Bcl-xL Cancer Research Results

Bcl-xL, Bcl-xL: Click to Expand ⟱
Source:
Type: pro-survival proteins
The proteins of BCL-2 family are classified into three subgroups, i.e., the anti-apoptotic/pro-survival proteins represented by BCL-2 and BCL-XL.
BCL-XL overexpressing cells exhibited higher tumors sphere formation capacity and expressed higher levels of some stem cell markers, supporting the concept that BCL-XL plays essential roles in the maintenance of cancer stem cell phenotype.
Scientific Papers found: Click to Expand⟱
6497- BCP,  Cisplatin,    Beta-Caryophyllene Enhances the Anti-Tumor Activity of Cisplatin in Lung Cancer Cell Lines through Regulating Cell Cycle and Apoptosis Signaling Molecules
- in-vitro, Lung, NA
TumCG↓, reported to reduce the growth and the proliferation as well as enhance the apoptosis in numerous cancer cells, including colorectal, ovarian, bladder cancer and lung cancer.
TumCP↓,
Apoptosis↑,
toxicity↓, results showed that BCP is not toxic at moderate doses and it can prevent lung cancer progression in doses above 75 µM.
ChemoSen↑, however, when being combined with CDDP, BCP improved the former chemotherapeutic function through regulating cell cycle, apoptosis and EMT signaling molecules.
P21↑, combined treatment of CDDP and BCP significantly upregulated the level of the cyclin-dependent kinase inhibitor, CDKN1A, and the inhibitor of the apoptosis, BCL-xl2.
Bcl-xL↑,
Bcl-2↓, combination treatment reduced the protein level of the apoptosis regulator, BCL-2.
EMT↓, BCP appears to prohibit the EMT process that is associated with CDDP chemotherapy since the combination treatment induced a significant increase in the level of the epithelial cell marker E-cad
E-cadherin↑,
eff↑, The dose of CDDP showed potential cytotoxicity at IC50 12 μM, this dose was reduced to be around two-fold lower when combined with 50 μM of BCP in a synergistic manner
MMP↓, combined treatment of CDDP and BCP induced more release of the mitochondrial contents and induced a significant decrease in membrane integrity

5891- CAR,  SRF,    Carvacrol enhances anti-tumor activity and mitigates cardiotoxicity of sorafenib in thioacetamide-induced hepatocellular carcinoma model through inhibiting TRPM7
- in-vivo, HCC, NA
eff↑, CARV/Sora combination significantly improved survival rate, and liver functions, reduced Alpha-Fetoprotein level, and attenuated HCC progression compared with Sora group
OS↑,
hepatoP↑,
AFP↓,
NOTCH↓, downregulating ATP-binding cassette subfamily G member 2, NOTCH1, Spalt like transcription factor 4, and CD133.
cycD1/CCND1↓, decreasing cyclin D1 and B-cell leukemia/lymphoma 2 and increasing BCL2-Associated X and caspase-3.
Bcl-xL↑,
Casp3↑,
TRPM7↓, CARV/Sora is a promising combination for tumor suppression and overcoming Sora resistance and cardiotoxicity in HCC by modulating TRPM7
Dose↝, CARV (15 mg/kg/day; orally) (Rats)

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↑,

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↓,

79- QC,    Chemopreventive Effect of Quercetin in MNU and Testosterone Induced Prostate Cancer of Sprague-Dawley Rats
- in-vivo, Pca, NA
GSH↑, The lipid peroxidation, H2O2, in (MNU+T) treated rats were increased and GSH level was decreased, whereas simultaneous quercetin-treated rats reverted back to normal level
SOD↑,
Catalase↑,
GPx↑, SOD, catalase, GPX, Glutathionereductase, GST activities were significantly decreased in VP & DLP ofcancer-induced rats compared to control. Whereas, simultaneousquercetin supplement showed increased activities. (PDF) Chemopreventive Effect of Que
GSR↑,
IGF-1R↓, IGFIR, AKT, AR, cell proliferative and anti-apoptotic proteins were increased in cancer-induced group whereas supplement of quercetin decreased its expression.
Akt↓,
AR↓, Protein expressions of AR were increased in both VP and DLP of cancer-induced rats and decreasedin quercetin supplemented rats.Fig. 2. Effect of quercetin on mRNA expressions of IGFIR, Bax, Bcl2, Caspase-3 and -8 in VP of cancer-induced male rats.G.
TumCP↓,
lipid-P↓,
H2O2↓,
Raf↓, Raf-1 and pMEK pro-tein expressions were increased significantly in cancer-induced rats compared to control whereas simultaneous quercetin treatment decreased the expressions
p‑MEK↓,
Bcl-2↑, Bcl2, Bcl-xl were significantly increased and apoptotic protein caspase-3,-8,-9 expressions were significantly decreased in cancer-induced rats compared to control in both ventral and dorsolateral prostate. But,this was the other way around when s
Bcl-xL↑,
Casp3↑,
Casp8↑,
Casp9↑,

1838- VitK3,  PDT,    Photodynamic Effects of Vitamin K3 on Cervical Carcinoma Cells Activating Mitochondrial Apoptosis Pathways
- in-vitro, Cerv, NA
eff↑, vitamin K3 (Vit K3) serves as a photosensitizer to produce Reactive Oxygen Species (ROS)
ROS↑,
tumCV↓, Vit K3 treatment plus UVA reduced tumor cell viability
TumCG↓, Vit K3 treatment plus UVA can inhibit tumor growth
Apoptosis↑, enhance the apoptosis of cervical cancer cells
cl‑Casp3↑, cleaved caspase-3, cleaved caspase-9, B-cell lymphoma- extra large (Bcl-xl), and cytochrome c (cyt-c) increased obviously,
cl‑Casp9↑,
Bcl-xL↑,
Cyt‑c↑,
Bcl-2↓, (Bcl-2) decreased


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(tgid=1) ⓘ

Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   GSR↑, 1,   H2O2↓, 1,   lipid-P↓, 1,   ROS↑, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

p‑MEK↓, 1,   MMP↓, 1,   Raf↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 2,   Bcl-2↑, 1,   Bcl-xL↑, 5,   cl‑BID↑, 1,   Casp3↑, 3,   cl‑Casp3↑, 1,   Casp8↑, 1,   proCasp8↑, 1,   Casp9↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↑, 2,   Fas↑, 1,   cl‑Mcl-1↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

EMT↓, 1,   IGF-1R↓, 1,   NOTCH↓, 1,   TRPM7↓, 1,   TumCG↓, 2,  

Migration(tgid=13) ⓘ

E-cadherin↑, 1,   TumCP↓, 2,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   Dose↝, 1,   eff↑, 4,  

Clinical Biomarkers(tgid=22) ⓘ

AFP↓, 1,   AR↓, 1,  

Functional Outcomes(tgid=23) ⓘ

hepatoP↑, 1,   OS↑, 1,   toxicity↓, 1,  
Total Targets: 48

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↓, 2,   SOD↑, 1,  

Cell Death(tgid=5) ⓘ

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

Protein Folding & ER Stress(tgid=8) ⓘ

HSP70/HSPA5↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

p‑ERK↑, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 1,   MMP9↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

HIF-1↓, 1,   NO↓, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL2↑, 1,   Inflam↓, 1,  
Total Targets: 18

Scientific Paper Hit Count for: Bcl-xL, Bcl-xL
1 Beta-Caryophyllene
1 Cisplatin
1 Carvacrol
1 Sorafenib (brand name Nexavar)
1 Cat’s Claw
1 Magnetic Fields
1 Quercetin
1 VitK3,menadione
1 Photodynamic Therapy
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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