cDC2 Cancer Research Results
cDC2, type 2 conventional dendritic cell: Click to Expand ⟱
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Play an important role in antitumor immunity by promoting cytotoxic T-cell responses and helper T-cell differentiation.
Dendritic cells (DCs) consist of three major subsets termed plasmacytoid (pDCs), type-1 (cDC1s), and type-2 (cDC2s) conventional (or classical) DCs.
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Scientific Papers found: Click to Expand⟱
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in-vitro, |
AML, |
HL-60 |
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in-vitro, |
AML, |
K562 |
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in-vitro, |
AML, |
TF1 |
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JAK↓,
PI3K↓, PI3K/PKB
cDC2↓,
STAT↓,
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in-vitro, |
Colon, |
HCT116 |
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CycB/CCNB1↓,
cDC2↓,
CDC25↓,
P53↑,
P21↑,
cl‑PARP↑, cleavage
proCasp8↓, Apigenin induced poly (ADP-ribose) polymerase (PARP) cleavage and decreased the levels of procaspase-8, -9 and -3
proCasp9↓,
proCasp3↓,
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in-vitro, |
Pca, |
PC3 |
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in-vitro, |
Pca, |
DU145 |
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ROS↑, WZ35 treatment for 30 min significantly induced reactive oxygen species (ROS) production in PC-3 cells.
Bcl-2↓,
PARP↑,
cDC2↓, decreased expression of CDC2, cyclinB1, and MDM2
CycB/CCNB1↓,
MDM2↓,
eff↓, Co-treatment with the ROS scavenger NAC completely abrogated the induction of WZ35 on cell apoptosis,
eIF2α↑, WZ35 treatment also induced a constant increase in the level of phosphorylated eIF2α 3 to 12 h after WZ35 treatment
ATF4↑, ATF4 expression also increased in a similar manner with p-eIF2α
CHOP↑, CHOP protein expression apparently increased 9-24 h after WZ35 treatment and peaked at 12 h
ER Stress↑, results suggest that WZ35 can induce ER stress in prostate cancer cells
TumCCA↑, WZ35 induced cell cycle arrest in G2/M phase in PC-3 cells
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in-vitro, |
BC, |
T47D |
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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, |
BC, |
MDA-MB-468 |
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CDC25↓,
cDC2↓,
P21↑,
p‑Akt↓,
p‑mTOR↓, phosphorylation
Bcl-2↓,
BAX↑,
Casp3↑,
TumCCA↑, G2/M arrest
P21↑,
Chk2↑,
CycB/CCNB1↓,
cDC2↓,
Apoptosis↑,
Cyt‑c↑, release of cytochrome c from mitochondria
Casp9↑,
Casp3↑,
ROS↑,
MMP↓,
Bax:Bcl2↑,
ER Stress↑,
TumCG↓, sodium butyrate inhibited the growth of SAS tongue cancer cells by 32% and 53% at concentrations of 1 and 2mM, respectively
ROS↑, These events were concomitant with induction of intracellular reactive oxygen species (ROS) production.
P21↑, An elevation in p21 mRNA and protein level was noted in SAS cells by sodium butyrate.
CycB/CCNB1↓, decline of cyclin Bl, cdc2 and cdc25C mRNA and protein expression in SAS cells was found after exposure to sodium butyrate
cDC2↓,
CDC25↓,
eff↓, Inclusion of N-acetyl-l-cysteine (NAC) (3mM), catalase (1000 U/ml) and dimethylthiourea (DMT, 5mM), and also SOD (500 U/ml) attenuated the sodium butyrate-induced ROS production in SAS cells.
TumCCA↑, sodium butyrate is toxic and inhibits the tongue cancer cell growth via induction of cell cycle arrest and apoptosis
Apoptosis↑,
P21↑, Addition of quercetin led to substantial decrease in the expression of Cdc2/Cdk-1, cyclin B1 and phosphorylated pRb and increase in p21.
cDC2↓, Cdc2/Cdk-1
CDK1↓, Cdc2/Cdk-1
CycB/CCNB1↓,
Casp3↑,
Bcl-2↓,
Bcl-xL↓, Apoptosis markers like Bcl-2 and Bcl-X(L) were significantly decreased and Bax and caspase-3 were increased.
BAX↑,
pRB↓,
TumCCA↑, Flowcytometric analysis showed that quercetin blocks G2-M transition, with significant induction of apoptosis.
Apoptosis↑,
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in-vitro, |
Pca, |
PC3 |
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in-vitro, |
Pca, |
DU145 |
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in-vitro, |
Pca, |
LNCaP |
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cycD1/CCND1↓, CCND1, CCND2, CCND3
cycE/CCNE↓, CCNE1, CCNE2
CDK2↓,
CDK4/6↓, CDK4, CDK8
E2Fs↓, E2F2, E2F3
PCNA↓,
cDC2↓,
PTEN↑,
MSH2↑,
P21↑,
EP300↑, p300
BRCA1↑,
NF2↑,
TSC1↑,
TGFβR1↑, TGFβR2
P53↑,
RB1↑, Rb
AKT1↓,
cMyc↓,
CDC7↓,
cycF↓, CCNF
CDC16↓,
CUL4B↑, CUL4B, a member of the cullin gene family that is also known to be involved in control of the cell cycle, was significantly up-regulated by quercetin.
CBP↑,
TSC2↑,
HER2/EBBR2↓, erb-2
BCR↓,
TumCCA↑, quercetin significantly inhibited the expression of specific oncogenes and genes controlling G1, S, G2, and M phases of the cell cycle.
chemoPv↑, Our results correlate with those of nutritional studies that support the roles of dietary bioflavonoids as cancer chemopreventive agents.
tumCV↓, TQ reduced cell viability, induced apoptosis and cell cycle arrest, depleted ROS, and altered protein expression in associated signaling pathways.
TumCCA↑,
ROS↓, With regards to ROS in the current study, TQ dose-dependently decreased intracellular ROS levels in all SCLC cells except H446 cells upon 24-hour treatment with TQ.
CycB/CCNB1↑, TQ induced upregulation of cyclin B1 and cyclin D3 in H69-adherent and H446 cells, respectively. Cyclins A2, E1, and cdc2 were downregulated, while cyclin D3 was upregulated in H841-adherent cells
CycD3↑,
cycA1/CCNA1↓,
cycE/CCNE↓,
cDC2↓,
antiOx↑, TQ acted as an antioxidant.
PARP↓, TQ downregulated intratumoral PARP
NRF2↓, TQ exerts its antioxidative effect by upregulating nuclear protein nuclear factor-erythroid 2 related factor 2 (Nrf2), hence amplifying antioxidant response element (ARE) expression.
ARE/EpRE↑,
eff↑, To confirm that the antioxidative action of TQ is anti-survival for cells, H841 cells were employed as a model and treated with NAC. NAC confirmed that ROS depletion led to a decrease in the cell viability of SCLC cells.
Showing Research Papers: 1 to 9 of 9
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, ARE/EpRE↑, 1, NRF2↓, 1, ROS↓, 1, ROS↑, 3,
Mitochondria & Bioenergetics ⓘ
BCR↓, 1, CDC16↓, 1, CDC25↓, 3, MMP↓, 1,
Core Metabolism/Glycolysis ⓘ
AKT1↓, 1, cMyc↓, 1,
Cell Death ⓘ
p‑Akt↓, 1, Apoptosis↑, 3, BAX↑, 2, Bax:Bcl2↑, 1, Bcl-2↓, 3, Bcl-xL↓, 1, Casp3↑, 3, proCasp3↓, 1, proCasp8↓, 1, Casp9↑, 1, proCasp9↓, 1, CBP↑, 1, Chk2↑, 1, Cyt‑c↑, 1, MDM2↓, 1,
Kinase & Signal Transduction ⓘ
CDC7↓, 1, HER2/EBBR2↓, 1, TSC2↑, 1,
Transcription & Epigenetics ⓘ
pRB↓, 1, tumCV↓, 1,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, eIF2α↑, 1, ER Stress↑, 2,
DNA Damage & Repair ⓘ
BRCA1↑, 1, CUL4B↑, 1, P53↑, 2, PARP↓, 1, PARP↑, 1, cl‑PARP↑, 1, PCNA↓, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 1, CDK2↓, 1, cycA1/CCNA1↓, 1, CycB/CCNB1↓, 5, CycB/CCNB1↑, 1, cycD1/CCND1↓, 1, CycD3↑, 1, cycE/CCNE↓, 2, cycF↓, 1, E2Fs↓, 1, P21↑, 6, RB1↑, 1, TumCCA↑, 6,
Proliferation, Differentiation & Cell State ⓘ
cDC2↓, 9, EP300↑, 1, p‑mTOR↓, 1, NF2↑, 1, PI3K↓, 1, PTEN↑, 1, STAT↓, 1, TumCG↓, 1,
Migration ⓘ
CDK4/6↓, 1, MSH2↑, 1, TSC1↑, 1,
Angiogenesis & Vasculature ⓘ
ATF4↑, 1,
Immune & Inflammatory Signaling ⓘ
JAK↓, 1,
Drug Metabolism & Resistance ⓘ
eff↓, 2, eff↑, 1,
Clinical Biomarkers ⓘ
BRCA1↑, 1, HER2/EBBR2↓, 1,
Functional Outcomes ⓘ
chemoPv↑, 1, TGFβR1↑, 1,
Total Targets: 73
Pathway results for Effect on Normal Cells:
Total Targets: 0
Scientific Paper Hit Count for: cDC2, type 2 conventional dendritic cell
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#:439 State#:% Dir#:1
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