Radiotherapy/Radiation Cancer Research Results
Rad, Radiotherapy/Radiation: Click to Expand ⟱
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Treatment of disease with radiation, especially by selective irradiation with x-rays or other ionizing radiation and by ingestion of radioisotopes.
Radiosensitizer
Atorvaqone, (mitochondria inhibitor) decrease O2 consumption making more O2 available as a radiosensitizer.
-Hypoxia (low oxygen levels) within tumors is a major cause of resistance to radiotherapy
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Scientific Papers found: Click to Expand⟱
ChemoSen↑, combination of 2DG and ionizing radiation resulted in greater inhibition of tumor growth and increased survival, relative to either agent alone
GlucoseCon↓,
ROS↑,
ATP↓, ATP production was severely inhibited in cancer cells treated with same concentration of 3-BP
HK2↓, It exerts potent anticancer effects by inhibiting hexokinase II enzyme of glycolysis pathway and ATP generation in cancer cells.
RadioS↑, We also observed that 3-BP in combination with low doses of irradiation was more effective in killing cancer cells than 3-BP alone.
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
BC, |
MDA-MB-468 |
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Glycolysis↓, Metabolomic analyses showed that 3BP causes inhibition of glycolysis
RadioS↑, Overall, MCT1-mediated metabolic perturbation in combination with radiotherapy is shown to be a promising strategy for the treatment of glycolytic tumors such as TNBC, overcoming the selectivity challenges of targeting glycolysis with glucose analogs
eff↑, 3BP is selectively toxic to cells expressing MCT1
GAPDH↓, 3BP inhibits GAPDH but not hexokinase
PPP↑, Pentose phosphate pathway is upregulated in response to 3BP
GSH↓, Glutathione and NADH are depleted at early time points
ECAR↓, prolonged incubation with 20 μM 3BP for 24 h resulted in a statistically significant selective decrease in ECAR
Apoptosis↑, higher rate of apoptotic cell death
TumAuto↑,
eff↑, Asharani et al compared the toxicity between 3–10 nm Pt, 5–35 nm Ag, and 15–35 nm Au NPs covered with PVA, and concluded that Ag NPs were the most toxic,
ROS↑, been suggested by different biological studies that they can produce ROS, and therefore can affect the concentration of intracellular calcium, activate transcription factors, and induce cytokine production
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in-vitro, |
BC, |
MCF7 |
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in-vitro, |
Ovarian, |
SKOV3 |
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in-vitro, |
GBM, |
U87MG |
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in-vitro, |
Melanoma, |
A431 |
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RadioS↑, Here, we, for the first time, present the results of the radiosensitizing properties of silver nanoparticles (AgNPs) (possessing low toxicity towards human body) against cancer cells under neutron irradiation.
ROS↑, The mechanism of AgNPs anticancer (intrinsic) effect includes oxidative stress, cell cycle arrest and apoptosis, activate endoplasmic reticulum stress, modulate various signaling pathways, etc
TumCCA↑,
Apoptosis↑,
ER Stress↑,
RadioS↑, silver nanoparticles (AgNPs) as radiation sensitizers and chitosan as a nanocarrier to deliver metformin to breast cancer cells.
DNAdam↑, 1.8-fold increase in DNA damage in cells pretreated with Met NPs and Ag NPs upon exposure to radiation.
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in-vitro, |
BC, |
MCF7 |
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in-vitro, |
Nor, |
MCF10 |
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
BC, |
BT549 |
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in-vivo, |
BC, |
MDA-MB-231 |
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ROS↑, AgNPs is known to cause dose-dependent toxicities, including induction of oxidative stress and DNA damage, which can lead to cell death.
DNAdam↑,
selectivity↑, We show that AgNPs are highly cytotoxic toward TNBC cells at doses that have little effect on nontumorigenic breast cells or cells derived from liver, kidney, and monocyte lineages.
TumCG↓, reduce TNBC growth and improve radiation therapy.
RadioS↑,
Dose↝, s 23±14 nm: particles were diluted to 40 μg/mL. 25 μg/mL AgNP dilution for 24 hours. zeta potential of AgNPs in water at pH 7 was approximately −36 mV, indicating good colloidal stability.
selectivity↑, Depending on AgNP dose, all three TNBC cell lines were 5- to 10-fold more sensitive to AgNP exposure than the nontumorigenic breast cells.
other↝, this study demonstrate that the cytotoxicity was dependent on exposure of cells to intact AgNPs and not due to Ag+ ions
eff↓, toxicity of AgNPs was significantly reduced in MDA-MB-231, MCF-7, and MCF-10A cells following pretreatment with GSH
eff↑, Selective depletion of GSH by BSO resulted in increased AgNP toxicity in all cell lines.
γH2AX↑, AgNPs significantly increased γH2AX in these cells compared to radiation alone.
Dose↓, Strikingly, an AgNP dose of as little as 1 μg/mL resulted in a dose enhancement of IR treatment (approximately 2-fold at the 2 Gy dose) f
eff↑, Moreover, intratumoral injection of AgNPs with or without radiation treatment can inhibit the growth of TNBC xenografts in mice
RadioS↑, AgNPs showed both radio and thermo sensitivity on U251 cells from the surviving fraction curve.
eff↑, both X-rays and heat could enhance the content of cells uptake of AgNPs.
TumCD↑, potential application in enhancing effect of RT with MHT combination therapy induced killing of cancer cells.
OS↑,
OS↑, 500% improvement
TumAuto↑,
ROS↑,
Apoptosis↑,
TumAuto↑, enhanced destructive autophagy
RadioS↑, allicin improves the sensitivity of X-ray radiotherapy in CRC, and its mechanism may be associated with inhibition of NF-κB signaling pathway.
NF-kB↓,
*ICAM-1↓, Allicin significantly inhibited gamma IR-induced surface expression of ICAM-1 and ICAM mRNA in a dose-dependent manner.
*AP-1↓, pretreatment with allicin resulted in the decrease of AP-1 activation and phosphorylation of the c-Jun NH2-terminal kinase (JNK) induced by gamma IR.
*p‑cJun↓,
*radioP↑, may be considered in therapeutic strategies for the management of patients treated with radiation therapy
JNK↓, downregulates gamma IR-induced ICAM-1 expression via inhibition of both AP-1 activation and the JNK pathway
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in-vitro, |
BC, |
MDA-MB-231 |
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Apoptosis↑,
P53↑,
p38↑,
NF-kB↑, NF-κB were significantly increased in the ALA+RT group compared to the control
TumCCA↑, G2/M cell cycle arrest.
*radioP↑, radio-protective role of alpha-lipoic acid.
*antiOx↑, Alpha-lipoic acid has anti-oxidant, anti-apoptosis, anti-inflammatory actions, etc.
*Inflam↓,
radioP↑, apigenin's radioprotective and radiosensitive properties
RadioS↑,
*COX2/PTGS2↓, When exposed to irradiation, apigenin reduces inflammation via cyclooxygenase-2 inhibition and modulates proapoptotic and antiapoptotic biomarkers.
*ROS↓, Apigenin's radical scavenging abilities and antioxidant enhancement mitigate oxidative DNA damage
VEGF↓, It inhibits radiation-induced mammalian target of rapamycin activation, vascular endothelial growth factor (VEGF), matrix metalloproteinase-2 (MMP), and STAT3 expression,
MMP2↓,
STAT3↓,
AMPK↑, while promoting AMPK, autophagy, and apoptosis, suggesting potential in cancer prevention.
Apoptosis↑,
MMP9↓, radiosensitizer, apigenin inhibits tumor growth by inducing apoptosis, suppressing VEGF-C, tumor necrosis factor alpha, and STAT3, reducing MMP-2/9 activity, and inhibiting cancer cell glucose uptake.
glucose↓,
*radioP↑, Withaferin A (WA) protected only normal lymphocytes, but not cancer cells, against IR-induced apoptosis
selectivity↑,
*Casp3↓, WA treatment led to significant inhibition of IR-induced caspase-3 activation and decreased IR-induced DNA damage to lymphocytes and bone-marrow cells.
*DNAdam↓,
*ROS↓, WA reduced intracellular ROS and GSH levels
*GSH↓,
*NRF2↑, WA induced pro-survival transcription factor, Nrf-2, and expression of cytoprotective genes HO-1, catalase, SOD, peroxiredoxin-2 via ERK.
*HO-1↑,
*Catalase↑,
*SOD↑,
*Prx↑,
*ERK↑, Activated ERK promotes the nuclear translocation and activity of Nrf2
tumCV↓, ATX inhibited viability of OSCC cells but not NHOK.
selectivity↑,
RadioS↑, In OSCC cells, ATX further enhanced the cell death induced by IR.
GPx4↓, ATX could synergize with IR, further inhibiting GPX4, SLC7A11 and promoting ACSL4 in OSCC cells.
Ferroptosis↑, ATX might synergize with IR treatment in OSCC partly via ferroptosis.
*radioP↑, First, with a mice model of RILI, the protected effects of astaxanthin were observed
Inflam↓, and reduces the elevation of inflammatory factors.
Apoptosis↑, ATV increased the percentage of apoptotic cells in irradiated breast and lung cancer cells.
RadioS↑, demonstrates that ATV has radiosensitizing effect on breast and lung cancer cells through increasing apoptosis, ROS production and cell death induced by IR.
TumCP↓, ATV exhibited anti-proliferative effect on cancer cells and increased cell death induced by IR.
ROS↑, ATV increased ROS production in irradiated cells.
radioP↑, Treatment with pravastatin for 24 hours after irradiation reduced the loss of endothelium‐dependent vasorelaxation and protected against enhanced vasoconstriction.
radioP↑, Treatment with pravastatin for 1 year after irradiation completely reversed irradiation‐induced changes.
radioP↑, conclude that the prophylactic use of Aloe vera reduces the intensity of radiationinduced dermatitis.
Dose↝, about two thirds of patients diagnosed with cancer are treated with radiotherapy. Acute dermatitis is a common side effect of radiation therapy, occurring in about 95% of patients treated with this modality
eff↑, The effect was more evident in patients undergoing radiotherapy with larger treatment fields and higher doses of radiation.
*radioP↑, Baicalein rebalances gut microbial composition pattern destroyed by irradiation. upport the potential of baicalein as a radioprotective medicine
GutMicro↑,
*P53↓, baicalein inhibited the activation of p53 and p53 mediated mitochondrial apoptosis and death receptor apoptosis in the intestine.
*Apoptosis↑,
*DR4↓,
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in-vitro, |
BC, |
MDA-MB-231 |
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in-vitro, |
BC, |
MCF7 |
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RadioS↑, BRF induced radiosensitization in all cells under 6 MV photon beam (SER of 1.06 to 1.35), and MDA-MB-231 cells only under 6 MeV electron beam (SER = 1.20)
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in-vitro, |
ESCC, |
Eca109 |
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in-vitro, |
ESCC, |
KYSE150 |
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12LOX↓, increased by 12-LOX upregulation but was suppressed by the well-established 12-LOX inhibitor, baicalein
RadioS↑, In prostate cancer cells, 12-LOX inhibition has been shown to increase radiation sensitivity,
Dose↝, Additionally, 12-LOX expression was significantly inhibited at 40 µmol/L
RANTES↓, post-radiotherapy protein levels of CCL5 increased in Eca109 and Kyse150 cells but were inhibited by baicalein
MCP1/CCL2↓, Baicalein, a recognized inhibitor of 12-LOX, successfully inhibited CCL2 and CCL5 expression, which was verified by RT-qPCR.
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in-vitro, |
ESCC, |
KYSE150 |
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TumCP↓, Radiation combined with baicalein could significantly inhibit the proliferation and migration of esophageal cancer cells compared with that of 6 Gy rays alone
TumCMig↓,
Glycolysis↓, 20μM baicalein reduced glycolysis in KYSE150 cells
cycD1/CCND1↓,
CDK4↓,
ECAR↓, Baicalein reduces ECAR and glycoPER
TumCCA↑, baicalein arrested cells in the G1 phase of the cell cycle
HK1↓, HK1 (4QS9),13 ALDH2, GPI and ALDOA are the key enzymes in the process of glycolysis.
ALDH↓,
ALDOA↓,
PKM2↓, protein levels of HIF-1A and PKM2 decreased significantly after baicalein treatment.
Hif1a↓,
*ROS↓, normal cells
*MDA↓, normal cells
*TNF-α↓, normal cells
*TGF-β↓, TGF-β1 normal cells
*IL10↑, normal cells
ROS↑, cancer cells
DNAdam↑, cancer cells
mtDam↑, cancer cells
MMP↓, cancer cells
Apoptosis↑, cancer cells
TumCCA↑, cancer cells
Hif1a↓, cancer cells
VEGF↓, cancer cells
RadioS↑, revealed radiosensitizing properties
RadioS↑, cytotoxic effect of the combination of berberine and irradiation was superior to that of berberine or irradiation alone
Apoptosis↑,
ROS↑, ROS generation was elevated by berberine with or without irradiation.
eff↑, antioxidant NAC inhibited berberine and radiation-induced cell death.
BAX↑,
Casp3↑,
P53↑,
p38↑,
JNK↑,
Bcl-2↓,
ERK↓,
HO-1↓,
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in-vitro, |
Ovarian, |
SKOV3 |
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RadioS↑, berberine might be a capable radiosensitizer for treating SKOV-3, because of oxidative DNA damage
ROS↑,
GSH↓, decreased level of (GSH) content supported the elevated ROS generation data
Apoptosis↑,
tumCV↓, IR and berberine treatment decreased the viability of MCF-7 spheroids and reduced OCT4 and SOX2 genes expression.
OCT4↓,
SOX2↓,
RadioS↑, Berberine has a radiosensitizing effect through targeting cancer stem cells
CSCs↓,
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in-vitro, |
Liver, |
SMMC-7721 cell |
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in-vitro, |
Nor, |
HL7702 |
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*toxicity↓, Berberine (Ber), an isoquinolin alkaloid with low toxicity and protective effects against radiotherapy
radioP↑,
BioAv↑, We preloaded Ber into folic acid targeting Janus gold mesoporous silica nanocarriers (FA-JGMSNs) for overcoming the poor bioavailability of Ber.
AntiTum↑, highly efficient anti-tumor effect, good biosafety
selectivity↑, as well as the effective protection of normal tissue of this nanoplatform.
eff↑, These selective distributions of Ber in cancer cells and normal cells originated from selective endocytosis as well as pH-responsive drug release, which were conducive to achieving an improved therapeutic effect of Ber.
chemoP↑, Notably, chemo/radio/photothermal therapeutics didn’t cause the amounts of deaths of HL-7702 cells, indicating an excellent biosafety of the triple-model therapy.
TumCG↓, Betulinic acid strongly and consistently suppressed the growth and colony-forming ability of all human melanoma cell lines investigated.
RadioS↑, In combination with ionizing radiation the effect of betulinic acid on growth inhibition was additive in colony-forming assays.
Apoptosis↑, Betulinic acid also induced apoptosis in human melanoma cells as demonstrated by Annexin V binding and by the emergence of cells with apoptotic morphology
selectivity↑, growth-inhibitory action of betulinic acid was more pronounced in human melanoma cell lines than in normal human melanocytes.
RadioS↑, We found that borneol administration along with radiotherapy significantly inhibited the growth of primary glioma cells in vitro and in vivo.
Beclin-1↑, coincided with increased expression of beclin-1 and LC3.
Hif1a↓, And the combination of borneol and radiation exposure significantly decreased the expression levels of HIF-1α, mTORC1 and eIF4E.
mTORC1↓,
EIF4E↓,
TumAuto↑, Our findings suggest that borneol sensitizes glioma cells to radiation by inducing autophagy via inhibition of the mTORC1/eIF4E/HIF-1α regulatory axis.
Risk↓, Increased groundwater boron concentrations, across the state of Texas, correlate with reduced risk of prostate cancer incidence and mortality.
TumCMig↓, boric acid improves the anti-proliferative effectiveness of chemo-preventative agents, selenomethionine and genistein, while enhancing ionizing radiation cell kill
Bcl-2↓,
Dose↝, treatment with micro-encapsulated sodium butyrate (MESB) (3 tablets/day). (600 mg of butyrate), a dosage recommended by the manufacturer (Butyrose® Lsc Microcaps-EP2352386B1, BLM, Sila Srl, Noale (VE), Italy).
radioP↑, MESB appears effective in reducing radiation-induced bowel toxicity during RT, minimizing stool changes, incontinence, and abdominal pain.
Pain↓,
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vitro+vivo, |
BC, |
MCF7 |
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NA, |
Liver, |
HepG2 |
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RadioS↑, Combined treatment of ZnO-CA NPs with γ-irradiation improved these effects.
TumVol↓, ZnO-CA NPs resulted in a considerable decline in tumor size and weight, down-regulation of B-cell lymphoma 2 (BCL2) and nuclear factor kappa B (NF-κB) gene expressions, decreased vascular cell adhesion molecule 1 (VCAM-1) level
Bcl-2↓,
NF-kB↓,
VCAM-1↓,
ERK↓, ownregulation of phosphorylated-extracellular-regulated kinase 1 and 2 (p-ERK1/2) protein expression, DNA fragmentation and a recognizable peak at sub-G0/G1 indicating dead cells’ population in cancer tissues.
DNAdam↑,
TumCCA↑,
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in-vivo, |
BC, |
MDA-MB-231 |
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tumCV↓, Cell viability decreased upon CAPE treatment in a dose dependent manner (IC50 53.5 ± 33.7 µM)
eff⇅, CAPE sensitized only p53 mutated or deficient cell lines to radiotherapy (p < 0.05), but not p53 proficient lines.
RadioS↑,
OS↑, Combination of radiotherapy and CAPE resulted in increased survival (22 days) compared to control
RadioS↑, Potentiation of radiation therapy in mice bearing a transplanted mouse mammary tumor (MTG-B) is reported as a supra-additive tumor growth delay when 60 mg/kg carboplatin is administered either 30 minutes before or immediately after 20 Gy of X-irradia
RadioS↑, ethanol extract of Centella asiatica: asiatic acid (1), madecassic acid (2), and asiaticoside (3). These compounds inhibited the ionizing radiation-induced migration and invasion of A549 human lung cancer cells at noncytotoxic concentrations.
OS↑, In elderly platinum-unfit patients, Cetuximab + RT treatment represents a valid option, associated with a reasonable survival rate at the cost of mostly manageable toxicity.
RadioS↓, CGA might be a potential tumor-protective compound upon irradiation and reduce the efficacy of radiotherapy via ROS scavenging and Nrf2 activation.
ROS↓,
NRF2↑,
RadioS↑, enhancement of the anticancer effects of chrysin upon exposure to gamma irradiation
ROS↑, excessive production of included reactive oxygen species, the dissipation of the mitochondrial membrane potential, regulation of the B cell lymphoma-2 family, activation of caspase-9, 3, and cleavage of poly (adenosine diphosphate-ribose) polymerase.
MMP↓,
Casp3↑,
Casp9↑,
cl‑PARP↑,
tumCV↓, Both crocin and eugenol independently decreased OSCC cell viability and triggered apoptosis in a dose-dependent way.
RadioS↑, When used with IR, they worked together to boost cytotoxicity at moderate doses (CI < 1).
TumCCA↑, Crocin caused early G1 arrest followed by G2/M accumulation, while eugenol strongly induced G2/M arrest and increased sub-G1 fractions.
BAX↑, activation of the intrinsic apoptotic pathway (↑Bax, ↑Caspase-3, ↓Bcl-2) and reduced levels of Cyclin A/B transcripts.
Casp3↑,
Bcl-2↓,
cycA1/CCNA1↓,
CycB/CCNB1↓,
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in-vitro, |
Cerv, |
HeLa |
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in-vitro, |
Laryn, |
FaDu |
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selectivity↑, previously demonstrated that curcumin radiosensitizes cervical tumor cells without increasing the cytotoxic effects of radiation on normal human fibroblasts
RadioS↑,
TrxR↓, inhibitory activity of curcumin on the anti-oxidant enzyme Thioredoxin Reductase-1 (TxnRd1) is required for curcumin-mediated radiosensitization of squamous carcinoma cells
ROS↑, induced reactive oxygen species
ERK↑, sustained ERK1/2 activation
Dose∅, Curcumin treatment resulted in a dose-dependent decrease in TxnRd activity with an IC50 of approximately 10 µM in both cell lines
cl‑PARP↑, curcumin induced a robust increase in cleaved PARP
RadioS↑, Although curcumin can sensitize cancer cells to irradiation, healthy cells are much less sensitive to this effect, and thus, curcumin is thought to be a potent, yet safe anti-cancer agent
*radioP↑, curcumin has been found to possess radioprotective properties, since it can lessen inflammatory toxicities associated with radiotherapy, like dermatitis, mucositis, and myelosuppression
EGFR↓, Curcumin can suppress the gene expression of EGFR, and downregulate the TGF-β pathway, thus leading to inhibition of cancer-associated fibroblasts (CAF)
TGF-β↓,
ROS↑, Curcumin can induce ROS generation and suppress DNA repair machinery, thus leading to increased radiation-induced cell death
P53↑, upregulation of both the expression and activity of p53, regulation of the anti-apoptotic PI3K signaling, and suppression of the activity of NF-κB and COX-2
PI3K↓,
NF-kB↓, curcumin increased radiation-induced apoptotic death primarily through inhibition of the NF-κB signaling pathway
COX2/PTGS2↓,
EMT↓, Curcumin was found to suppress radiation-induced EMT resulting in the inhibition of NSCLC migration and invasion
Hif1a↓, inhibition of the expression of both hypoxia-inducible factor 1-alpha (HIF-1a) and heat shock protein 90 (HSP90) proteins and increase in the levels of ROS
HSP90↓,
mTOR↓, In cervical cancer, curcumin has been studied as a potent mTOR inhibitor when given together with irradiation.
*Catalase↑, 40 rats were exposed to curcumin 1 day before irradiation to 3 consecutive days after irradiation, the levels of antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD), and malondialdehyde (MDA), were found to be considerably eleva
*SOD↑,
*MDA↑,
*Wound Healing↑, treatment with curcumin stimulated wound healing,
*hepatoP↑, curcumin treatment prior to radiation can prevent liver damages, mainly through the modulation of the NF-κB pathway and reduction of oxidative stress (upregulation of SOD, CAD and GSH levels in the curcumin-treated group)
*NF-kB↓,
*ROS↓,
ChemoSen↑, Such effects of curcumin were due to its ability to sensitize cancer cells for increased production of ROS
NF-kB↓, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF-κB, STAT3, COX2, Akt
*STAT3↓, curcumin acts as a chemosensitizer and radiosensitizer has also been studied extensively. For example, it downregulates various growth regulatory pathways and specific genetic targets including genes for NF-kB, STAT3, COX2, Akt,
*COX2/PTGS2↓,
*Akt↓,
*NRF2↑, The protective effects of curcumin appear to be mediated through its ability to induce the activation of NRF2 and induce the expression of antioxidant enzymes (e.g., hemeoxygenase-1, glutathione peroxidase
*HO-1↑,
*GPx↑,
*NADPH↑,
*GSH↑, increase glutathione (a product of the modulatory subunit of gamma-glutamyl-cysteine ligase)
*ROS↓, dietary curcumin can inhibit chemotherapy-induced apoptosis via inhibition of ROS generation and blocking JNK signaling
*p300↓, inhibit p300 HAT activity
radioP↑, radioprotector for normal organs
chemoP↑, curcumin has also been shown to protect normal organs such as liver, kidney, oral mucosa, and heart from chemotherapy and radiotherapy-induced toxicity.
RadioS↑,
eff↑, As compared to its parent molecule curcumin, DIMC showed a very potent radiosensitizing effect as seen by clonogenic survival assay.
ROS↑, significant increase in cellular ROS
GSH/GSSG↓, decrease in GSH to GSSG ratio
TrxR↓, inhibition of thioredoxin reductase enzyme by DIMC
selectivity↑, DIMC can synergistically enhance the cancer cell killing when combined with radiation by targeting thioredoxin system.
survivin↓, In the group treated with curcumin + radiation, 15 (75%) patients had decreased survivin levels, and 5 (25%) patients had increased survivin levels.
RadioS↑, curcumin is an effective, alternative radiosensitizer agent for application in cervical cancer treatment.
toxicity↓, One advantage to curcumin is its low risk of side effects compared with other radiosensitizers. Up to 12 g of curcumin per day does not cause side effects in patients
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 137
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
Ferroptosis↑, 1, GPx4↓, 1, GSH↓, 2, GSH/GSSG↓, 1, HK1↓, 1, HO-1↓, 1, NRF2↑, 1, ROS↓, 1, ROS↑, 13, TrxR↓, 2,
Mitochondria & Bioenergetics(tgid=3) ⓘ
ATP↓, 1, MMP↓, 2, mtDam↑, 1,
Core Metabolism/Glycolysis(tgid=4) ⓘ
12LOX↓, 1, ALDOA↓, 1, AMPK↑, 1, ECAR↓, 2, GAPDH↓, 1, glucose↓, 1, GlucoseCon↓, 1, Glycolysis↓, 2, HK2↓, 1, PKM2↓, 1, PPP↑, 1,
Cell Death(tgid=5) ⓘ
Apoptosis↑, 10, BAX↑, 2, Bcl-2↓, 4, Casp3↑, 3, Casp9↑, 1, Ferroptosis↑, 1, JNK↓, 1, JNK↑, 1, p38↑, 2, survivin↓, 1, TumCD↑, 1,
Transcription & Epigenetics(tgid=7) ⓘ
other↝, 1, tumCV↓, 4,
Protein Folding & ER Stress(tgid=8) ⓘ
ER Stress↑, 1, HSP90↓, 1,
Autophagy & Lysosomes(tgid=9) ⓘ
Beclin-1↑, 1, TumAuto↑, 4,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↑, 4, P53↑, 3, cl‑PARP↑, 2, γH2AX↑, 1,
Cell Cycle & Senescence(tgid=11) ⓘ
CDK4↓, 1, cycA1/CCNA1↓, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 1, TumCCA↑, 6,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ALDH↓, 1, CSCs↓, 1, EIF4E↓, 1, EMT↓, 1, ERK↓, 2, ERK↑, 1, mTOR↓, 1, mTORC1↓, 1, OCT4↓, 1, PI3K↓, 1, SOX2↓, 1, STAT3↓, 1, TumCG↓, 2,
Migration(tgid=13) ⓘ
MMP2↓, 1, MMP9↓, 1, TGF-β↓, 1, TumCMig↓, 2, TumCP↓, 2, VCAM-1↓, 1,
Angiogenesis & Vasculature(tgid=14) ⓘ
EGFR↓, 1, Hif1a↓, 4, VEGF↓, 2,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 1, Inflam↓, 1, MCP1/CCL2↓, 1, NF-kB↓, 4, NF-kB↑, 1, RANTES↓, 1,
Drug Metabolism & Resistance(tgid=21) ⓘ
BioAv↑, 1, ChemoSen↑, 2, Dose↓, 1, Dose↝, 4, Dose∅, 1, eff↓, 1, eff↑, 9, eff⇅, 1, RadioS↓, 1, RadioS↑, 28, selectivity↑, 8,
Clinical Biomarkers(tgid=22) ⓘ
EGFR↓, 1, GutMicro↑, 1,
Functional Outcomes(tgid=23) ⓘ
AntiTum↑, 1, chemoP↑, 2, OS↑, 4, Pain↓, 1, radioP↑, 7, Risk↓, 1, toxicity↓, 1, TumVol↓, 1,
Total Targets: 99
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress(tgid=1) ⓘ
antiOx↑, 1, Catalase↑, 2, GPx↑, 1, GSH↓, 1, GSH↑, 1, HO-1↑, 2, MDA↓, 1, MDA↑, 1, NRF2↑, 2, Prx↑, 1, ROS↓, 5, SOD↑, 2,
Core Metabolism/Glycolysis(tgid=4) ⓘ
NADPH↑, 1,
Cell Death(tgid=5) ⓘ
Akt↓, 1, Apoptosis↑, 1, Casp3↓, 1, DR4↓, 1,
Transcription & Epigenetics(tgid=7) ⓘ
p‑cJun↓, 1,
DNA Damage & Repair(tgid=10) ⓘ
DNAdam↓, 1, P53↓, 1,
Proliferation, Differentiation & Cell State(tgid=12) ⓘ
ERK↑, 1, p300↓, 1, STAT3↓, 1,
Migration(tgid=13) ⓘ
AP-1↓, 1, TGF-β↓, 1,
Immune & Inflammatory Signaling(tgid=16) ⓘ
COX2/PTGS2↓, 2, ICAM-1↓, 1, IL10↑, 1, Inflam↓, 1, NF-kB↓, 1, TNF-α↓, 1,
Functional Outcomes(tgid=23) ⓘ
hepatoP↑, 1, radioP↑, 6, toxicity↓, 1, Wound Healing↑, 1,
Total Targets: 35
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#:201 Target#:% State#:% Dir#:%
wNotes= sortOrder:rid,rpid
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