DNArepair Cancer Research Results
DNArepair, DNA repair: Click to Expand ⟱
| Source: HalifaxProj(enhance) |
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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.
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Scientific Papers found: Click to Expand⟱
ChemoSen↑, Beta-Caryophyllene (BCP), was highlighted in several recent preclinical studies to enhance chemo-sensitization in chemo-resistant tumors and to efficiently inhibit angiogenesis and cancer cells’ ability to invade and metastasize.
angioG↓,
TumCI↓,
TumMeta↓,
ROS↑, BCP seems to work as a dual modulator of oxidative stress, increasing reactive oxygen species (ROS) in cancer cells, and thus enhancing apoptosis, but reducing ROS in normal cells to protect them from damage
*ROS↓,
chemoP↑,
CB2 / CNR2↑, important issue in BCP is its ability to bind to the body’s cannabinoid receptor 2 (CB2), where it binds selectively to the CB2 receptors and not the CB1 receptor, which makes it non-psychoactive and therapeutically appealing.
Inflam↓, activation of the CB2 receptor by BCP can suppress pro-inflammatory cytokines production, helping to create an anti-tumor immune environment
AntiTum↑,
*BioAv↑, Beta-Caryophyllene, a food additive approved by the Food and Drug Administration, is efficiently absorbed in the gastro-intestinal tract and can penetrate the blood–brain barrier and has a well-established safety profile, making it an attractive biom
*BBB↑,
Apoptosis↑, Induces apoptosis and suppresses proliferative activity of lung cancer cells
TumCP↑,
TumCCA↑, Induces G1 cell cycle arrest by dysregulating cyclins and other molecules
RadioS↑, GBM: Works as a potential radiosensitizer for improving RT outcomes by inhibiting DNA repair, inducing apoptosis, and suppressing anti-apoptotic and survival pathways
DNArepair↓,
ROS↑, BC: Enhances sensitization and promotes the cigarette smoke condensate (CSC)-induced apoptosis in MDA-MB-468 cells, mainly by triggering oxidative stress and inhibition of STAT3
STAT3↓,
*BioEnh↑, BCP is considered a key component in black pepper’s ability to enhance nutrient absorption, including compounds like curcumin.
Pain↓, BCP in cloves further supports their role in pain management and infection prevention.
AntiBio↓,
ROS↑, selectively induce apoptosis and oxidative stress in cancer cells while sparing normal cells at lower concentrations.
Dose↝, I50, for many cancer cell lines typically ranges from 19 to 64 μM
NF-kB↓, Beta-Caryophyllene was reported to inhibit the central to the regulators of inflammation, NF-κB and MAPK pathways, leading to a decrease in pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6) production
MAPK↓,
TNF-α↓,
IL1β↓,
IL6↓,
cl‑PARP↑, through increasing the levels of cleaved PARP, caspases and Bax, and the downregulation of Bcl-2, directly by interaction with CB2.
Casp↑,
BAX↑,
Bcl-2↓,
VEGF↓, BCP blocks migration of endothelial cells by inhibiting the secretion of VEGF, and thus blocking the activity of the tyrosine kinase VEGFR2
VEGFR2↓,
MMP2↓, BCP can also prohibit the secretion of MMP-2, p-p38 and p-ERK
p‑p38↓,
p‑ERK↓,
EPR↑, BCP was suggested to accumulate in the cancer cell membrane, altering the cells’ permeability, leading to the accumulation of anticancer drugs, and consequently strengthening the drugs’ activity.
P-gp↓, direct inhibition of P-glycoprotein (P-gp/ABCB1) and multidrug resistance-associated protein 1 (MRP1/ABCC1), which are overexpressed in resistant tumors
MRP1/ABCC1↓,
*NRF2↑, Importantly, BCP’s selective antioxidant activity—activating Nrf2 in normal cells while increasing ROS in cancer cells—minimizes off-target toxicity,
*antiOx↑,
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.
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in-vitro, |
BC, |
MCF7 |
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in-vitro, |
BC, |
MDA-MB-468 |
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in-vitro, |
Nor, |
MCF10 |
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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
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in-vivo, |
Melanoma, |
B16-F10 |
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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
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 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:
NA, unassigned(tgid=0) ⓘ
AntiBio↓, 1,
Redox & Oxidative Stress(tgid=1) ⓘ
GSH↓, 1, H2O2↑, 1, ROS↑, 5, i-ROS?, 1, xCT↓, 1,
Mitochondria & Bioenergetics(tgid=3) ⓘ
MMP?, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
Glycolysis↓, 1, HK2↓, 1, LDHA↓, 1, PKM2↓, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↑, 2, ASK1↑, 1, BAX↑, 2, Bcl-2↓, 2, Casp↑, 2, Casp3↑, 2, Casp8↑, 1, Cyt‑c↝, 1, JNK↑, 1, MAPK↓, 1, p‑p38↓, 1, p‑p38↑, 1, survivin↓, 1, Telomerase↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other?, 1,
Protein Folding & ER Stress(tgid=8) ⓘ
CHOP↑, 1, ER Stress↓, 1, GRP78/BiP↓, 1, HSP27↑, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
LAMP2↑, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1, DNArepair↓, 5, cl‑PARP↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
P21↑, 1, TumCCA↑, 4,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↑, 1, p‑ERK↓, 1, HDAC↓, 2, IGFBP3↑, 1, STAT3↓, 1,
Migration(tgid=13) ⓘ
FAK↓, 1, MMP2↓, 1, TumCI↓, 1, TumCP↑, 1, TumMeta↓, 2,
Angiogenesis & Vasculature(tgid=14) ⓘ
angioG↓, 2, EPR↑, 1, Hif1a↓, 1, VEGF↓, 2, VEGFR2↓, 1,
Barriers & Transport(tgid=15) ⓘ
P-gp↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
CB2 / CNR2↑, 1, IL1β↓, 1, IL6↓, 1, Inflam↓, 1, NF-kB↓, 1, TNF-α↓, 1,
Hormonal & Nuclear Receptors(tgid=20) ⓘ
AR↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
ChemoSen↑, 1, Dose↝, 4, eff↑, 1, MRP1/ABCC1↓, 1, RadioS↓, 1, RadioS↑, 1, selectivity↑, 2,
Clinical Biomarkers(tgid=22) ⓘ
AR↓, 1, IL6↓, 1,
Functional Outcomes(tgid=23) ⓘ
AntiTum↑, 1, chemoP↑, 1, Pain↓, 1,
Total Targets: 71
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, NRF2↑, 1, ROS↓, 1, ROS∅, 1,
Barriers & Transport(tgid=15) ⓘ
BBB↑, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 1, BioEnh↑, 1,
Functional Outcomes(tgid=23) ⓘ
toxicity↓, 1,
Total Targets: 8
Scientific Paper Hit Count for: DNArepair, DNA repair
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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