BMI1 Cancer Research Results

BMI1, B cell-specific Moloney murine leukemia virus integration site 1: Click to Expand ⟱
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BMI1 (B cell-specific Moloney murine leukemia virus integration site 1) is a protein that plays a crucial role in the regulation of cell growth, differentiation, and survival. It is a key component of the Polycomb repressive complex 1 (PRC1), which is involved in the silencing of genes through histone modification.
Overexpression of BMI1 has been observed in many types of cancer, and it is often associated with poor prognosis and reduced survival rates.
Scientific Papers found: Click to Expand⟱
5437- AG,    Modulation of PD-L1 by Astragalus polysaccharide attenuates the induction of melanoma stem cell properties and overcomes immune evasion
- in-vivo, Melanoma, B16-F10
CSCs↓, APS attenuated the tumor sphere formation of MSCs in vitro as well as the tumorigenicity in vivo.
CD133↓, It also decreased the expression of CD133, BMI1 and CD47.
BMI1↓,
PD-L1↓, it was confirmed that APS inhibited the induction of MSCs by down-regulating PD-L1 expression.
TumCG↓, Accordingly, the CSC properties were also attenuated, accompanied by a slower tumor growth rate. F

2730- BetA,    Betulinic acid induces autophagy-dependent apoptosis via Bmi-1/ROS/AMPK-mTOR-ULK1 axis in human bladder cancer cells
- in-vitro, Bladder, T24/HTB-9
tumCV↓, The present study showed that BA exposure significantly suppressed viability, proliferation, and migration of EJ and T24 human bladder cancer cells
TumCP↓,
TumCMig↓,
Casp↑, These effects reflected caspase 3-mediated apoptosis
TumAuto↑, BA-induced autophagy was evidenced by epifluorescence imaging of lentivirus-induced expression of mCherry-GFP-LC3B and increased expression of two autophagy-related proteins, LC3B-II and TEM.
LC3B-II↑,
p‑AMPK↑, Moreover, enhanced AMPK phosphorylation and decreased mTOR and ULK-1 phosphorylation suggested BA activates autophagy via the AMPK/mTOR/ULK1 pathway.
mTOR↓,
BMI1↓, decreased Bmi-1 expression in BA-treated T24 cell xenografts in nude mice suggested that downregulation of Bmi-1 is the underlying mechanism in BA-mediated, autophagy-dependent apoptosis.
ROS↑, BA induced ROS production dose-dependently
eff↓, Co-incubation with NAC effectively blocked ROS production (Figure 4B), rescued cell viability,

2047- Buty,    Sodium butyrate inhibits migration and induces AMPK-mTOR pathway-dependent autophagy and ROS-mediated apoptosis via the miR-139-5p/Bmi-1 axis in human bladder cancer cells
- in-vitro, CRC, T24/HTB-9 - in-vitro, Nor, SV-HUC-1 - in-vitro, Bladder, 5637 - in-vivo, NA, NA
HDAC↓, Sodium butyrate (NaB) is a histone deacetylase inhibitor and exerts remarkable antitumor effects in various cancer cells
AntiTum↑,
TumCMig↓, NaB inhibited migration
AMPK↑, induced AMPK/mTOR pathway-activated autophagy and reactive oxygen species (ROS) overproduction via the miR-139-5p/Bmi-1 axis
mTOR↑,
TumAuto↑,
ROS↑, NaB initiates ROS overproduction
miR-139-5p↑, NaB upregulates miR-139-5p and depletes Bmi-1 in bladder cancer cells
BMI1↓,
TumCI?, NaB significantly inhibited cell migration dose-dependently
E-cadherin↑, E-cadherin was markedly increased, while the expression of N-cadherin, Vimentin, and Snail was decreased
N-cadherin↓,
Vim↓,
Snail↓,
cl‑PARP↑, increased expression levels of cleaved PARP, cleaved caspase-3, and Bax and the concurrent decrease in Bcl-2 and Bcl-xl
cl‑Casp3↑,
BAX↑,
Bcl-2↓,
Bcl-xL↓,
MMP↓, impairs mitochondrial membrane potential
PINK1↑, activates the PINK1/ PARKIN pathway
PARK2↑,
TumMeta↓, NaB inhibits tumor metastasis and growth in vivo
TumCG↓,
LC3II↑, a significant increase in the levels of cleaved caspase3, p-AMPK, and LC3B-II along with decreased Bmi-1 and Vimentin
p62↓, elevated LC3B-II levels and degradation of p62
eff↓, NAC abolished the impairment of MMP and ROS overproduction. Interestingly, NAC also significantly inhibited apoptosis induced by NaB

679- EGCG,  5-FU,    Epigallocatechin-3-gallate targets cancer stem-like cells and enhances 5-fluorouracil chemosensitivity in colorectal cancer
- in-vitro, CRC, NA
NOTCH1↓, Furthermore, EGCG suppressed Notch1
BMI1↓,
SUZ12↓,
EZH2↓,
miR-34a↑,
miR-200c↑,
miR-145↑,
CSCs↓, (EGCG), an active catechin present in green tea, has been shown to suppress CSC growth in various cancers

4928- PEITC,    Dietary phytochemical PEITC restricts tumor development via modulation of epigenetic writers and erasers
- vitro+vivo, Colon, SW-620
Risk↓, Dietary intake of bioactive phytochemicals including the cruciferous vegetable derivative phenethyl isothiocyanate (PEITC) can reduce risk of human cancers, but possible epigenetic mechanisms of these effects are yet unknown.
HDAC↓, Sustained PEITC exposure not only blocked HDAC binding to euchromatin but was also associated with hypomethylation of PcG target genes that are typically hypermethylated in cancer.
TumW↓, The mean weight of tumors generated by SW620-PEITC cells was 63.6% of that generated by SW620-CON cells assessed at the same time point
TumCG↓, indicating that long-term exposure to low concentration of PEITC can potently restrict tumor growth in vivo.
AP-1↓, Unlike SW620-CON cells, tumor cells treated with PEITC displayed impaired signaling via AP-1 (activator protein 1), CRE/CREB (cAMP response elements), and NFkB pathways (Fig. 4c).
cAMP↓,
NF-kB↓,
BMI1↓, substantial down-regulation of PcG complex proteins including BMI-1 (B cell-specific Moloney murine leukemia virus integration site 1), SUZ12 (suppressor of zeste 12 homolog), EZH2 (enhancer of zeste homolog 2), Ring1A, and Ring1B.
SUZ12↓,
EZH2↓,
selectivity↑, ntriguingly, this PEITC-induced decrease in expression of PcG complex proteins was more pronounced in metastatic SW620 cells than in non-metastatic SW480 cells.

5163- PLB,    Plumbagin suppresses epithelial to mesenchymal transition and stemness via inhibiting Nrf2-mediated signaling pathway in human tongue squamous cell carcinoma cells
- in-vitro, SCC, SCC25
TumCP↓, PLB inhibited cell proliferation, activated death receptor-mediated apoptotic pathway,
NRF2↓, PLB induces intracellular ROS generation and regulates redox homeostasis via suppressing Nrf2-mediated oxidative signaling pathway in SCC25 cells
TumCCA↑, PLB markedly induced cell cycle arrest at G2/M phase and extrinsic apoptosis
EMT↓, and inhibited epithelial to mesenchymal transition (EMT) and stemness in SCC25 cells.
CSCs↓,
eff↓, Of note, N-acetyl-l-cysteine (NAC) and l-glutathione (GSH) abolished the effects of PLB on cell cycle arrest, apoptosis induction, EMT inhibition, and stemness a
ROS↑, PLB on ROS generation-related molecules
CycB/CCNB1↓, PLB induces G2/M arrest in SCC25 cells via downregulation of cyclin B1, CDK1/cdc2, and cdc25
CDK1↓,
CDK2↓,
CDC25↓,
Vim↓, PLB inhibited the expression of vimentin in a concentration- and time-dependent manner
OCT4↓, PLB significantly decreased the expression level of Oct-4, Sox-2, Nanog, and Bmi-1.
SOX2↓,
Nanog↓,
BMI1↓,
NQO1↓, The expression levels of NQO1, GST, and HSP90 were all markedly decreased
GSTA1↓,
HSP90↓,
toxicity↓, PLB exhibits anticancer activities with minimal side effect in vitro and in vivo,

3199- SFN,    Sulforaphane improves chemotherapy efficacy by targeting cancer stem cell-like properties via the miR-124/IL-6R/STAT3 axis
- in-vitro, GC, NA
CSCs↓, It also plays important roles in mediating CSCs. For example, overexpression of miR-124 reduced neurosphere formation, CD133+ cell subpopulations, and stem cell markers such as BMI1, Nanog, and nestin in glioma cells
CD133↓,
BMI1↓,
Nanog↓,
Nestin↓,


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 ⓘ

GSTA1↓, 1,   NQO1↓, 1,   NRF2↓, 1,   PARK2↑, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

CDC25↓, 1,   MMP↓, 1,   PINK1↑, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   p‑AMPK↑, 1,   cAMP↓, 1,  

Cell Death ⓘ

BAX↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp↑, 1,   cl‑Casp3↑, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 2,   miR-145↑, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

HSP90↓, 1,  

Autophagy & Lysosomes ⓘ

LC3B-II↑, 1,   LC3II↑, 1,   p62↓, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   CycB/CCNB1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

BMI1↓, 7,   CD133↓, 2,   CSCs↓, 4,   EMT↓, 1,   HDAC↓, 2,   miR-34a↑, 1,   mTOR↓, 1,   mTOR↑, 1,   Nanog↓, 2,   Nestin↓, 1,   NOTCH1↓, 1,   OCT4↓, 1,   SOX2↓, 1,   SUZ12↓, 2,   TumCG↓, 3,  

Migration ⓘ

AP-1↓, 1,   E-cadherin↑, 1,   miR-139-5p↑, 1,   miR-200c↑, 1,   N-cadherin↓, 1,   Snail↓, 1,   TumCI?, 1,   TumCMig↓, 2,   TumCP↓, 2,   TumMeta↓, 1,   Vim↓, 2,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,   PD-L1↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 3,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

EZH2↓, 2,   PD-L1↓, 1,   SUZ12↓, 2,  

Functional Outcomes ⓘ

AntiTum↑, 1,   Risk↓, 1,   toxicity↓, 1,   TumW↓, 1,  
Total Targets: 66

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: BMI1, B cell-specific Moloney murine leukemia virus integration site 1
1 Astragalus
1 Betulinic acid
1 Butyrate
1 EGCG (Epigallocatechin Gallate)
1 5-fluorouracil
1 Phenethyl isothiocyanate
1 Plumbagin
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:%  Cells:%  prod#:%  Target#:837  State#:%  Dir#:1
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