BRCA1 Cancer Research Results

BRCA1, BReast CAncer gene 1: Click to Expand ⟱
Source: CGL-Driver Genes
Type: TSG
BRCA1 and BRCA2 are tumor suppressor genes, which, when they function normally, keep tumors from forming.
BRCA1 mutations are associated with an increased risk for:
Breast cancer, including an aggressive form called Triple Negative Breast Cancer
Ovarian cancer
Pancreatic cancer
Prostate cancer
BRCA1/BRCA2 are used as clinical biomarker for PARP inhibitor use.
Scientific Papers found: Click to Expand⟱
6140- Cin,  HCAs,    Cinnamaldehyde: Pharmacokinetics, anticancer properties and therapeutic potential (Review)
- Review, Var, NA
Dose↝, Cinnamaldehyde (CA), an active compound derived from the natural plant cinnamon, has garnered attention in pharmacological research due to its diverse therapeutic applications.
TumCP↓, CA and its derivatives have antitumor effects, which encompass inhibiting cell proliferation, arresting the cell cycle, inducing apoptosis, limiting cell migration and invasion, and suppressing angiogenesis.
TumCCA↑,
Apoptosis↑,
TumCMig↓,
TumCI↓,
angioG↓,
*Inflam↓, including anti-inflammatory (3), antioxidant (4), antiviral (5), anti-bacterial (6), antithrombic (7), hypoglycemic (8), hepatoprotective (9), anti-diabetic (10), neuroprotective (11) and anticancer effects
*antiOx↑,
*Bacteria↓,
*AntiThr↑,
*hepatoP↑,
*AntiDiabetic↑,
*neuroP↑,
AntiCan↑,
ChemoSen↑, can enhance the effectiveness of anticancer drugs and ensure patient safety.
*BioAv↝, the bioavailability of intravenous administration of CA was superior to that of oral administration
*BioAv↑, A into CA solid lipid nanoparticles, which increased the oral bioavailability of CA by >1.69 times.
eff↑, Especially when combined with hyperthermia therapy at 42°C and 43°C, CA could inhibit cell proliferation
CDK1↓, CB403 (Fig. 1) is a cinnamaldehyde derivative that inhibits the activity of cyclin-dependent kinases (CDKs), particularly CDK1, CDK2 and CDK4, thereby halting cell cycle progression.
CDK2↓,
CDK4↓,
cJun↓, 2-hydroxycinnamaldehyde (HCA; Fig. 1) inhibits the growth of SW620 colon cancer cells by reducing the expression of c-Jun and c-Fos, inhibiting the DNA binding activity of activator protein 1, and inducing cell apoptosis
cFos↓,
Apoptosis↑,
PI3K↓, CA can induce apoptosis in colon cancer cells by inhibiting the PI3K/Akt signaling pathway
Akt↓,
E-cadherin↑, CA upregulates the expression of E-cadherin while downregulating the expression of matrix metalloproteinase-2 (MMP2) and MMP9
MMP2↓,
MMP9↓,
TOP1↓, increases the sensitivity of CRC cells to 5-FU by reducing the expression of thymidylate synthase, ERCC1, DNA topoisomerase 1 and BRCA1
BRCA1↓,
ROS↑, CA was also able to induce apoptosis in cancer cells by increasing intracellular ROS levels
BAX↑, A induces cell apoptosis by upregulating Bax expression, and downregulating Bcl-2 and X-linked inhibitor of apoptosis (XIAP) expression
Bcl-2↓,
XIAP↓,
MMP↓, CA can also induce apoptosis in leukemia K562 cells by reducing the mitochondrial transmembrane potential via mitochondrial-mediated pathways
STAT3↓, figure 2
mTOR↓,
NF-kB↓, ↓NF-κB
eff↑, CA-Cu-PDA was able to release copper ions and CA in tumor cells, and weakened the antioxidant system by binding to glutathione (GSH), which in turn produced additional ROS, thereby inducing enhanced oxidative stress effects
toxicity↓, Consistent with these findings, another study has demonstrated that CA does not exhibit genotoxic or carcinogenic effects on the body
cardioP↑, CA has demonstrated a capacity to alleviate cardiotoxicity induced by DOX

2043- PB,  Cisplatin,    Phenylbutyrate interferes with the Fanconi anemia and BRCA pathway and sensitizes head and neck cancer cells to cisplatin
- in-vitro, HNSCC, UM-SCC-1
ChemoSen↑, phenylbutyrate sensitizes head and neck cancer cell lines to cisplatin
eff↑, Furthermore, we found that cancer cells defective in the FA pathway were also sensitized to cisplatin by phenylbutyrate suggesting that phenylbutyrate targets additional pathways.
HDAC↓, HDAC inhibitor phenylbutyrate has shown a good clinical safety record when used to treat urea cycle disorders and cystic fibrosis
BRCA1↓, Phenylbutyrate attenuates BRCA1 expression
RadioS↑, inhibition of double strand break repair and thus phenylbutyrate and other HDAC inhibitors may have sensitizing properties when combined with radiotherapy or chemotherapeutic agents

5022- UA,    Ursolic Acid’s Alluring Journey: One Triterpenoid vs. Cancer Hallmarks
- Review, Var, NA
TumCP↓, inhibition of cell proliferation, induction of apoptosis, suppression of angiogenesis, inhibition of metastasis, and modulation of the tumor microenvironment
Apoptosis↑,
angioG↑,
TumMeta↓,
BioAv↓, acknowledges hurdles related to UA’s low bioavailability,
Hif1a↓, graphical abstract
Glycolysis↓,
mitResp↓,
Akt↓,
MAPK↓,
ERK↓,
mTOR↓,
P53↑,
P21↑,
E2Fs↑,
STAT3↓,
MMP↓,
NLRP3↓,
iNOS↓,
CHK1↓,
Chk2↓,
BRCA1↓,
E-cadherin↑,
N-cadherin↓,
Casp↑,
p62↓,
LC3II↑,
Vim↓,
ROS↑, administration of UA has effectively modulated the generation of both cellular and mitochondrial ROS
CSCs↓, This, in turn, triggers a response in embryonic CSCs known as DNA damage response (DDR), strongly suggesting the potential for UA-induced cell death
DNAdam↑,
GutMicro↑, UA has shown potential in modulating the composition of the gut microbiota and improving the microenvironment within the digestive system
VEGF↓, UA treatment significantly reduced the expression of VEGF-A and FGF-β in both CRC tumors and HT-29 cells (


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 ⓘ

ROS↑, 2,  

Mitochondria & Bioenergetics ⓘ

mitResp↓, 1,   MMP↓, 2,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 3,   BAX↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   Chk2↓, 1,   iNOS↓, 1,   MAPK↓, 1,  

Transcription & Epigenetics ⓘ

cJun↓, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   p62↓, 1,  

DNA Damage & Repair ⓘ

BRCA1↓, 3,   CHK1↓, 1,   DNAdam↑, 1,   P53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   CDK4↓, 1,   E2Fs↑, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

cFos↓, 1,   CSCs↓, 1,   ERK↓, 1,   HDAC↓, 1,   mTOR↓, 2,   PI3K↓, 1,   STAT3↓, 2,   TOP1↓, 1,  

Migration ⓘ

E-cadherin↑, 2,   MMP2↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   angioG↑, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   ChemoSen↑, 2,   Dose↝, 1,   eff↑, 3,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

BRCA1↓, 3,   GutMicro↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   cardioP↑, 1,   toxicity↓, 1,  
Total Targets: 59

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Transcription & Epigenetics ⓘ

AntiThr↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   hepatoP↑, 1,   neuroP↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,  
Total Targets: 9

Scientific Paper Hit Count for: BRCA1, BReast CAncer gene 1
1 Cinnamon
1 Hydroxycinnamic-acid
1 Phenylbutyrate
1 Cisplatin
1 Ursolic acid
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#:32  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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