RB1 Cancer Research Results
RB1, retinoblastoma 1 gene: Click to Expand ⟱
| Source: CGL-Driver Genes |
| Type: TSG |
The RB1 gene is a critical tumor suppressor gene that plays a significant role in regulating the cell cycle, thereby preventing uncontrolled cell growth and tumor formation.
The RB1 gene encodes the retinoblastoma protein (pRB), which helps control the cell cycle by regulating the transition from the G1 (gap 1) phase to the S (synthesis) phase. When functioning properly, pRB binds to and inhibits transcription factors that promote cell division.
The loss of RB1 function is often associated with a more aggressive tumor phenotype and poorer clinical outcomes.
|
Scientific Papers found: Click to Expand⟱
| - |
Review, |
Var, |
NA |
|
|
|
- |
Review, |
IBD, |
NA |
|
|
|
Inflam↓, anti-inflammatory, antidiabetic, antibacterial, antiparasitic, antidiarrheal, antihypertensive, hypolipidemic, and fungicide.
AntiCan↑, elaborated on the anticancer effects of BBR through the regulation of different molecular pathways such as: inducing apoptosis, autophagy, arresting cell cycle, and inhibiting metastasis and invasion.
Apoptosis↑,
TumAuto↑,
TumCCA↑,
TumMeta↓,
TumCI↓,
eff↑, BBR is shown to have beneficial effects on cancer immunotherapy.
eff↑, BBR inhibited the release of Interleukin 1 beta (IL-1β), Interferon gamma (IFN-γ), Interleukin 6 (IL-6), and Tumor Necrosis Factor-alpha (TNF-α) from LPS stimulated lymphocytes by acting as a dopamine receptor antagonist
CD4+↓, BBR inhibited the proliferation of CD4+ T cells and down-regulated TNF-α and IL-1 and thus, improved autoimmune neuropathy.
TNF-α↓,
IL1↓,
BioAv↓, On the other hand, P-Glycoprotein (P-gp), a secretive pump located in the epithelial cell membrane, restricts the oral bioavailability of a variety of medications, such as BBR. The use of P-gp inhibitors is a common and effective way to prevent this
BioAv↓, Regardless of its low bioavailability, BBR has shown great therapeutic efficacy in the treatment of a number of diseases.
other↓, BBR has been also used as an effective therapeutic agent for Inflammatory Bowel Disease (IBD) for several years
AMPK↑, inhibitory effects on inflammation by regulating different mechanisms such as 5′ Adenosine Monophosphate-Activated Protein Kinase (AMPK. Increase of AMPK
MAPK↓, Mitogen-Activated Protein Kinase (MAPK), and NF-κB signaling pathways
NF-kB↓,
IL6↓, inhibiting the expression of proinflammatory genes such as IL-1, IL-6, Monocyte Chemoattractant Protein 1 (MCP1), TNF-α, Prostaglandin E2 (PGE2), and Cyclooxygenase-2 (COX-2)
MCP1↓,
PGE2↓,
COX2↓,
*ROS↓, BBR protected PC-12 cells (normal) from oxidative damage by suppressing ROS through PI3K/AKT/mTOR signaling pathways
*antiOx↑, BBR therapy improved the antioxidant function of mice intestinal tissue by enhancing the levels of glutathione peroxidase and catalase enzymes.
*GPx↑,
*Catalase↑,
AntiTum↑, Besides, BBR leaves great antitumor effects on multiple types of cancer such as breast cancer,69 bladder cancer,70 hepatocarcinoma,71 and colon cancer.72
TumCP↓, BBR exerts its antitumor activity by inhibiting proliferation, inducing apoptosis and autophagy, and suppressing angiogenesis and metastasis
angioG↓,
Fas↑, by increasing the amounts of Fas receptor (death receptor)/FasL (Fas ligand), ROS, ATM, p53, Retinoblastoma protein (Rb), caspase-9,8,3, TNF-α, Bcl2-associated X protein (Bax), BID
FasL↑,
ROS↑,
ATM↑,
P53↑,
RB1↑,
Casp9↑,
Casp8↑,
Casp3↓,
BAX↑,
Bcl-2↓, and declining Bcl2, Bcl-X, c-IAP1 (inhibitor of apoptosis protein), X-linked inhibitor of apoptosis protein (XIAP), and Survivin levels
Bcl-xL↓,
IAP1↓,
XIAP↓,
survivin↓,
MMP2↓, Furthermore, BBR suppressed Matrix Metalloproteinase-2 (MMP-2), and MMP-9 expression.
MMP9↓,
CycB/CCNB1↓, Inhibition of cyclin B1, cdc2, cdc25c
CDC25↓,
CDC25↓,
Cyt‑c↑, BBR inhibited tumor cell proliferation and migration and induced mitochondria-mediated apoptosis pathway in Triple Negative Breast Cancer (TNBC) by: stimulating cytochrome c release from mitochondria to cytosol
MMP↓, decreased the mitochondrial membrane potential, and enabled cytochrome c release from mitochondria to cytosol
RenoP↑, BBR significantly reduced the destructive effects of cisplatin on the kidney by inhibiting autophagy, and exerted nephroprotective effects.
mTOR↓, U87 cell, Inhibition of m-TOR signaling
MDM2↓, Downregulation of MDM2
LC3II↑, Increase of LC3-II and beclin-1
ERK↓, BBR stimulated AMPK signaling, resulting in reduced extracellular signal–regulated kinase (ERK) activity and COX-2 expression in B16F-10 lung melanoma cells
COX2↓,
MMP3↓, reducing MMP-3 in SGC7901 GC and AGS cells
TGF-β↓, BBR suppressed the invasion and migration of prostate cancer PC-3 cells by inhibiting TGF-β-related signaling molecules which induced Epithelial-Mesenchymal Transition (EMT) such as Bone morphogenetic protein 7 (BMP7),
EMT↑,
ROCK1↓, inhibiting metastasis-associated proteins such as ROCK1, FAK, Ras Homolog Family Member A (RhoA), NF-κB and u-PA, leading to in vitro inhibition of MMP-1 and MMP-13.
FAK↓,
RAS↓,
Rho↓,
NF-kB↓,
uPA↓,
MMP1↓,
MMP13↓,
ChemoSen↑, recent studies have indicated that it can be used in combination with chemotherapy agents
Apoptosis↑,
TumCCA↓, CAPE (1-80 uM) can stimulate apoptosis and cell cycle arrest (G1 phase
TumCMig↓,
TumMeta↓,
ChemoSen↑,
eff↑, Nanoparticles promote therapeutic effect of CA and CAPE in reducing cancer cell malignancy.
eff↑, improve capacity of CA and CAPE in cancer suppression, it has been co-administered with other anti-tumor compounds such as gallic acid
eff↓, Currently, solvent extraction is utilized by methanol and ethyl acetate
combination at high temperatures. However, a low amount of CA is
yielded via this pathway
eff↝, Decyl CA (DCA) is a
novel derivative of CA but its role in affecting colorectal cancer has not
been completely understood.
Dose∅, The CAPE administration (0-60 uM) induces both
autophagy and apoptosis in C6 glioma cells.
AMPK↑, CAPE induces autophagy via AMPK upregulation.
p62↓, CAPE can induce autophagy via p62 down-regulation and LC3-II upregulation
LC3II↑,
Ca+2↑, CA (0-1000 uM) enhances Ca2+ accumulation in cells in a concentration-dependent manner
Bax:Bcl2↑, CA can promote Bax/Bcl-2 ratio i
CDK4↑, The administration of CAPE (1–80 μM)
can stimulate apoptosis and cell cycle arrest (G1 phase) via upregulation of Bax, CDK4, CDK6 and Rb
CDK6↑,
RB1↑,
EMT↓, CAPE has demonstrated high potential in inhibiting EMT in nasopharyngeal caner via enhancing E-cadherin levels, and reducing vimentin and β-catenin levels.
E-cadherin↑,
Vim↓,
β-catenin/ZEB1↓,
NF-kB↓,
angioG↑, CAPE (0.01-1ug/ml) inhibited angiogenesis via VEGF down-regulation
VEGF↓,
TSP-1↑, and furthermore, CAPE is capable of increasing TSP-1 levels
MMP9↓, CAPE was found to reduce MMP-9 expression
MMP2↓, CAPE can also down-regulate MMP-2
ChemoSen↑, role of CA and its derivatives in enhancing therapy sensitivity of cancer cells.
eff↑, CA administration (100 uM) alone or its combination with metformin (10 mM) can induce AMPK signaling
ROS↑, CA can promote ROS levels to induce cell death in human squamous cell carcinoma
CSCs↓, CA can reduce self-renewal capacity of CSCs and their migratory ability in vitro and in vivo.
Fas↑, CAPE (0-100 uM) is capable of inducing Fas signaling to promote p53 expression, leading to apoptotic cell death via Bax and caspase activation
P53↑,
BAX↑,
Casp↑,
β-catenin/ZEB1↓, anti-tumor activity of CAPE is mediated via reducing β-catenin levels
NDRG1↑, CAPE (30 uM) can promote NDRG1 expression via MAPK activation and down-regulation of STAT3
STAT3↓,
MAPK↑, CAPE stimulates mitogen-activated protein kinase (MAPK) and ERK
ERK↑,
eff↑, Res, thymoquinone and CAPE mediate lung tumor cell death via Bax
upregulation and Bcl-2 down-regulation.
eff↑, co-administration of CA (100 μM) and
metformin (10 mM) is of interest in cervical squamous cell carcinoma
therapy.
eff↑, in addition to CA, propolis contains other agents such as chrysin, p-coumaric acid and ferulic acid that are beneficial in tumor suppression.
TumCG↓,
TumCCA↑, increase in G1 cell population
P21↑,
CDK4↓,
cycD1/CCND1↓,
RB1↑,
E2Fs↓,
| - |
in-vitro, |
Pca, |
PC3 |
|
|
|
- |
in-vitro, |
Pca, |
DU145 |
|
|
|
- |
in-vitro, |
Pca, |
LNCaP |
|
|
|
cycD1/CCND1↓, CCND1, CCND2, CCND3
cycE/CCNE↓, CCNE1, CCNE2
CDK2↓,
CDK4/6↓, CDK4, CDK8
E2Fs↓, E2F2, E2F3
PCNA↓,
cDC2↓,
PTEN↑,
MSH2↑,
P21↑,
EP300↑, p300
BRCA1↑,
NF2↑,
TSC1↑,
TGFβR1↑, TGFβR2
P53↑,
RB1↑, Rb
AKT1↓,
cMyc↓,
CDC7↓,
cycF↓, CCNF
CDC16↓,
CUL4B↑, CUL4B, a member of the cullin gene family that is also known to be involved in control of the cell cycle, was significantly up-regulated by quercetin.
CBP↑,
TSC2↑,
HER2/EBBR2↓, erb-2
BCR↓,
TumCCA↑, quercetin significantly inhibited the expression of specific oncogenes and genes controlling G1, S, G2, and M phases of the cell cycle.
chemoPv↑, Our results correlate with those of nutritional studies that support the roles of dietary bioflavonoids as cancer chemopreventive agents.
hepatoP↑, well as hepatoprotective agents.
chemoP↑, silymarin could be beneficial to oncology patients, especially for the treatment of the side effects of anticancer chemotherapeutics.
*lipid-P↓, Silymarin has been shown to significantly reduce lipid peroxidation and exhibit anti-oxidant, antihypertensive, antidiabetic, and hepatoprotective effects
*antiOx↑,
tumCV↓, reduces the viability, adhesion, and migration of tumor cells by induction of apoptosis and formation of reactive oxygen species (ROS), reducing glutathione levels, B-cell lymphoma 2 (Bcl-2), survivin, cyclin D1, Notch 1 intracellular domain (NICD),
TumCMig↓,
Apoptosis↑,
ROS↑,
GSH↓,
Bcl-2↓,
survivin↓,
cycD1/CCND1↓,
NOTCH1↓,
BAX↑, as well as enhancing the amount of Bcl-2-associated X protein (Bax) level (
NF-kB↓, The suppression of NK-κB-regulated gene products (e.g., cyclooxygenase-2 (COX-2), lipoxygenase (LOX), inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF), and interleukin-1 (IL-1)) mediates the anti-inflammatory effect of silymarin
COX2↓,
LOX1↓,
iNOS↓,
TNF-α↓,
IL1↓,
Inflam↓,
*toxicity↓, Silymarin is also safe for humans, hence at therapeutic doses patients demonstrated no negative effects at the high dose of 700 mg, three times a day, for 24 weeks
CXCR4↓, fig 2
EGFR↓,
ERK↓,
MMP↓, reduction in mitochondrial transmembrane potential due to an increase in cytosolic cytochrome complex (Cyt c) levels.
Cyt‑c↑,
TumCCA↑, Moreover, silymarin increased the percentage of cells in the gap 0/gap 1 (G0/G1) phase and decreased the percentage of cells in the synthesis (S)-phase,
RB1↑, concomitant up-regulation of retinoblastoma protein (Rb), p53, cyclin-dependent kinase inhibitor 1 (p21Cip1), and cyclin-dependent kinase inhibitor 1B (p27Kip1)
P53↑,
P21↑,
p27↑,
cycE/CCNE↓, and down-regulation of cyclin D1, cyclin E, cyclin-dependent kinase 4 (CDK4), and phospho-Rb
CDK4↓,
p‑pRB↓,
Hif1a↓, silibinin inhibited proliferation of Hep3B cells due to simultaneous induction of apoptosis and prevented the accumulation
cMyc↓, Silibinin also reduces cellular myelocytomatosis oncogene (c-MYC) expression, a key regulator of cancer metabolism in pancreatic cancer cells
IL1β↓, Silymarin can also inhibit the production of inflammatory cytokines, such as interleukin-1beta (IL-1β), interferon-gamma (IFNγ),
IFN-γ↓,
PCNA↓, ilymarin suppresses the high proliferative activity of cells started with a carcinogen so that it significantly inhibits proliferating cell nuclear antigen (PCNA) and cyclin D1 labeling indices
PSA↓, In another patent, S. marianum has been used as an estrogen receptor β-agonist and an inhibitor of PSA for treating prostate cancer
CYP1A1↓, Silymarin prevents the expression of CYP1A1 and COX-2
Showing Research Papers: 1 to 5 of 5
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
CYP1A1↓, 1, GSH↓, 1, ROS↑, 3,
Mitochondria & Bioenergetics ⓘ
BCR↓, 1, CDC16↓, 1, CDC25↓, 2, MMP↓, 2, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
AKT1↓, 1, AMPK↑, 2, cMyc↓, 2,
Cell Death ⓘ
Apoptosis↑, 3, BAX↑, 3, Bax:Bcl2↑, 1, Bcl-2↓, 2, Bcl-xL↓, 1, Casp↑, 1, Casp3↓, 1, Casp8↑, 1, Casp9↑, 1, CBP↑, 1, Cyt‑c↑, 2, Fas↑, 2, FasL↑, 1, IAP1↓, 1, iNOS↓, 1, MAPK↓, 1, MAPK↑, 1, MDM2↓, 1, p27↑, 1, survivin↓, 2,
Kinase & Signal Transduction ⓘ
CDC7↓, 1, HER2/EBBR2↓, 1, TSC2↑, 1,
Transcription & Epigenetics ⓘ
other↓, 1, p‑pRB↓, 1, tumCV↓, 1,
Autophagy & Lysosomes ⓘ
LC3II↑, 2, p62↓, 1, TumAuto↑, 1,
DNA Damage & Repair ⓘ
ATM↑, 1, BRCA1↑, 1, CUL4B↑, 1, P53↑, 4, PCNA↓, 2,
Cell Cycle & Senescence ⓘ
CDK2↓, 1, CDK4↓, 2, CDK4↑, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 3, cycE/CCNE↓, 2, cycF↓, 1, E2Fs↓, 2, P21↑, 3, RB1↑, 5, TumCCA↓, 1, TumCCA↑, 4,
Proliferation, Differentiation & Cell State ⓘ
cDC2↓, 1, CSCs↓, 1, EMT↓, 1, EMT↑, 1, EP300↑, 1, ERK↓, 2, ERK↑, 1, mTOR↓, 1, NF2↑, 1, NOTCH1↓, 1, PTEN↑, 1, RAS↓, 1, STAT3↓, 1, TumCG↓, 1,
Migration ⓘ
Ca+2↑, 1, CDK4/6↓, 1, E-cadherin↑, 1, FAK↓, 1, MMP1↓, 1, MMP13↓, 1, MMP2↓, 2, MMP3↓, 1, MMP9↓, 2, MSH2↑, 1, Rho↓, 1, ROCK1↓, 1, TGF-β↓, 1, TSC1↑, 1, TSP-1↑, 1, TumCI↓, 1, TumCMig↓, 2, TumCP↓, 1, TumMeta↓, 2, uPA↓, 1, Vim↓, 1, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, angioG↑, 1, EGFR↓, 1, Hif1a↓, 1, LOX1↓, 1, VEGF↓, 1,
Immune & Inflammatory Signaling ⓘ
CD4+↓, 1, COX2↓, 3, CXCR4↓, 1, IFN-γ↓, 1, IL1↓, 2, IL1β↓, 1, IL6↓, 1, Inflam↓, 2, MCP1↓, 1, NF-kB↓, 4, PGE2↓, 1, PSA↓, 1, TNF-α↓, 2,
Hormonal & Nuclear Receptors ⓘ
CDK6↑, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, ChemoSen↑, 3, Dose∅, 1, eff↓, 1, eff↑, 8, eff↝, 1,
Clinical Biomarkers ⓘ
BRCA1↑, 1, EGFR↓, 1, HER2/EBBR2↓, 1, IL6↓, 1, PSA↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, AntiTum↑, 1, chemoP↑, 1, chemoPv↑, 1, hepatoP↑, 1, NDRG1↑, 1, RenoP↑, 1, TGFβR1↑, 1,
Total Targets: 132
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 2, Catalase↑, 1, GPx↑, 1, lipid-P↓, 1, ROS↓, 1,
Functional Outcomes ⓘ
toxicity↓, 1,
Total Targets: 6
Scientific Paper Hit Count for: RB1, retinoblastoma 1 gene
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#:270 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
Home Page