosine kinase (BMX), cyclin-dependent kinase 2 (CDK2), and polo-like kinase 1 (PLK1) had decreased expression with SFN treatment
TumCP↓, suppression of Sp1 expression decreased prostate cancer cells proliferation.
BID↑, SFN treatment produced a significant increase in the expression of the apoptosis related genes Bid, Smac/Diablo, and ICAD only in PC-3 cells (
Smad1↑,
Diablo↑,
ICAD↑,
Cyt‑c↑, It also increased the expression of cytochrome c, c-IAP1, and HSP27 in PC-3 cells while it decreased expression in PREC cells.
IAP1↑,
HSP27↑,
*Cyt‑c↓,
*IAP1↓,
*HSP27↓,
survivin↓, In these studies, inhibition of Sp1 is associated with inhibition of the cancer promoting genes survivin, CDK4, VEGF and the androgen receptor.
CDK4↓,
VEGF↓,
AR↓,

1465-

SFN,

TRAIL attenuates sulforaphane-mediated Nrf2 and sustains ROS generation, leading to apoptosis of TRAIL-resistant human bladder cancer cells

NA,

Bladder,

eff↑, Combined treatment with SFN and TRAIL (SFN/TRAIL) significantly induced apoptosis
Apoptosis↑,
Casp↑,
MMP↓,
BID↑,
DR5↑,
ROS↑, SFN increased both the generation of reactive oxygen species (ROS) and the activation of nuclear factor erythroid 2-related factor 2 (Nrf2), which is an anti-oxidant enzyme.
NRF2↑,
eff↑, Interestingly, TRAIL effectively suppressed SFN-mediated nuclear translocation of Nrf2, and the period of ROS generation was more extended compared to that of treatment with SFN alone.
eff↓, blockade of ROS generation inhibited apoptotic activity

978-

SIL,

A comprehensive evaluation of the therapeutic potential of silibinin: a ray of hope in cancer treatment

Review,

NA,

10uM

 200 to 570 μM

PI3K↓,
Akt↓,
NF-kB↓,
Wnt/(β-catenin)↓,
MAPK↓,
TumCP↓,
TumCCA↑, G0/G1 cell cycle arrest
Apoptosis↑, In T24 and UM-UC-3 human bladder cancer cells, silibinin treatment at a concentration of 10 μM significantly inhibited proliferation, migration, invasion, and induced apoptosis.
p‑EGFR↓,
JAK2↓,
STAT5↓,
cycD1/CCND1↓,
hTERT/TERT↓,
AP-1↓,
MMP9↓,
miR-21↓,
miR-155↓,
Casp9↑,
BID↑,
ERK↓, ERK1/2
Akt2↓,
DNMT1↓,
P53↑,
survivin↓,
Casp3↑,
ROS↑, cytotoxicity of silibinin in Hep-2 cells was associated with the accumulation of intracellular reactive oxygen species (ROS), which could be mitigated by the ROS scavenger NAC.

Showing Research Papers: 1 to 25 of 25

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 25

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

GSH↑, 1, ROS↓, 1, SOD↑, 1,

Core Metabolism/Glycolysis ⓘ

LDHA↑, 1,

Cell Death ⓘ

Cyt‑c↓, 1, IAP1↓, 1,

Protein Folding & ER Stress ⓘ

HSP27↓, 1,

Autophagy & Lysosomes ⓘ

Beclin-1↓, 1,

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,

Functional Outcomes ⓘ

neuroP↑, 1, toxicity↓, 1,
Total Targets: 12

Scientific Paper Hit Count for: BID, BH3 interacting-domain death agonist

4 Baicalein
4 Phenethyl isothiocyanate
2 Silver-NanoParticles
2 Curcumin
2 Docetaxel
2 Sulforaphane (mainly Broccoli)
1 Camptothecin
1 Apigenin (mainly Parsley)
1 Boron
1 Caffeic acid
1 Cat’s Claw
1 Celecoxib
1 Chrysin
1 Fucoidan
1 Fisetin
1 Luteolin
1 nelfinavir/Viracept
1 Phenylbutyrate
1 Silymarin (Milk Thistle) silibinin

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

BID Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

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 ⓘ

Cellular Microenvironment ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

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