cMYB Cancer Research Results

cMYB, c-MYB: Click to Expand ⟱
Source:
Type: marker
c‑MYB is a transcription factor that plays critical roles in cell proliferation, differentiation, and apoptosis.
– c‑MYB is a transcription factor essential for normal hematopoiesis and the regulation of genes involved in cell cycle progression, differentiation, and survival.

– Aberrant or sustained expression of c‑MYB is found in several malignancies, particularly hematological cancers such as acute leukemias, as well as solid tumors including breast and colon cancers.
– Overexpression or mutation of c‑MYB can lead to enhanced cell proliferation and impaired differentiation, creating an environment conducive to malignant transformation and tumor maintenance.
– In several studies, high levels of c‑MYB correlate with more aggressive tumor behavior and poorer clinical outcomes, such as reduced overall survival and an increased likelihood of relapse.

c‑MYB plays a pivotal role in the regulation of cell proliferation, differentiation, and survival. Its dysregulation in cancer contributes to unchecked growth and resistance to cell death, correlating with aggressive disease and poorer clinical outcomes.
Scientific Papers found: Click to Expand⟱
1358- Ash,    Withaferin A: A Dietary Supplement with Promising Potential as an Anti-Tumor Therapeutic for Cancer Treatment - Pharmacology and Mechanisms
- Review, Var, NA
TumCCA↑,
Apoptosis↑,
TumAuto↑,
Ferroptosis↑,
TumCP↓,
CSCs↓,
TumMeta↓,
EMT↓,
angioG↓,
Vim↓,
HSP90↓,
annexin II↓, annexin II proteins directly bind to WA
m-FAM72A↓,
BCR-ABL↓,
Mortalin↓,
NRF2↓,
cMYB↓,
ROS↑, WA inhibits proliferation through ROS-mediated intrinsic apoptosis
ChemoSen↑, WA and cisplatin, WA produced ROS, while cisplatin caused DNA damage, suggesting that lower doses of cisplatin combined with suboptimal doses of WA could achieve the same effect
eff↑, sulforaphane and WA showed synergistic effects on epigenetic modifiers and cell proliferation in breast cancer cells
ChemoSen↑, WA and sorafenib caused G2/M arrest in anaplastic and papillary thyroid cancer cells
ChemoSen↑, combination of WA and 5-FU executed PERK axis-mediated endoplasmic reticulum (ER) stress-induced autophagy and apoptosis
eff↑, WA and carnosol also exhibit a synergistic effect on pancreatic cancer
*BioAv↓, Saurabh by Saurabh et al and Tianming et al reported oral bioavailability values 1.8% and 32.4 ± 4.8%, respectively, in male rats.
ROCK1↓, In another study, WA reduces macrophage infiltration and inhibits the expression of protein tyrosine kinase-2 (Pyk2), rho-associated kinase 1 (ROCK1), and VEGF in a hepatocellular carcinoma xenograft model, thereby suppressing tumor invasion and angi
TumCI↓,
Sp1/3/4↓, Furthermore, WA exerts potent anti-angiogenic activity in vivo.174 In the Ehrlich ascites tumor model, WA exerts its anti-angiogenic activity by reducing the binding of the transcription factor specificity protein 1 (Sp1) to VEGF
VEGF↓, n another study, WA reduces macrophage infiltration and inhibits the expression of protein tyrosine kinase-2 (Pyk2), rho-associated kinase 1 (ROCK1), and VEGF in a hepatocellular carcinoma xenograft model, thereby suppressing tumor invasion and angio
Hif1a↓, Furthermore, WA suppresses the AK4-HIF-1α signaling axis and acts as a potent antimetastatic agent in lung cancer.Citation79
EGFR↓, WA synergistically inhibited wild-type epidermal growth factor receptor (EGFR) lung cancer cell viability

1498- SFN,    Prolonged sulforaphane treatment activates survival signaling in nontumorigenic NCM460 colon cells but apoptotic signaling in tumorigenic HCT116 colon cells
- in-vitro, CRC, HCT116 - in-vitro, Nor, NCM460
selectivity↑, we demonstrated that SFN (15 μmol/L) exposure (72 h) inhibited cell proliferation by up to 95% in colon cancer cells (HCT116) and by 52% in normal colon mucosa-derived (NCM460) cells
TumCCA↑, reduction of G1 phase cell distribution
Apoptosis↑, apoptosis in HCT116 cells, but to a much lesser extent in NCM460 cells
*p‑ERK↑, in NCM460 cells but not in HCT116 cells
cMYB↓, decreased c-Myc expression in HCT116 cells but not NCM460 cells.
selectivity↑, decreased c-Myc expression in HCT116 cells but not NCM460 cells.
selectivity↑, upregulated p-ERK1/2 in NCM460 cells but not in HCT116 cells

1508- SFN,    Nrf2 targeting by sulforaphane: A potential therapy for cancer treatment
- Review, Var, NA
*BioAv↑, RAW: higher amounts were detected when broccoli were eaten raw (bioavailability equal to 37%), compared to the cooked broccoli (bioavailability 3.4%)
HDAC↓, Sulforaphane is able to down-regulate HDAC activity and induce histone hyper-acetylation in tumor cell
TumCCA↓, Sulforaphane induces cell cycle arrest in G1, S and G2/M phases,
eff↓, in leukemia stem cells, sulforaphane potentiates imatinib effect through inhibition of the Wnt/β-catenin functions
Wnt↓,
β-catenin/ZEB1↓,
Casp12?, inducing caspases activation
Bcl-2↓,
cl‑PARP↑,
Bax:Bcl2↑, unbalancing the ratio Bax/Bcl-2
IAP1↓, down-regulating IAP family proteins
Casp3↑,
Casp9↑,
Telomerase↓, In Hep3B cells, sulforaphane reduces telomerase activity
hTERT/TERT↓, inhibition of hTERT expression;
ROS?, increment of ROS, induced by this compound, is essential for the downregulation of transcription and of post-translational modification of hTERT in suppression of telomerase activity
DNMTs↓, (2.5 - 10 μM) represses hTERT by impacting epigenetic pathways, in particular through decreased DNA methyltransferases activity (DNMTs)
angioG↓, inhibit tumor development through regulation of angiogenesis
VEGF↓,
Hif1a↓,
cMYB↓,
MMP1↓, inhibition of migration and invasion activities induced by sulforaphane in oral carcinoma cell lines has been associated to the inhibition of MMP-1 and MMP-2
MMP2↓,
MMP9↓,
ERK↑, inhibits invasion by activating ERK1/2, with consequent upregulation of E-cadherin (an invasion inhibitor)
E-cadherin↑,
CD44↓, downregulation of CD44v6 and MMP-2 (invasion promoters)
MMP2↓,
eff↑, ombination of sulforaphane and quercetin synergistically reduces the proliferation and migration of melanoma (B16F10) cells
IL2↑, induces upregulation of IL-2 and IFN-γ
IFN-γ↑,
IL1β↓, downregulation of IL-1beta, IL-6, TNF-α, and GM-CSF
IL6↓,
TNF-α↓,
NF-kB↓, sulforaphane inhibits the phorbol ester induction of NF-κB, inhibiting two pathways, ERK1/2 and NF-κB
ERK↓,
NRF2↑, At molecular level, sulforaphane modulates cellular homeostasis via the activation of the transcription factor Nrf2.
RadioS↑, sulforaphane could be used as a radio-sensitizing agent in prostate cancer if clinical trials will confirm the pre-clinical results.
ChemoSideEff↓, chemopreventive effects of sulforaphane


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   NRF2↓, 1,   NRF2↑, 1,   ROS?, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

BCR-ABL↓, 1,   Mortalin↓, 1,  

Cell Death ⓘ

Apoptosis↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 1,   Casp12?, 1,   Casp3↑, 1,   Casp9↑, 1,   Ferroptosis↑, 1,   hTERT/TERT↓, 1,   IAP1↓, 1,   Telomerase↓, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,  

Protein Folding & ER Stress ⓘ

HSP90↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNMTs↓, 1,   m-FAM72A↓, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

CD44↓, 1,   cMYB↓, 3,   CSCs↓, 1,   EMT↓, 1,   ERK↓, 1,   ERK↑, 1,   HDAC↓, 1,   Wnt↓, 1,  

Migration ⓘ

annexin II↓, 1,   E-cadherin↑, 1,   MMP1↓, 1,   MMP2↓, 2,   MMP9↓, 1,   ROCK1↓, 1,   TumCI↓, 1,   TumCP↓, 1,   TumMeta↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   EGFR↓, 1,   Hif1a↓, 2,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

IFN-γ↑, 1,   IL1β↓, 1,   IL2↑, 1,   IL6↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 3,   eff↓, 1,   eff↑, 3,   RadioS↑, 1,   selectivity↑, 3,  

Clinical Biomarkers ⓘ

EGFR↓, 1,   hTERT/TERT↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

ChemoSideEff↓, 1,  
Total Targets: 63

Pathway results for Effect on Normal Cells:


Proliferation, Differentiation & Cell State ⓘ

p‑ERK↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 1,  
Total Targets: 3

Scientific Paper Hit Count for: cMYB, c-MYB
2 Sulforaphane (mainly Broccoli)
1 Ashwagandha(Withaferin A)
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#:1077  State#:%  Dir#:1
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