condition found tbRes List
CUR, Curcumin: Click to Expand ⟱
Features:
Curcumin is the main active ingredient in Tumeric. Member of the ginger family.Curcumin is a polyphenol extracted from turmeric with anti-inflammatory and antioxidant properties.
- Has iron-chelating, iron-chelating properties. Ferritin. But still known to increase Iron in Cancer cells.
- GSH depletion in cancer cells, exhaustion of the antioxidant defense system. But still raises GSH↑ in normal cells.
- Higher concentrations (5-10 μM) of curcumin induce autophagy and ROS production
- Inhibition of TrxR, shifting the enzyme from an antioxidant to a prooxidant
- Strong inhibitor of Glo-I, , causes depletion of cellular ATP and GSH
- Curcumin has been found to act as an activator of Nrf2, (maybe bad in cancer cells?), hence could be combined with Nrf2 knockdown

Clinical studies testing curcumin in cancer patients have used a range of dosages, often between 500 mg and 8 g per day; however, many studies note that doses on the lower end may not achieve sufficient plasma concentrations for a therapeutic anticancer effect in humans.
• Formulations designed to improve curcumin absorption (like curcumin combined with piperine, nanoparticle formulations, or liposomal curcumin) are often employed in clinical trials to enhance its bioavailability.

-Note half-life 6 hrs.
BioAv is poor, use piperine or other enhancers
Pathways:
- induce ROS production at high concentration. Lowers ROS at lower concentrations
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: GSH↓ Catalase↓ HO1↓ GPx↓
but conversely is known as a NRF2↑ activator in cancer
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, uPA↓, VEGF↓, NF-κB↓, CXCR4↓, SDF1↓, TGF-β↓, α-SMA↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓, Sp proteins↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, GLUT1↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, HK2↓, ECAR↓, OXPHOS↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓,
- inhibits Cancer Stem Cells : CSC↓, CK2↓, Hh↓, GLi1↓, CD133↓, CD24↓, β-catenin↓, n-myc↓, sox2↓, OCT4↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK, TrxR**,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells


Akt, PKB-Protein kinase B: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
Akt1 is involved in cellular survival pathways, by inhibiting apoptotic processes; Akt2 is an important signaling molecule in the insulin signaling pathway. It is required to induce glucose transport.

Inhibitors:
-Curcumin: downregulate AKT phosphorylation and signaling.
-Resveratrol
-Quercetin: inhibit the PI3K/AKT pathway.
-Epigallocatechin Gallate (EGCG)
-Luteolin and Apigenin: inhibit AKT phosphorylation


Scientific Papers found: Click to Expand⟱
463- CUR,    Curcumin induces autophagic cell death in human thyroid cancer cells
- in-vitro, Thyroid, K1 - in-vitro, Thyroid, FTC-133 - in-vitro, Thyroid, BCPAP - in-vitro, Thyroid, 8505C
TumAuto↑,
LC3II↑,
Beclin-1↑,
p‑p38↑,
p‑JNK↑,
p‑ERK↑, p-ERK1/2
p62↓,
p‑PDK1↓,
p‑Akt↓,
p‑p70S6↓,
p‑PIK3R1↓,
p‑S6↓,
p‑4E-BP1↓,

471- CUR,    Curcumin induces apoptotic cell death and protective autophagy by inhibiting AKT/mTOR/p70S6K pathway in human ovarian cancer cells
- in-vitro, Ovarian, SKOV3 - in-vitro, Ovarian, A2780S
Apoptosis↑,
TumAuto↑,
p62↓,
p‑Akt↓,
p‑mTOR↓,
p‑P70S6K↓,
Casp9↑,
PARP↑,
ATG3↑,
Beclin-1↑,
LC3‑Ⅱ/LC3‑Ⅰ↑,

476- CUR,    The effects of curcumin on proliferation, apoptosis, invasion, and NEDD4 expression in pancreatic cancer
- in-vitro, PC, PATU-8988 - in-vitro, PC, PANC1
TumCMig↓,
TumCI↓,
Apoptosis↑,
NEDD9↓,
p‑Akt↓,
p‑mTOR↓,
PTEN↑,
p73↑,
β-TRCP↑,

448- CUR,    Heat shock protein 27 influences the anti-cancer effect of curcumin in colon cancer cells through ROS production and autophagy activation
- in-vitro, CRC, HT-29
Apoptosis↑,
TumCCA↑, G2/M cell cycle arrest
p‑Akt↓,
Akt↓,
Bcl-2↓,
p‑BAD↓,
BAD↑,
cl‑PARP↑,
ROS↑,
HSP27↑,
Beclin-1↑,
p62↑,
GPx1↓,
GPx4↓,

452- CUR,    Curcumin downregulates the PI3K-AKT-mTOR pathway and inhibits growth and progression in head and neck cancer cells
- vitro+vivo, HNSCC, SCC9 - vitro+vivo, HNSCC, FaDu - vitro+vivo, HNSCC, HaCaT
TumCCA↑, arrested cell cycle at phase G2 /M
PI3k/Akt/mTOR↓,
Casp3↑,
EGFR↓, 0.18 fold
EGF↑, Curcumin induced a noticeable increase in the expression of EGF (11.3-fold change)
PRKCG↑, 13.2 fold
p‑Akt↓,
p‑mTOR↓,
RPS6KA1↓, 0.17 fold
EIF4E↓, 0.18 fold
proCasp3↓,

457- CUR,    Curcumin regulates proliferation, autophagy, and apoptosis in gastric cancer cells by affecting PI3K and P53 signaling
- in-vitro, GC, SGC-7901 - in-vitro, GC, BGC-823
TumCP↓,
Apoptosis↑,
TumAuto↑,
P53↑,
PI3K↓,
P21↑,
p‑Akt↓,
p‑mTOR↓,
Bcl-2↓,
Bcl-xL↓,
LC3I↓, LC3I
BAX↑,
Beclin-1↑,
cl‑Casp3↑,
cl‑PARP↑,
LC3II↑,
ATG3↑,
ATG5↑,

2654- CUR,    Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence
- Review, Var, NA
ROS↑, ROS induction has been implicated as one of the mechanisms of the anticancer activity of curcumin and its derivatives in various cancers
Catalase↓, Curcumin induces ROS by inhibiting the activity of various ROS-related metabolic enzymes, such as CAT, SOD1, glyoxalase 1, and NAD(P)H dehydrogenase [quinone] 1 [146,149]
SOD1↓,
GLO-I↓,
NADPH↓,
TumCCA↑, ROS accumulation further mediates G1 or G2/M cell cycle arrest [146,147,150,154], senescence [146], and apoptosis.
Apoptosis↑,
Akt↓, downregulation of AKT phosphorylation [145
ER Stress↑, endoplasmic reticulum stress (namely through the PERK–ATF4–CHOP axis)
JNK↑, activation of the JNK pathway [151],
STAT3↓, and inhibition of STAT3 [155].
BioAv↑, Additionally, the combination of curcumin and piperine, a pro-oxidative phytochemical that drastically increases the bioavailability of curcumin in humans

480- CUR,    Curcumin exerts its tumor suppressive function via inhibition of NEDD4 oncoprotein in glioma cancer cells
- in-vitro, GBM, SNB19
TumCP↓,
TumCMig↓,
Apoptosis↑,
TumCCA↑, G2/M phase
NEDD9↓,
NOTCH1↓,
p‑Akt↓,

485- CUR,  PDT,    Red Light Combined with Blue Light Irradiation Regulates Proliferation and Apoptosis in Skin Keratinocytes in Combination with Low Concentrations of Curcumin
- in-vitro, Melanoma, NA
NF-kB↓,
Casp8↑,
Casp9↑,
p‑Akt↓,
p‑ERK↓,

1485- CUR,  Chemo,  Rad,    Curcumin, the golden spice from Indian saffron, is a chemosensitizer and radiosensitizer for tumors and chemoprotector and radioprotector for normal organs
- Review, Var, NA
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↓,
*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↑,

152- CUR,    Anti-cancer activity of curcumin loaded nanoparticles in prostate cancer
- in-vivo, Pca, NA
β-catenin/ZEB1↓,
AR↓,
STAT3↓,
p‑Akt↓,
Mcl-1↓,
Bcl-xL↓,
cl‑PARP↑, cleavage
miR-21↓,
miR-205↑,

12- CUR,    Curcumin inhibits the Sonic Hedgehog signaling pathway and triggers apoptosis in medulloblastoma cells
- in-vitro, MB, DAOY
HH↓,
Shh↓,
Gli1↓,
PTCH1↓,
cMyc↓,
n-MYC↓,
cycD1↓,
Bcl-2↓,
NF-kB↓,
Akt↓,
β-catenin/ZEB1↓,
survivin↓,

15- CUR,  UA,    Effects of curcumin and ursolic acid in prostate cancer: A systematic review
NF-kB↝,
Akt↝,
AR↝,
Apoptosis↝,
Bcl-2↝,
Casp3↝,
BAX↝,
P21↝,
ROS↝,
Apoptosis↝,
Bcl-xL↝,
JNK↝,
MMP2↝,
P53↝,
PSA↝,
VEGF↝,
COX2↝,
cycD1↝,
EGFR↝,
IL6↝,
β-catenin/ZEB1↝,
mTOR↝,
NRF2↝,
p‑Akt↝,
AP-1↝,
Cyt‑c↝,
PI3K↝,
PTEN↝,
Cyc↝,
TNF-α↝,

424- CUR,    Curcumin inhibits autocrine growth hormone-mediated invasion and metastasis by targeting NF-κB signaling and polyamine metabolism in breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
Src↓,
p‑STAT1↓, pSTAT-1
p‑Akt↓,
p‑p44↓, p-p44
p‑p42↓, p-p42
RAS↓,
Raf↓, c-RAF
Vim↓,
β-catenin/ZEB1↓,
P53↓,
Bcl-2↓,
Mcl-1↓,
PIAS-3↑,
SOCS-3↑,
SOCS1↑,
ROS↑,
NF-kB↓, NF-kB inactivation, ROS generation and PA depletion in MCF-7, MDA-MB-453 and MDA-MB-231 breast can- cer cells
PAO↑,
SSAT↑,
P21↑,
Bak↑,

425- CUR,    Curcumin inhibits proliferation and promotes apoptosis of breast cancer cells
- in-vitro, BC, T47D - in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468
CDC25↓,
cDC2↓,
P21↑,
p‑Akt↓,
p‑mTOR↓, phosphorylation
Bcl-2↓,
BAX↑,
Casp3↑,

434- CUR,    Curcumin induces apoptosis in lung cancer cells by 14-3-3 protein-mediated activation of Bad
- in-vitro, Lung, A549
14-3-3 proteins↓,
p‑BAD↓, p-Bad
p‑Akt↓,
Akt↓,
cl‑Casp9↑, cleaved
cl‑PARP↑, cleaved

435- CUR,    Antitumor activity of curcumin by modulation of apoptosis and autophagy in human lung cancer A549 cells through inhibiting PI3K/Akt/mTOR pathway
- in-vitro, Lung, A549
Apoptosis↑,
TumAuto↑,
LC3‑Ⅱ/LC3‑Ⅰ↑,
Beclin-1↑,
p62↓,
PI3K↓,
Akt↓,
mTOR↓,
p‑Akt↓,
p‑mTOR↓,
NA↓,

165- CUR,    Curcumin interrupts the interaction between the androgen receptor and Wnt/β-catenin signaling pathway in LNCaP prostate cancer cells
- in-vitro, Pca, LNCaP
AR↓,
β-catenin/ZEB1↓,
p‑Akt↓,
GSK‐3β↓,
p‑β-catenin/ZEB1↑, phosphorylated
cycD1↓,
cMyc↓,

168- CUR,    Curcumin inhibits Akt/mammalian target of rapamycin signaling through protein phosphatase-dependent mechanism
- in-vitro, Pca, PC3
Akt↓,
mTOR↓,
AMPK↑,
TAp63α↑, MAP kinases

2979- CUR,  GB,    Curcumin overcome primary gefitinib resistance in non-small-cell lung cancer cells through inducing autophagy-related cell death
- in-vitro, Lung, H157 - in-vitro, Lung, H1299
EGFR↓, Combination treatment with curcumin and gefitinib markedly downregulated EGFR activity through suppressing Sp1 and blocking interaction of Sp1 and HADC1,
Sp1/3/4↓,
ERK↓, and markedly suppressed receptor tyrosine kinases as well as ERK/MEK and AKT/S6K pathways in the resistant NSCLC cells.
MEK↓,
Akt↓,
S6K↓,

3576- CUR,    Protective Effects of Indian Spice Curcumin Against Amyloid-β in Alzheimer's Disease
- Review, AD, NA
*Inflam↓, known to have protective effects, including anti-inflammatory, antioxidant, anti-arthritis, pro-healing, and boosting memory cognitive functions.
*antiOx↑,
*memory↑,
*Aβ↓, curcumin prevents Aβ aggregation and crosses the blood-brain barrier,
*BBB↑,
*cognitive↑, curcumin ameliorates cognitive decline and improves synaptic functions in mouse models of AD
*tau↓, curcumin's effect on inhibition of A and tau,copper binding ability, cholesterol lowering ability, anti-inflammatory and modulation of microglia, acetylcholinesterase (AChE) inhibition, antioxidant properties,
*LDL↓,
*AChE↓,
*IL1β↓, Curcumin reduced the levels of oxidized proteins and IL1B in the brains of APP mice
*IronCh↑, Curcumin binds to redox-active metals, iron and copper
*neuroP↑, Curcumin, a neuroprotective agent, has poor brain bioavailability.
*BioAv↝,
*PI3K↑, They found that curcumin significantly upregulates phosphatidylinositol 3-kinase (PI3K), Akt, nuclear factor E2-related factor-2 (Nrf2), heme oxygenase 1, and ferritin expression
*Akt↑,
*NRF2↑,
*HO-1↑,
*Ferritin↑,
*HO-2↓, and that it significantly downregulates heme oxygenase 2, ROS, and A40/42 expression.
*ROS↓,
*Ach↑, significant increase in brain ACh, glutathione, paraoxenase, and BCL2 levels with respect to untreated group associated with significant decrease in brain AChE activity,
*GSH↑,
*Bcl-2↑,
*ChAT↑, nvestigation revealed that the selected treatments caused marked increase in ChAT positive cells.

2688- CUR,    Effects of resveratrol, curcumin, berberine and other nutraceuticals on aging, cancer development, cancer stem cells and microRNAs
- Review, Var, NA - Review, AD, NA
*ROS↓, CUR reduced the production of ROS
*SOD↑, CUR also upregulated the expression of superoxide dismutase (SOD) genes
p16↑, The effects of CUR on gene expression in cancer-associated fibroblasts obtained from breast cancer patients has been examined. CUR increased the expression of the p16INK4A and other tumor suppressor proteins
JAK2↓, CUR decreased the activity of the JAK2/STAT3 pathway
STAT3↓,
CXCL12↓, and many molecules involved in cellular growth and metastasis including: stromal cell-derived factor-1 (SDF-1), IL-6, MMP2, MMP9 and TGF-beta
IL6↓,
MMP2↓,
MMP9↓,
TGF-β↓,
α-SMA↓, These effects reduced the levels of alpha-smooth muscle actin (alpha-SMA) which was attributed to decreased migration and invasion of the cells.
LAMs↓, CUR suppressed Lamin B1 and
DNAdam↑, induced DNA damage-independent senescence in proliferating but not quiescent breast stromal fibroblasts in a p16INK4A-dependent manner.
*memory↑, CUR has recently been shown to suppress memory decline by suppressing beta-site amyloid precursor protein cleaving enzyme 1 (BACE1= Beta-secretase 1, an important gene in AD) expression which is implicated in beta-amyoid pathology in 5xFAD transgenic
*cognitive↑, CUR was found to decrease adiposity and improve cognitive function in a similar fashion as CR in 15-month-old mice.
*Inflam↓, The effects of CUR and CR were positively linked with anti-inflammatory or antioxidant actions
*antiOx↓,
*NO↑, CUR treatment increased nNOS expression, acidity and NO concentration
*MDA↓, CUR treatment resulted in decreased levels of MDA
*ROS↓, CUR treatment was determined to cause reduction of ROS in the AMD-RPEs and protected the cells from H2O2-induced cell death by reduction of ROS levels.
DNMT1↓, CUR has been shown to downregulate the expression of DNA methyl transferase I (DNMT1)
ROS↑, induction of ROS and caspase-3-mediated apoptosis
Casp3↑,
Apoptosis↑,
miR-21↓, CUR was determined to decrease both miR-21 and anti-apoptotic protein expression.
LC3II↓, CUR also induced proteins associated with cell death such as LC3-II and other proteins in U251 cells
ChemoSen↑, The combined CUR and temozolomide treatment resulted in enhanced toxicity in U-87 glioblastoma cells.
NF-kB↓, suppression of NF-kappaB activity
CSCs↓, Dendrosomal curcumin increased the expression of miR-145 and decreased the expression of stemness genes including: NANOG, OCT4A, OCT4B1, and SOX2 [113]
Nanog↓,
OCT4↓,
SOX2↓,
eff↑, A synergistic interaction was observed when emodin and CUR were combined in terms of inhibition of cell growth, survival and invasion.
Sp1/3/4↓, CUR inducing ROS which results in suppression of specificity protein expression (SP1, SP3 and SP4) as well as miR-27a.
miR-27a-3p↓,
ZBTB10↑, downregulation of miR-27a by CUR, increased expression of ZBTB10 occurred
SOX9?, This resulted in decreased SOX9 expression.
ChemoSen↑, CUR used in combination with cisplatin resulted in a synergistic cytotoxic effect, while the effects were additive or sub-additive in combination with doxorubicin
VEGF↓, Some of the effects of CUR treatment are inhibition of NF-κB activity and downstream effector proteins, including: VEGF, MMP-9, XIAP, BCL-2 and Cyclin-D1.
XIAP↓,
Bcl-2↓,
cycD1↓,
BioAv↑, Piperine is an alkaloid found in the seeds of black pepper (Piper nigrum) and is known to enhance the bioavailability of several therapeutic agents, including CUR
Hif1a↓, CUR inhibits HIF-1 in certain HCC cell lines and in vivo studies with tumor xenografts. CUR also inhibited EMT by suppressing HIF-1alpha activity in HepG2 cells
EMT↓,
BioAv↓, CUR has a poor solubility in aqueous enviroment, and consequently it has a low bioavailability and therefore low concentrations at the target sites.
PTEN↑, CUR treatment has been shown to result in activation of PTEN, which is a target of miR-21.
VEGF↓, CUR treatment resulted in a decrease of VEGF and activated Akt.
Akt↑,
EZH2↓, CUR also suppressed EZH2 expression by induction of miR-let 7c and miR-101.
NOTCH1↓, The expression of NOTCH1 was inhibited upon EZH2 suppression [
TP53↑, CUR has been shown to activate the TP53/miR-192-5p/miR-215/XIAP pathway in NSCLC.
NQO1↑, CUR can also induce the demethylation of the nuclear factor erythroid-2 (NF-E2) related factor-2 (NRT2) gene which in turn activates (NQO1), heme oxygenase-1 (HO1) and an antioxidant stress pathway which can prevent growth in mouse TRAMP-C1 prostate
HO-1↑,

2821- CUR,    Antioxidant curcumin induces oxidative stress to kill tumor cells (Review)
- Review, Var, NA
*antiOx↑, Curcumin is a plant polyphenol in turmeric root and a potent antioxidant
*NRF2↑, regulation by nuclear factor erythroid 2-related factor 2, thereby suppressing reactive oxygen species (ROS) and exerting anti-inflammatory, anti-infective and other pharmacological effects
*ROS↓,
*Inflam↓,
ROS↑, Of note, curcumin induces oxidative stress in tumors. curcumin-induced accumulation of ROS in tumors to kill tumor cells has been noted in several studies
p‑ERK↑, Curcumin promoted ERK/JNK phosphorylation, causing elevated ROS levels and triggering mitochondria-dependent apoptosis
ER Stress↑, Curcumin triggered disturbances in Ca2+ homeostasis, leading to endoplasmic reticulum stress, mitochondrial damage and apoptosis
mtDam↑,
Apoptosis↑,
Akt↓, Curcumin inhibited the AKT/mTOR/p70S6K signaling pathway
mTOR↓,
HO-1↑, Curcumin-induced HO-1 overexpression led to a disturbed intracellular iron distribution and triggered the Fenton reaction
Fenton↑,
GSH↓, Non-small cell lung cancer: Curcumin induced a decrease in GSH and an increase in ROS levels and iron accumulation
Iron↑,
p‑JNK↑, Curcumin causes mitochondrial damage by promoting phosphorylation of ERK and JNK, resulting in the increased release of ROS and cytochrome c into the cytoplasm, thereby triggering a mitochondrion-dependent pathway of apoptosis
Cyt‑c↑,
ATF6↑, thyroid cancer with curcumin, both activating transcription factor (ATF) 6 and the ER stress marker C/EBP homologous protein (CHOP) were activated by curcumin and Ca2+-ATPase activity was also affected.
CHOP↑,

150- NRF,  CUR,  docx,    Subverting ER-Stress towards Apoptosis by Nelfinavir and Curcumin Coexposure Augments Docetaxel Efficacy in Castration Resistant Prostate Cancer Cells
- in-vitro, Pca, C4-2B
p‑Akt↓,
p‑eIF2α↑, phosphorylated
ER Stress↑, ER stress
ATFs↑, ATF4
CHOP↑,
TRIB3↑,

139- Tomatine,  CUR,    Combination of α-Tomatine and Curcumin Inhibits Growth and Induces Apoptosis in Human Prostate Cancer Cells
- in-vitro, Pca, PC3
NF-kB↓,
Bcl-2↓,
p‑Akt↓,
p‑ERK↓, ERK1/2

2133- TQ,  CUR,  Cisplatin,    Thymoquinone and curcumin combination protects cisplatin-induced kidney injury, nephrotoxicity by attenuating NFκB, KIM-1 and ameliorating Nrf2/HO-1 signalling
- in-vitro, Nor, HEK293 - in-vivo, NA, NA
*creat↓, BUN, creatinine, CK and pro-inflammatory cytokines like TNF-α, IL-6 and MRP-1 to be elevated in the cisplatin-treated group while reducing glomerular filtration rate. Tq + Cur treatment significantly improved these conditions.
*TNF-α↓,
*IL6↓,
*MRP↓,
*GFR↑,
*mt-ATPase↑, antioxidant enzyme levels and mitochondrial ATPases were restored upon treatment,
*p‑Akt↑, Tq + Cur treatment increased the expressions of phosphorylated Akt, Nrf2 and HO-1 proteins while decreasing the levels of cleaved caspase 3 and NFκB in kidney homogenates.
*NRF2↑,
*HO-1↑,
*Casp3↓,
*NF-kB↓,
*RenoP↑, In summary, Tq + Cur had protective effects on cisplatin-induced nephrotoxicity and renal injury


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 26

Results for Effect on Cancer/Diseased Cells:
14-3-3 proteins↓,1,   p‑4E-BP1↓,1,   Akt↓,8,   Akt↑,1,   Akt↝,1,   p‑Akt↓,16,   p‑Akt↝,1,   AMPK↑,1,   AP-1↝,1,   Apoptosis↑,9,   Apoptosis↝,2,   AR↓,2,   AR↝,1,   ATF6↑,1,   ATFs↑,1,   ATG3↑,2,   ATG5↑,1,   BAD↑,1,   p‑BAD↓,2,   Bak↑,1,   BAX↑,2,   BAX↝,1,   Bcl-2↓,7,   Bcl-2↝,1,   Bcl-xL↓,2,   Bcl-xL↝,1,   Beclin-1↑,5,   BioAv↓,1,   BioAv↑,2,   Casp3↑,3,   Casp3↝,1,   cl‑Casp3↑,1,   proCasp3↓,1,   Casp8↑,1,   Casp9↑,2,   cl‑Casp9↑,1,   Catalase↓,1,   cDC2↓,1,   CDC25↓,1,   chemoP↑,1,   ChemoSen↑,3,   CHOP↑,2,   cMyc↓,2,   COX2↝,1,   CSCs↓,1,   CXCL12↓,1,   Cyc↝,1,   cycD1↓,3,   cycD1↝,1,   Cyt‑c↑,1,   Cyt‑c↝,1,   DNAdam↑,1,   DNMT1↓,1,   eff↑,1,   EGF↑,1,   EGFR↓,2,   EGFR↝,1,   p‑eIF2α↑,1,   EIF4E↓,1,   EMT↓,1,   ER Stress↑,3,   ERK↓,1,   p‑ERK↓,2,   p‑ERK↑,2,   EZH2↓,1,   Fenton↑,1,   Gli1↓,1,   GLO-I↓,1,   GPx1↓,1,   GPx4↓,1,   GSH↓,1,   GSK‐3β↓,1,   HH↓,1,   Hif1a↓,1,   HO-1↑,2,   HSP27↑,1,   IL6↓,1,   IL6↝,1,   Iron↑,1,   JAK2↓,1,   JNK↑,1,   JNK↝,1,   p‑JNK↑,2,   LAMs↓,1,   LC3‑Ⅱ/LC3‑Ⅰ↑,2,   LC3I↓,1,   LC3II↓,1,   LC3II↑,2,   Mcl-1↓,2,   MEK↓,1,   miR-205↑,1,   miR-21↓,2,   miR-27a-3p↓,1,   MMP2↓,1,   MMP2↝,1,   MMP9↓,1,   mtDam↑,1,   mTOR↓,3,   mTOR↝,1,   p‑mTOR↓,6,   n-MYC↓,1,   NA↓,1,   NADPH↓,1,   Nanog↓,1,   NEDD9↓,2,   NF-kB↓,6,   NF-kB↝,1,   NOTCH1↓,2,   NQO1↑,1,   NRF2↝,1,   OCT4↓,1,   p16↑,1,   P21↑,3,   P21↝,1,   p‑p38↑,1,   p‑p42↓,1,   p‑p44↓,1,   P53↓,1,   P53↑,1,   P53↝,1,   p62↓,3,   p62↑,1,   p‑p70S6↓,1,   p‑P70S6K↓,1,   p73↑,1,   PAO↑,1,   PARP↑,1,   cl‑PARP↑,4,   p‑PDK1↓,1,   PI3K↓,2,   PI3K↝,1,   PI3k/Akt/mTOR↓,1,   PIAS-3↑,1,   p‑PIK3R1↓,1,   PRKCG↑,1,   PSA↝,1,   PTCH1↓,1,   PTEN↑,2,   PTEN↝,1,   radioP↑,1,   RadioS↑,1,   Raf↓,1,   RAS↓,1,   ROS↑,5,   ROS↝,1,   RPS6KA1↓,1,   p‑S6↓,1,   S6K↓,1,   Shh↓,1,   SOCS-3↑,1,   SOCS1↑,1,   SOD1↓,1,   SOX2↓,1,   SOX9?,1,   Sp1/3/4↓,2,   Src↓,1,   SSAT↑,1,   p‑STAT1↓,1,   STAT3↓,3,   survivin↓,1,   TAp63α↑,1,   TGF-β↓,1,   TNF-α↝,1,   TP53↑,1,   TRIB3↑,1,   TumAuto↑,4,   TumCCA↑,4,   TumCI↓,1,   TumCMig↓,2,   TumCP↓,2,   VEGF↓,2,   VEGF↝,1,   Vim↓,1,   XIAP↓,1,   ZBTB10↑,1,   α-SMA↓,1,   β-catenin/ZEB1↓,4,   β-catenin/ZEB1↝,1,   p‑β-catenin/ZEB1↑,1,   β-TRCP↑,1,  
Total Targets: 180

Results for Effect on Normal Cells:
Ach↑,1,   AChE↓,1,   Akt↓,1,   Akt↑,1,   p‑Akt↑,1,   antiOx↓,1,   antiOx↑,2,   mt-ATPase↑,1,   Aβ↓,1,   BBB↑,1,   Bcl-2↑,1,   BioAv↝,1,   Casp3↓,1,   ChAT↑,1,   cognitive↑,2,   COX2↓,1,   creat↓,1,   Ferritin↑,1,   GFR↑,1,   GPx↑,1,   GSH↑,2,   HO-1↑,3,   HO-2↓,1,   IL1β↓,1,   IL6↓,1,   Inflam↓,3,   IronCh↑,1,   LDL↓,1,   MDA↓,1,   memory↑,2,   MRP↓,1,   NADPH↑,1,   neuroP↑,1,   NF-kB↓,1,   NO↑,1,   NRF2↑,4,   p300↓,1,   PI3K↑,1,   RenoP↑,1,   ROS↓,5,   SOD↑,1,   STAT3↓,1,   tau↓,1,   TNF-α↓,1,  
Total Targets: 44

Scientific Paper Hit Count for: Akt, PKB-Protein kinase B
26 Curcumin
1 Photodynamic Therapy
1 Chemotherapy
1 Radiotherapy/Radiation
1 Ursolic acid
1 gefitinib, erlotinib
1 nelfinavir/Viracept
1 Docetaxel
1 Tomatine
1 Thymoquinone
1 Cisplatin
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:65  Target#:4  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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