DNArepair Cancer Research Results

DNArepair, DNA repair: Click to Expand ⟱
Source: HalifaxProj(enhance)
Type:
DNA repair is a crucial cellular process that maintains the integrity of the genome by correcting damage that can occur due to various factors, including environmental stress, radiation, and normal metabolic activities.
Radiation and Chemotherapy: These treatments often work by inducing DNA damage, and cancer cells with defective repair mechanisms may be more susceptible to these therapies.
Scientific Papers found: Click to Expand⟱
2028- PB,    Potential of Phenylbutyrate as Adjuvant Chemotherapy: An Overview of Cellular and Molecular Anticancer Mechanisms
- Review, Var, NA
HDAC↓, Phenylbutyrate is one of the first drugs encountered in cancer therapy as a histone deacetylase inhibitor (HDACI).
TumCCA↑, phenylbutyrate treatment that results in reduced proliferation and cell-cycle arrest in G1 or G2 phases.
P21↑, common sequela of phenylbutyrate treatment is the upregulation of p21,
Dose↝, In prostate cancer, phenylbutyrate at clinically achievable concentrations (0.1 mM-8 mM),
Telomerase↓, butyrate or its derivatives was also evident in several other types of cancers and was associated with loss of telomerase activity
IGFBP3↑, Upregulation of insulin-like growth factor binding protein 3 (IGFBP-3) is another unique antiproliferative mechanism of sodium butyrate in breast cancer cells
p‑p38↑, Phenylbutyrate and its derivatives upregulated p21, gelsolin, phosphorylated p38, JNK, and ERK (MAPK pathway members), Bax, caspases-3,
JNK↑,
ERK↑,
BAX↑,
Casp3↑,
Bcl-2↓, downregulated Bcl-X L , Bcl-2, cytochrome c, FAK, and survivin
Cyt‑c↝,
FAK↓,
survivin↓,
VEGF↓, Butyrate treatment reduced the level of vascular endothelial growth factor (VEGF)
angioG↓,
DNArepair↓, Inhibition of DNA Repair.
TumMeta↓,
HSP27↑, Moreover, butyrate treatment in colorectal cancer cells resulted in an acute stress response that was associated with HSP27 activation, activation of ASK1 (MAP3K) and p38 MAPK pathway consequently.
ASK1↑,
ROS↑, Also it resulted in elevated cellular levels of reactive oxygen species (ROS) in oral and tongue cancer cells.
eff↑, phenylbutyrate enhanced the cytotoxicity of temozolamide in malignant glioma cells via suppression of the endoplasmic reticulum stress revealed by the decreased expression of GRP78 and GADD153.
ER Stress↓,
GRP78/BiP↓,
CHOP↑, GADD153
AR↓, Sodium butyrate treatment of prostate cancer cells was associated with downregulation of androgen receptor
other?, lots of references in this paper.

2046- PB,    Sodium butyrate promotes apoptosis in breast cancer cells through reactive oxygen species (ROS) formation and mitochondrial impairment
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-468 - in-vitro, Nor, MCF10
Apoptosis↑, NaBu induced a dose and time-dependent cell toxicity in breast cancer cells which was related to the cell cycle arrest and induction of apoptosis.
i-ROS?, NaBu-elicited apoptosis was accompanied by the elevated level of ROS
Casp↑, increased caspase activity
MMP?, reduced mitochondrial membrane potential (Δψm) in MCF-7 and MDA-MB-468 cells
selectivity↑, and with no effect on the above mentioned factors in MCF-10A cells.
*ROS∅, however the level of ROS production was remained approximately unchanged in MCF-10A cells.
HDAC↓, Sodium butyrate (NaBu), one of the well-studied HDACi, is a short-chain fatty acid and the byproduct of carbohydrate metabolism in the gut
DNArepair↓, Sodium butyrate including the inhibition of DNA double strand break repair and stress oxidative
Casp3↑, effect of sodium butyrate on the cell cycle distribution, intracellular formation of Reactive oxygen species (ROS), the caspase 3 and 8 activity,
Casp8↑,
*toxicity↓, MCF-10A cells were treated with the same concentrations of sodium butyrate (0.1–20 mM) for 24, 48, 72 h and the subsequent cytotoxic effect was significantly lower comparing to the breast cancer cells.
TumCCA↑, significant elevation in the percentage of accumulated cells in the sub-G1 phase which was observed in MCF-7 and MDA-MB-468 cells however the effect of sodium butyrate on MCF-10A cell cycle distribution was inconsiderable

5038- SAS,  Rad,    Sulfasalazine, an inhibitor of the cystine-glutamate antiporter, reduces DNA damage repair and enhances radiosensitivity in murine B16F10 melanoma
- in-vivo, Melanoma, B16-F10
xCT↓, Sulfasalazine is an inhibitor of xCT that is known to increase cellular oxidative stress, giving it anti-tumor potential.
ROS↑,
RadioS↓, radio-sensitizing effect of sulfasalazine using a B16F10 melanoma model.
GSH↓, Sulfasalazine decreased glutathione concentrations and resistance to H2O2 in B16F10 melanoma cells, but not in mouse embryonic fibroblasts.
selectivity↑,
DNArepair↓, It inhibited cellular DNA damage repair and prolonged cell cycle arrest after X-irradiation.
TumCCA↑,
H2O2↑, SAS decreases cellular GSH and increases H2O2 cytotoxicity in B16F10 cells
Dose↝, At lower SAS concentrations (10–100 μM), we did not observe any increase in intracellular ROS. At higher concentrations of SAS (800–1,000 μM), intracellular ROS increased approximately 2.3-fold in B16F10 cells

2406- SFN,    Sulforaphane and Its Protective Role in Prostate Cancer: A Mechanistic Approach
- Review, Pca, NA
HK2↓, When TRAMP mice were given 6 μmol/mouse (1 mg/mouse) three times a week for 17–19 weeks, the prostate tumor expression of glycolysis-promoting enzymes such as (HKII), 2 (PKM2) and (LDHA) was decreased by 32–45%
PKM2↓,
LDHA↓,
Glycolysis↓, These results provide evidence that sulforaphane suppresses in vivo glycolysis in prostate cancer cells
LAMP2↑, The study shows that 10–20 μM of sulforaphane significantly increased lysosome-associated membrane protein 2 (LAMP2) in the cell lines
Hif1a↓, sulforaphane has been shown to suppress HIF-1α
DNAdam↓, SFN causes DNA damage and prevents DNA repair in prostate cancer cell
DNArepair↓,
Dose↝, 5 to 100 mg/kg of sulforaphane reduce tumors in animal models [ 5 , 19]. For a 70 kg human, this translates to 350–7000 mg/kg, which is significantly above the upper threshold of tolerable doses


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   H2O2↑, 1,   ROS↑, 2,   i-ROS?, 1,   xCT↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP?, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,   HK2↓, 1,   LDHA↓, 1,   PKM2↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   ASK1↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   Casp3↑, 2,   Casp8↑, 1,   Cyt‑c↝, 1,   JNK↑, 1,   p‑p38↑, 1,   survivin↓, 1,   Telomerase↓, 1,  

Transcription & Epigenetics ⓘ

other?, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↓, 1,   GRP78/BiP↓, 1,   HSP27↑, 1,  

Autophagy & Lysosomes ⓘ

LAMP2↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,   DNArepair↓, 4,  

Cell Cycle & Senescence ⓘ

P21↑, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,   HDAC↓, 2,   IGFBP3↑, 1,  

Migration ⓘ

FAK↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

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

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 3,   eff↑, 1,   RadioS↓, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

AR↓, 1,  
Total Targets: 46

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS∅, 1,  

Functional Outcomes ⓘ

toxicity↓, 1,  
Total Targets: 2

Scientific Paper Hit Count for: DNArepair, DNA repair
2 Phenylbutyrate
1 Sulfasalazine
1 Radiotherapy/Radiation
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

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