Diablo Cancer Research Results

Diablo, Diablo/Smac: Click to Expand ⟱

Source:

Type:

Diablo homolog is a mitochondrial protein that in humans is encoded by the DIABLO gene on chromosome 12. DIABLO is also referred to as second mitochondria-derived activator of caspases or SMAC. This protein binds inhibitor of apoptosis proteins, thus freeing caspases to activate apoptosis.
SMAC/Diablo is known to be a pro-apoptotic protein and its overexpression has been observed to oppose progression of a variety of tumor types. SMAC/Diablo possesses a new lipid synthesis-related function essential for cancer growth, rendering SMAC/Diablo a promising therapeutic target in cancer. Suggesting that the role of SMAC/Diablo in cancer can be a double-edged sword.

High levels of Diablo expression have been associated with increased sensitivity to chemotherapy and better prognosis in some cancers, as it may promote apoptosis in cancer cells. Conversely, low levels of Diablo expression might correlate with resistance to treatment and poorer outcomes.

Var, Various Cancer: Click to Expand ⟱

Cyclooxygenase (COX)-2 overexpression has been noted in various cancers. PI3Ks/AKT pathways are over-activated in several types of cancers.
EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity.
Activating protein-1 transcription factor has been associated with pathogenesis including cancer.
Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics.
The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors.
The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50.
Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25].
The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell.
Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.
Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer.
Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research.
Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy.
Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer.
Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis.
More than 50% of human cancers have a mutated nonfunctional p53.

Scientific Papers found: Click to Expand⟱

2736-

BetA,

Chemo,

Multifunctional Roles of Betulinic Acid in Cancer Chemoprevention: Spotlight on JAK/STAT, VEGF, EGF/EGFR, TRAIL/TRAIL-R, AKT/mTOR and Non-Coding RNAs in the Inhibition of Carcinogenesis and Metastasis

Review,

Var,

chemoPv↑, p‑STAT3↓, JAK1↓, JAK2↓, VEGF↓, EGFR↓, Cyt‑c↑, Diablo↑, AMPK↑, mTOR↓, Sp1/3/4↓, DNAdam↑, Gli1↓, GLI2↓, PTCH1↓, MMP2↓, MMP9↓, miR-21↓, SOD2↓, ROS↑, Apoptosis↑,

2748-

BetA,

Betulinic Acid: Recent Advances in Chemical Modifications, Effective Delivery, and Molecular Mechanisms of a Promising Anticancer Therapy

Review,

Var,

Bcl-2↓, MMP↓, Cyt‑c↑, Casp↑, Diablo↑, AIF↑, angioG↓, BioAv↓, NF-kB↓,

2776-

Bos,

Anti-inflammatory and anti-cancer activities of frankincense: Targets, treatments and toxicities

Review,

Var,

*5LO↓, *TNF-α↓, *MMP3↓, *COX1↓, *COX2↓, *PGE2↓, *Th2↑, *Catalase↑, *SOD↑, *NO↑, *PGE2↑, *IL1β↓, *IL6↓, *Th1 response↓, *Th2↑, *iNOS↓, *NO↓, *p‑JNK↓, *p38↓, GutMicro↑, p‑Akt↓, GSK‐3β↓, cycD1/CCND1↓, Akt↓, STAT3↓, CSCs↓, AR↓, P21↑, DR5↑, CHOP↑, Casp3↑, Casp8↑, cl‑PARP↑, DNAdam↑, p‑RB1↓, FOXM1↓, TOP2↓, CDC25↓, p‑CDK1↓, p‑ERK↓, MMP9↓, VEGF↓, angioG↓, ROS↑, Cyt‑c↑, AIF↑, Diablo↑, survivin↓, ICAD↓, ChemoSen↑, SOX9↓, ER Stress↑, GRP78/BiP↑, cal2↓, AMPK↓, mTOR↓, ROS↓,

1605-

EA,

Ellagic Acid and Cancer Hallmarks: Insights from Experimental Evidence

Review,

Var,

*BioAv↓, antiOx↓, Inflam↓, TumCP↓, TumCCA↑, cycD1/CCND1↓, cycE/CCNE↓, P53↑, P21↑, COX2↓, NF-kB↓, Akt↑, NOTCH↓, CDK2↓, CDK6↓, JAK↓, STAT3↓, EGFR↓, p‑ERK↓, p‑Akt↓, p‑STAT3↓, TGF-β↓, SMAD3↓, CDK6↓, Wnt/(β-catenin)↓, Myc↓, survivin↓, CDK8↓, PKCδ↓, tumCV↓, RadioS↑, eff↑, MDM2↓, XIAP↓, p‑RB1↓, PTEN↑, p‑FAK↓, Bax:Bcl2↑, Bcl-xL↓, Mcl-1↓, PUMA↑, NOXA↑, MMP↓, Cyt‑c↑, ROS↑, Ca+2↝, Endoglin↑, Diablo↑, AIF↑, iNOS↓, Casp9↑, Casp3↑, cl‑PARP↑, RadioS↑, Hif1a↓, HO-1↓, HO-2↓, SIRT1↓, selectivity↑, Dose∅, NHE1↓, Glycolysis↓, GlucoseCon↓, lactateProd↓, PDK1?, PDK1?, ECAR↝, COX1↓, Snail↓, Twist↓, cMyc↓, Telomerase↓, angioG↓, MMP2↓, MMP9↓, VEGF↓, Dose↝, PD-L1↓, eff↑, SIRT6↑, DNAdam↓,

3238-

EGCG,

Green tea catechin, epigallocatechin-3-gallate (EGCG): mechanisms, perspectives and clinical applications

Review,

Var,

Telomerase↓, DNMTs↓, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, CDK6↓, HATs↓, HDAC↓, selectivity↑, uPA↓, NF-kB↓, TNF-α↓, *ROS↓, *antiOx↑, Hif1a↓, VEGF↓, MMP2↓, MMP9↓, FAK↓, TIMP2↑, Mcl-1↓, survivin↓, XIAP↓, PCNA↓, p16↑, P21↑, p27↑, pRB↑, P53↑, MDM2↑, ROS↑, Casp3↑, Casp8↑, Casp9↑, Cyt‑c↑, Diablo↑, BAX⇅, cl‑PPARα↓, PDGF↓, EGFR↓, FOXO↑, AP-1↓, JNK↓, COX2↓, angioG↓,

2857-

FIS,

A review on the chemotherapeutic potential of fisetin: In vitro evidences

Review,

Var,

COX2↓, PGE2↓, EGFR↓, Wnt↓, β-catenin/ZEB1↓, TCF↑, Apoptosis↑, Casp3↑, cl‑PARP↑, Bcl-2↓, Mcl-1↓, BAX↑, BIM↑, BAD↑, Akt↓, mTOR↓, ACC↑, Cyt‑c↑, Diablo↑, cl‑Casp8↑, Fas↑, DR5↑, TRAIL↑, Securin↓, CDC2↓, CDC25↓, HSP70/HSPA5↓, CDK2↓, CDK4↓, cycD1/CCND1↓, MMP2↓, uPA↓, NF-kB↓, cFos↓, cJun↓, MEK↓, p‑ERK↓, N-cadherin↓, Vim↓, Snail↓, Fibronectin↓, E-cadherin↓, NF-kB↑, ROS↑, DNAdam↑, MMP↓, CHOP↑, eff↑, ChemoSen↑,

2845-

FIS,

Fisetin: A bioactive phytochemical with potential for cancer prevention and pharmacotherapy

Review,

Var,

PI3K↓, Akt↓, mTOR↓, p38↓, *antiOx↑, *neuroP↑, Casp3↑, Bcl-2↓, Mcl-1↓, BAX↑, BIM↑, BAD↑, AMPK↑, ACC↑, DNAdam↑, MMP↓, eff↑, ROS↑, cl‑PARP↑, Cyt‑c↑, Diablo↑, P53↑, p65↓, Myc↓, HSP70/HSPA5↓, HSP27↓, COX2↓, Wnt↓, EGFR↓, NF-kB↓, TumCCA↑, CDK2↓, CDK4↓, cycD1/CCND1↓, cycA1/CCNA1↓, P21↑, MMP2↓, MMP9↓, TumMeta↓, MMP1↓, MMP3↓, MMP7↓, MET↓, N-cadherin↓, Vim↓, Snail↓, Fibronectin↓, E-cadherin↑, uPA↓, ChemoSen↑, EMT↓, Twist↓, Zeb1↓, cFos↓, cJun↓, EGF↓, angioG↓, VEGF↓, eNOS↓, *NRF2↑, HO-1↑, NRF2↓, GSTs↓, ATF4↓,

2825-

FIS,

Exploring the molecular targets of dietary flavonoid fisetin in cancer

Review,

Var,

*Inflam↓, *antiOx↓, *ERK↑, *p‑cMyc↑, *NRF2↑, *GSH↑, *HO-1↑, mTOR↓, PI3K↓, Akt↓, TumCCA↑, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, CDK6↓, P21↑, p27↑, JNK↑, MMP2↓, MMP9↓, uPA↓, NF-kB↓, cFos↓, cJun↓, E-cadherin↑, Vim↓, N-cadherin↓, EMT↓, MMP↓, Cyt‑c↑, Diablo↑, Casp↑, cl‑PARP↑, P53↑, COX2↓, PGE2↓, HSP70/HSPA5↓, HSP27↓, DNAdam↑, Casp3↑, Casp9↑, ROS↑, AMPK↑, NO↑, Ca+2↑, mTORC1↓, p70S6↓, ROS↓, ER Stress↑, IRE1↑, ATF4↑, GRP78/BiP↑, eff↑, eff↑, eff↑, RadioS↑, ChemoSen↑, Half-Life↝,

2827-

FIS,

The Potential Role of Fisetin, a Flavonoid in Cancer Prevention and Treatment

Review,

Var,

*antiOx↑, *Inflam↓, neuroP↑, hepatoP↑, RenoP↑, cycD1/CCND1↓, TumCCA↑, MMPs↓, VEGF↓, MAPK↓, NF-kB↓, angioG↓, Beclin-1↑, LC3s↑, ATG5↑, Bcl-2↓, BAX↑, Casp↑, TNF-α↓, Half-Life↓, MMP↓, mt-ROS↑, cl‑PARP↑, CDK2↓, CDK4↓, Cyt‑c↑, Diablo↑, DR5↑, Fas↑, PCNA↓, Ki-67↓, p‑H3↓, chemoP↑, Ca+2↑, Dose↝, CDC25↓, CDC2↓, CHK1↑, Chk2↑, ATM↑, PCK1↓, RAS↓, p‑p38↓, Rho↓, uPA↓, MMP7↓, MMP13↓, GSK‐3β↑, E-cadherin↑, survivin↓, VEGFR2↓, IAP2↓, STAT3↓, JAK1↓, mTORC1↓, mTORC2↓, NRF2↑,

2832-

FIS,

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

Review,

Var,

MMP↓, mtDam↑, Cyt‑c↑, Diablo↑, Casp↑, cl‑PARP↑, Bak↑, BIM↑, Bcl-xL↓, Bcl-2↓, P53↑, ROS↑, AMPK↑, Casp9↑, Casp3↑, BID↑, AIF↑, Akt↓, mTOR↓, MAPK↓, Wnt↓, β-catenin/ZEB1↓, TumCCA↑, P21↑, p27↑, cycD1/CCND1↓, cycE/CCNE↓, CDK2↓, CDK4↓, CDK6↓, TumMeta↓, uPA↓, E-cadherin↑, Vim↓, EMT↓, Twist↓, DNAdam↑, ROS↓, COX2↓, PGE2↓, HSF1↓, cFos↓, cJun↓, AP-1↓, Mcl-1↓, NF-kB↓, IRE1↑, ER Stress↑, ATF4↑, GRP78/BiP↑, MMP2↓, MMP9↓, TCF-4↓, MMP7↓, RadioS↑, TOP1↓, TOP2↓,

3930-

PTS,

A Review of Pterostilbene Antioxidant Activity and Disease Modification

Review,

Var,

Review,

adrenal,

Review,

Stroke,

*BioAv↑, *antiOx↑, *neuroP↑, *Inflam↓, *ROS↓, *H2O2↓, *GSH↑, *GPx↑, *GSR↑, *SOD↑, TumCG↓, PTEN↑, HGF/c-Met↓, PI3K↓, Akt↓, NF-kB↓, TumMeta↓, MMP2↓, MMP9↓, Ki-67↓, Casp3↑, MMP↓, H2O2↑, ROS↑, ChemoSen↑, *cardioP↑, *CDK2↓, *CDK4↓, *cycE/CCNE↓, *cycD1/CCND1↓, *RB1↓, *PCNA↓, *CREB↑, *GABA↑, *memory↑, *IGF-1↑, *ERK↑, TIMP1↑, BAX↑, Cyt‑c↑, Diablo↑, SOD2↑,

3368-

QC,

The potential anti-cancer effects of quercetin on blood, prostate and lung cancers: An update

Review,

Var,

*Inflam↓, *antiOx↑, *AntiCan↑, Casp3↓, p‑Akt↓, p‑mTOR↓, p‑ERK↓, β-catenin/ZEB1↓, Hif1a↓, AntiAg↓, VEGFR2↓, EMT↓, EGFR↓, MMP2↓, MMP↓, TumMeta↓, MMPs↓, Akt↓, Snail↓, N-cadherin↓, Vim↓, E-cadherin↑, STAT3↓, TGF-β↓, ROS↓, P53↑, BAX↑, PKCδ↓, PI3K↓, COX2↓, cFLIP↓, cycD1/CCND1↓, cMyc↓, IL6↓, IL10↓, Cyt‑c↑, TumCCA↑, DNMTs↓, HDAC↓, ac‑H3↑, ac‑H4↑, Diablo↑, Casp3↑, Casp9↑, PARP1↑, eff↑, PTEN↑, VEGF↓, NO↓, iNOS↓, ChemoSen↑, eff↑, eff↑, eff↑, uPA↓, CXCR4↓, CXCL12↓, CLDN2↓, CDK6↓, MMP9↓, TSP-1↑, Ki-67↓, PCNA↓, ROS↑, ER Stress↑,

3061-

RES,

The Anticancer Effects of Resveratrol: Modulation of Transcription Factors

Review,

Var,

AhR↓, NRF2↑, *NQO1↑, *HO-1↑, *GSH↑, P53↑, Cyt‑c↑, Diablo↑, Bcl-2↓, Bcl-xL↓, survivin↓, XIAP↓, FOXO↑, p‑PI3K↓, p‑Akt↓, BIM↑, DR4↑, DR5↑, p27↑, cycD1/CCND1↓, SIRT1↑, NF-kB↓, ATF3↑,

1726-

SFN,

Sulforaphane: A Broccoli Bioactive Phytocompound with Cancer Preventive Potential

Review,

Var,

Dose↝, eff↝, IL1β↓, IL6↓, IL12↓, TNF-α↓, COX2↓, CXCR4↓, MPO↓, HSP70/HSPA5↓, HSP90↓, VCAM-1↓, IKKα↓, NF-kB↓, HO-1↑, Casp3↑, Casp7↑, Casp8↑, Casp9↑, cl‑PARP↑, Cyt‑c↑, Diablo↑, CHOP↑, survivin↓, XIAP↓, p38↑, Fas↑, PUMA↑, VEGF↓, Hif1a↓, Twist↓, Zeb1↓, Vim↓, MMP2↓, MMP9↓, E-cadherin↑, N-cadherin↓, Snail↓, CD44↓, cycD1/CCND1↓, cycA1/CCNA1↓, CycB/CCNB1↓, cycE/CCNE↓, CDK4↓, CDK6↓, p50↓, P53↑, P21↑, GSH↑, SOD↑, GSTs↑, mTOR↓, Akt↓, PI3K↓, β-catenin/ZEB1↓, IGF-1↓, cMyc↓, CSCs↓,

Showing Research Papers: 1 to 14 of 14

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↓, 1, antiOx↑, 5, Catalase↑, 1, GPx↑, 1, GSH↑, 3, GSR↑, 1, H2O2↓, 1, HO-1↑, 2, NQO1↑, 1, NRF2↑, 2, ROS↓, 2, SOD↑, 2,

Core Metabolism/Glycolysis ⓘ

p‑cMyc↑, 1, CREB↑, 1,

Cell Death ⓘ

iNOS↓, 1, p‑JNK↓, 1, p38↓, 1,

DNA Damage & Repair ⓘ

PCNA↓, 1,

Cell Cycle & Senescence ⓘ

CDK2↓, 1, CDK4↓, 1, cycD1/CCND1↓, 1, cycE/CCNE↓, 1, RB1↓, 1,

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 2, IGF-1↑, 1,

Migration ⓘ

5LO↓, 1, MMP3↓, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 1, NO↑, 1,

Immune & Inflammatory Signaling ⓘ

COX1↓, 1, COX2↓, 1, IL1β↓, 1, IL6↓, 1, Inflam↓, 4, PGE2↓, 1, PGE2↑, 1, Th1 response↓, 1, Th2↑, 2, TNF-α↓, 1,

Synaptic & Neurotransmission ⓘ

GABA↑, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↑, 1,

Clinical Biomarkers ⓘ

IL6↓, 1,

Functional Outcomes ⓘ

AntiCan↑, 1, cardioP↑, 1, memory↑, 1, neuroP↑, 2,
Total Targets: 47

Scientific Paper Hit Count for: Diablo, Diablo/Smac

5 Fisetin
2 Betulinic acid
1 Chemotherapy
1 Boswellia (frankincense)
1 Ellagic acid
1 EGCG (Epigallocatechin Gallate)
1 Pterostilbene
1 Quercetin
1 Resveratrol
1 Sulforaphane (mainly Broccoli)

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:26  Cells:%  prod#:%  Target#:395  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

Diablo Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

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 ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

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 ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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