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⟱
TumCP↓, Berbamine inhibits the proliferation of KM3 cells in a dose- and time-dependent manner.
eff↑, Combination of berbamine with dexamethasone (Dex), doxorubicin (Dox) or arsenic trioxide (ATO) resulted in enhanced inhibition of cell growth.
TumCCA↑, KM3 cells were arrested at G1 phase and apoptotic cells increased from 0.54% to 51.83% for 36 h.
IKKα↓, Berbamine treatment led to increased expression of A20, down-regulation of IKKα, p-IκBα, and followed by inhibition of p65 nuclear localization.
p65↓,
Bcl-xL↓, As a result, NF-κB downstream targets such as cyclinD1, Bcl-xL, Bid and survivin were down-regulated.
BID↓,
survivin↓,
BID↓, EGCG, a green tea polyphenol, induces ER stress-mediated apoptosis in colorectal cancer cells, an effect associated with BiP upregulation
UPR↑, Natural compounds have also been identified as BiP modulators, including palmatine and epigallocatechin gallate (EGCG), which impair BiP function, leading to unfolded protein accumulation and UPR activation.
ER Stress↑,
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
*cardioP↑, kaempferol has been linked to various cardiovascular, cancer, inflammatory, neurodegenerative, and obese diseases
*AntiCan↑,
*Inflam↓,
*neuroP↑,
*BioAv↓, in a 2002 study by Radtke, the plasma concentration of kaempferol was reported to be 10.7 nM, while the intake amount was 4.7 mg/day
selectivity?, Their study showed that kaempferol was a potent inhibitor in bladder cancer with high safety on normal cells.
p‑Akt↓, it suppressed the phosphorylation of AKT, CyclinD1, CDK4, Bid, Mcl-1, and Bcl-xL, while boosting the expression of p-BRCA1, ATM, p53, p21, and p38, as well as Bax and Bid.
p‑cycD1/CCND1↓,
p‑CDK4↓,
p‑BID↓,
p‑Mcl-1↓,
p‑BRCA1↑,
ATM↑,
P53↑,
P21↑,
p38↑,
BAX↑,
BID↑,
MMP↓, decrease mitochondrial membrane potential and increase caspase-3, -7, and -9 activities in the U-2 OS cell line.
Casp3↑,
Casp7↑,
Casp9↑,
AIF↑, A rise in AIF protein levels was also observed, indicating that apoptosis was induced through a caspase-independent mitochondrial mechanism.
ER Stress↑, The endoplasmic reticulum stress pathways are the other mechanism induced by kaempferol in the human osteosarcoma cell line.
TumMeta↓, kaempferol inhibited cell metastasis in U-2 OS cells by inhibiting various signaling pathways (e.g., ERK, AP-1, JNK, and p38)
ERK↓,
AP-1↓,
JNK↓,
p38↓,
GLUT1↓, suggested chemoprotective mechanism of kaempferol can result in toxicity and proliferation arrest due to the downregulation of glucose transporter 1 (GLUT1) gene expression and inhibition of cellular glucose uptake in cancer cell lines.
GlucoseCon↓,
MMP9↓, Downregulation of the matrix metalloproteinase-9 (MMP) expression and activity was the other process in breast cancer invasion treated with kaempferol using the MDA-MB-231 cell line
CYP1A1↓, kaempferol influenced the aryl hydrocarbon receptor in inhibiting CYP1A1 transcription
ChemoSen↑, Cancer stem cell markers, such as Oct-4, Nanog, ABCB1, and ALDH1A1, were significantly reduced in MCF-7 cells treated with kaempferol and docetaxel.
OCT4↓,
Nanog↓,
P-gp/ABCB1↓,
ALDH1A1↓,
TumCCA↑, Kaempferol could also suppress the proliferation of triple-negative breast cancer, contribute to the G2/M arrest induction, induce apoptosis and DNA damage, increase the expression of γ-H2AX and cleave the caspase-9, caspase-3, and p-ATM
DNAdam↑,
γH2AX↑,
COX2/PTGS2↓, The new derivative showed downregulation of the expression of COX-2, inhibited migration, decreased intracellular ROS and calcium cation levels, decreased Bcl-2 expression, and increased Bax expression in MCF-7 cells
i-ROS↓,
Ca+2↓,
eff↑, The activation of death receptor 5 (DR5) by kaempferol increased the sensitivity of colon cancer cells to TRAIL-induced apoptosis
DR5↑,
ChemoSen↑, combination of doxorubicin (DOX) and kaempferol was more efficient in induction of apoptosis and cytotoxic effect against HT-29 colon cancer cell line in comparison with each drug alone
Akt↓, kaempferol inhibits PI3K/Akt signaling pathways
PI3K↓,
ROS↑, rat model of hepatocellular carcinoma through the mitochondrial-dependent pathway by targeting upstream activities such as the enhancement of ROS formation, MMP downregulation, and the increasing of the caspase-3 activity in the cytosol
EMT↓, kaempferol inhibits the EMT, migration, and MMP-2 activation induced by TGF-1 in these cancer cells
survivin↓, Kaempferol was also responsible for downregulating phosphorylated Akt and reducing the quantity of survivin protein to stop survivin
ROS⇅, It appears that the cellular and/or physiological context(s)
determines whether TQ acts as a pro-oxidant or an anti-ox-
idant in vivo
Fas↑, Figure 2, cell death
DR5↑,
TRAIL↑,
Casp3↑,
Casp8↑,
Casp9↑,
P53↑,
mTOR↓,
Bcl-2↓,
BID↓,
CXCR4↓,
JNK↑,
p38↑,
MAPK↑,
LC3II↑,
ATG7↑,
Beclin-1/ATG6↑,
AMPK↑,
PPARγ↑, cell survival
eIF2α↓,
P70S6K↓,
VEGF↓,
ERK↓,
NF-kB↓,
XIAP↓,
survivin↓,
p65↓,
DLC1↑, epigenetic
FOXO↑,
TET2↑,
CYP1B1↑,
UHRF1↓,
DNMT1↓,
HDAC1↓,
IL2↑, inflammation
IL1↓,
IL6↓,
IL10↓,
IL12↓,
TNF-α↓,
iNOS↓,
COX2/PTGS2↓,
5LO↓,
AP-1↓,
PI3K↓, invastion
Akt↓,
cMET↓,
VEGFR2/KDR/Flk1↓,
CXCL1↓,
ITGA5↓,
Wnt↓,
β-catenin/ZEB1↓,
GSK‐3β↓,
Myc↓,
cycD1/CCND1↓,
N-cadherin↓,
Snail↓,
Slug↓,
Vim↓,
Twist↓,
Zeb1↓,
MMP2↓,
MMP7↓,
MMP9↓,
JAK2↓, cell proliferiation
STAT3↓,
NOTCH↓,
cycA1/CCNA1↓,
CDK2↓,
CDK4↓,
CDK6↓,
CDC2↓,
CDC25↓,
Mcl-1↓,
E2Fs↓,
p16↑,
p27/CDKN1B↑,
P21↑,
ChemoSen↑, Such chemo-potentiating effects of TQ in
different cancer cells have been observed with 5-fluorouracil
in gastric cancer and colorectal cancer models
Showing Research Papers: 1 to 5 of 5
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
CYP1A1↓, 1, ROS↑, 2, ROS⇅, 1, i-ROS↓, 1, TrxR↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
AIF↑, 1, CDC2↓, 1, CDC25↓, 1, MMP↓, 2, OCR↓, 1, XIAP↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
AMPK↑, 1, ATG7↑, 1, GlucoseCon↓, 1, PPARγ↑, 1, SIRT1↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 3, p‑Akt↓, 1, BAD↓, 1, BAX↑, 2, Bcl-2↓, 2, Bcl-xL↓, 1, BID↓, 4, BID↑, 1, p‑BID↓, 1, Casp3↑, 3, Casp7↑, 1, Casp8↑, 2, Casp9↑, 3, cFLIP↓, 1, DR5↑, 2, Fas↑, 1, hTERT/TERT↓, 1, iNOS↓, 1, JNK↓, 1, JNK↑, 1, MAPK↑, 1, Mcl-1↓, 1, p‑Mcl-1↓, 1, Myc↓, 2, p27/CDKN1B↑, 1, p38↓, 1, p38↑, 2, survivin↓, 4, Telomerase↓, 1, TRAIL↑, 1,
Kinase & Signal Transduction(tgid=6) ⓘ
FOXD3↑, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
eIF2α↓, 1, ER Stress↑, 2, HSP90↓, 1, UPR↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1/ATG6↑, 1, LC3II↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
ATM↑, 1, p‑BRCA1↑, 1, CYP1B1↑, 1, DNAdam↑, 1, DNMT1↓, 1, p16↑, 1, P53↑, 3, UHRF1↓, 1, γH2AX↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK2↓, 1, CDK4↓, 1, p‑CDK4↓, 1, cycA1/CCNA1↓, 1, cycD1/CCND1↓, 1, p‑cycD1/CCND1↓, 1, E2Fs↓, 1, P21↑, 2, TumCCA↑, 2,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ALDH1A1↓, 1, cMET↓, 1, EMT↓, 1, ERK↓, 3, FOXO↑, 1, GSK‐3β↓, 1, HDAC1↓, 1, mTOR↓, 1, Nanog↓, 1, NOTCH↓, 1, OCT4↓, 1, P70S6K↓, 1, PI3K↓, 3, STAT3↓, 2, TumCG↓, 1, Wnt↓, 1,
Migration(tgid=13) ⓘ
5LO↓, 1, AP-1↓, 2, Ca+2↓, 1, DLC1↑, 1, ITGA5↓, 1, MMP2↓, 2, MMP7↓, 1, MMP9↓, 3, N-cadherin↓, 1, Slug↓, 1, Snail↓, 1, TumCP↓, 1, TumMeta↓, 2, Twist↓, 1, Vim↓, 1, Zeb1↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 1, Hif1a↓, 1, VEGF↓, 2, VEGFR2/KDR/Flk1↓, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1, GLUT1↓, 1, P-gp/ABCB1↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 2, CXCL1↓, 1, CXCR4↓, 1, IKKα↓, 1, IL1↓, 1, IL10↓, 1, IL12↓, 1, IL2↑, 1, IL6↓, 1, JAK2↓, 1, NF-kB↓, 2, p65↓, 2, TNF-α↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
CDK6↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1, BioAv↑, 2, ChemoSen↑, 4, eff↓, 1, eff↑, 2, RadioS↑, 1, selectivity?, 1, TET2↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
p‑BRCA1↑, 1, hTERT/TERT↓, 1, IL6↓, 1, Myc↓, 2,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1,
Total Targets: 138
Pathway results for Effect on Normal Cells:
Immune & Inflammatory Signaling(tgid=16) ⓘ
Inflam↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiCan↑, 1, cardioP↑, 1, neuroP↑, 1,
Total Targets: 5
Scientific Paper Hit Count for: BID, BH3 interacting-domain death agonist
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#:1
wNotes=on sortOrder:rid,rpid
Home Page