Bcl-xL Cancer Research Results
Bcl-xL, Bcl-xL: Click to Expand ⟱
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| 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.
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Scientific Papers found: Click to Expand⟱
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
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)
*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↑,
*antiOx↑, Molecular hydrogen is gaining increasing attention as an antioxidant, anti-inflammatory, and antiapoptotic agent.
*Inflam↓,
*Apoptosis↓,
*Dose↓, It reaches a maximum level of about 0.78 mM (≈1.6 mg/L) at room temperature with a loss of about 2–5% per 3 min
*Dose↝, It is produced (and consumed) by bacteria of the gut microbiota .The most prominent bacterial phyla involved in this process are the Firmicutes and Bacteroidetes phyla, which include the anaerobic Clostridium species
*eff↑, hydrogen mixed with oxygen at a ratio of 96%-to-4%, known as the Hydrox gas mixture, was used by deep-sea divers to prevent decompression sickness and allow diving to depths of up to 500 m
*ROS↓, The antioxidant activity of H2 is based on two processes: a direct scavenging of the most toxic reactive oxygen and nitrogen species (ROS/RNS),
*RNS↓,
*NRF2↑, H2 activates the Nrf2 (nuclear factor erythroid 2-related factor 2) pathway, a key transcription factor involved in oxidative stress-related responses, including cytoprotective, antioxidant, and detoxifying enzymes such as HO-1
*HO-1↑,
*Fenton↓, removal of free heme and inhibition of the Fenton reaction
*NLRP3↓, the activation of the Nrf2 pathway has been shown to inhibit the NLRP3 (NLR family pyrin domain containing 3) inflammasome,
*NADPH↓, H2 suppresses the activation of the NADPH oxidase pathway and downregulates the expression of NOX2 and NOX4
*NOX4↓,
*NOX↓,
*MPO↓, H2 has been shown to reduce the overactivation of myeloperoxidase (MPO)
*NF-kB↓, would further suppress the NFκB
*TNF-α↓, figure 3
*IL6↓,
*IL1β↓,
*HMGB1↓,
*IL4↑,
*IL10↑,
*M2 MC↑, Additionally, H2 promotes the polarization of macrophages from the proinflammatory M1 type to the anti-inflammatory M2 type
*Treg lymp↝, It also inhibits Th2 responses, restores regulatory T cells (Treg), and, thus, normalizes an overactivated immune system
*Bcl-2↑, upregulate the antiapoptotic factors, including Bcl-2 and Bcl-xl.
*Bcl-xL↑,
*PI3K↑, phenomenon is likely facilitated by the activation of the PI3K/Akt and JAK2/STAT3 signaling pathways
*Akt↑,
*JAK2↑,
*STAT3↑,
*Dose↑, The consumption of certain prebiotics, especially those rich in dietary fiber, indigestible starches, and sugars (lactulose), has been demonstrated to enhance intestinal H2 production through the activity of intestinal flora
*CD4+↑, H2 increased the population of CD4+CD25+Foxp3+ Treg cells, which are often decreased in allergic rhinitis (AR)
*CD25+↑,
*FOXP3↑,
*MDA↓, H2 administration attenuated oxidative stress expressed as lower MDA and other lipid peroxidation markers along with an enhancement in the expression and activity of endogenous antioxidant enzymes such as SOD or CAT
*SOD↑,
*Catalase↑,
*Casp3↓, inhibition of proapoptotic processes like the caspase 3 and 9 pathways
*Casp9↓,
*TBARS↓, drinking of HRW by patients with asthma and COPD leads to an increase in blood oxygen saturation, vitamin E levels, along with lower oxidative stress markers such as thiobarbituric acid reactive substances (TBARS), MDA,
*SpO2↑,
*VitE↓,
*OS↑, COPD:In general, H2 administration has been found to lead to enhanced survival and reduced weight loss [110], improved lung function and static lung compliance, and decreased arterial blood pressure
*Weight↑,
*DNAdam↓, reduction in levels of oxidative DNA damage markers
*PGE2↓, H2 reduced elevated inflammatory markers, including IL-1β, IL-6, TNF-α, prostaglandin E2 (PGE2) [29,65,71,128,130], macrophage protein 1α 2 (MP1α), and monocyte chemoattractant protein-1 (MCP-1)
*MCP1/CCL2↓,
*lipid-P↓, Further, a reduction in oxidative stress markers such as lipid peroxidation and proapoptotic markers, including Bax and caspase-3, was observed.
*TumCP↓, H2-rich medium reduced the colony size and formation of tongue cancer cells and decreased proliferation in human fibrosarcoma and esophageal cancer cells, as well as A549 cells
*tumCV↓, decrease in cell viability, migration, and invasion
*TumCMig↓,
*TumCI↓,
TumW↓, A reduction in tumor weight and size, as well as a lower number of cells of squamous cell carcinoma, was revealed by animal studies.
TumVol↓,
selectivity↑, Notably, as previously reported, H2 administration exhibited no effect on healthy animals or non-cancerous cell lines
QoL↑, Patients reported improved quality of life with better physical status and fewer pulmonary symptoms
ChemoSen↑, In combination with conventional (such as cis-platin) and modern (including antibodies like nivolumab) therapeutics, H2 enhanced drug activity, resulting in enhanced outcomes and improved disease control
chemoP↑, and reduced side effects of the treatment, such as nephrotoxicity, weight loss, insomnia, pain, or hearing loss in the case of radiotherapy
radioP↑, radioprotective effects of H2 are primarily attributed to its hydroxyl radical scavenging activity
ROS↑, As indicated by Yang et al., the latter include the activation of the ROS/NLRP3/caspase-3/gasdermin D-mediated pyroptotic pathways
NLRP3↑,
Casp3↑,
VEGF↓, suppression of vascular endothelial growth factor (VEGF) expression
Wnt↓, H2 result in the suppression of the overactivated Wnt/beta-catenin signaling pathways, which further leads to suppression of tumor progression
β-catenin/ZEB1↓,
*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↓,
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↑,
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 7 of 7
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7
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↑, 2, 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↑, 4, 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, Wnt↓, 1,
Migration(tgid=13) ⓘ
E-cadherin↑, 1, TumCP↓, 2, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
VEGF↓, 1,
Protein Aggregation(tgid=19) ⓘ
NLRP3↑, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
AR↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 2, Dose↝, 1, eff↑, 4, selectivity↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
AFP↓, 1, AR↓, 1,
Functional Outcomes(tgid=23) ⓘ
chemoP↑, 1, hepatoP↑, 1, OS↑, 1, QoL↑, 1, radioP↑, 1, toxicity↓, 1, TumVol↓, 1, TumW↓, 1,
Total Targets: 58
Pathway results for Effect on Normal Cells:
NA, unassigned(tgid=0) ⓘ
SpO2↑, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, Catalase↑, 1, Fenton↓, 1, HO-1↑, 1, lipid-P↓, 1, MDA↓, 1, MPO↓, 1, NOX4↓, 1, NRF2↑, 1, RNS↓, 1, ROS↓, 3, SOD↑, 2, TBARS↓, 1, VitE↓, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
NADPH↓, 1,
Cell Death(tgid=5) ⓘ
Akt↑, 1, p‑Akt↑, 1, Apoptosis↓, 2, BAD↓, 1, BAX↓, 1, Bcl-2↑, 1, Bcl-xL↑, 2, Casp3↓, 2, Casp9↓, 1, p38↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
tumCV↓, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
HSP70/HSPA5↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
p‑ERK↑, 1, PI3K↑, 1, STAT3↑, 1,
Migration(tgid=13) ⓘ
Ca+2↓, 1, MMP9↓, 1, Treg lymp↝, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
HIF-1↓, 1, NO↓, 1, VEGF↑, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CD25+↑, 1, CD4+↑, 1, FOXP3↑, 1, HMGB1↓, 1, IL10↑, 1, IL1β↓, 1, IL2↑, 1, IL4↑, 1, IL6↓, 1, Inflam↓, 2, JAK2↑, 1, M2 MC↑, 1, MCP1/CCL2↓, 1, NF-kB↓, 1, PGE2↓, 1, TNF-α↓, 1,
Cellular Microenvironment(tgid=17) ⓘ
NOX↓, 1,
Protein Aggregation(tgid=19) ⓘ
NLRP3↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
Dose↓, 1, Dose↑, 1, Dose↝, 1, eff↑, 1,
Clinical Biomarkers(tgid=22) ⓘ
IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
OS↑, 1, Weight↑, 1,
Total Targets: 66
Scientific Paper Hit Count for: Bcl-xL, Bcl-xL
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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