TP53 Cancer Research Results
TP53, tumor protein p53: Click to Expand ⟱
| Source: CGL-Driver Genes |
| Type: TSG |
TP53 is a gene that encodes the p53 protein, which plays a crucial role in regulating the cell cycle, maintaining genomic stability, and preventing tumor formation. It is often referred to as the "guardian of the genome" due to its role in protecting cells from DNA damage and stress.
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Scientific Papers found: Click to Expand⟱
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in-vivo, |
CRC, |
HCT116 |
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in-vitro, |
CRC, |
SW480 |
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ChemoSen↑, combined treatment
Casp9↑,
Ferroptosis↑, activation of ferroptosis and suppression of β-catenin/Wnt-signaling pathways were the key mediators for the anti-cancer and chemosensitizing effects of andrographis.
Wnt/(β-catenin)↓,
FTL↑,
TP53↑,
ACSL5↑,
GCLC↑,
GCLM↑,
SAT1↑,
STEAP3↑,
ACSL5↑,
Apoptosis↑,
ROS↑,
MMP↓,
ATP↓,
AMPK↑,
TP53↑,
p‑MAPK↓, decreased phosphorylated-MAPK3/1 expression
p‑ERK↓,
TumCCA↑, G1 phase, G0/G1 phase, or G2/M phase
TP53↑,
COX2↓,
Bax:Bcl2↑,
ROS↑,
VEGFR2↓,
Akt↓,
ERK↓,
MMP2↓, Berberine also decreased MMP-2, MMP-9, E-cadherin, EGF, bFGF, and fibronectin in the breast cancer cells.
MMP9↓,
IL8↑,
P21↑,
p27↑,
E-cadherin↓,
Fibronectin↓,
cMyc↓, The results indicated that these derivatives could selectively induce and stabilize the formation of the c-myc in the parallel molecular G-quadruplex. Accordingly, transcription of c-myc was down-regulated in the cancer cell line
*memory↑, treatment with berberine significantly improved spatial learning and memory in mice with cognitive decline induced by D-gal
*cognitive↑,
MAPK↑, core targets of berberine for improving cognitive function, include Mapk1, Src, Ctnnb1, Akt1, Pik3ca, Tp53, Jun, and Hsp90aa1.
*Akt↑,
*PI3K↑, PI3K-Akt signaling pathway and MAPK signaling pathway were significantly enriched.
*TP53↑, Tp53 and Jun expression showed a decreasing trend and were significantly lower in the BBR-H group
*Jun↓,
*HSP90↑, src, Ctnnb1, Akt1, Pik3ca, and Hsp90aa1 exhibited an increasing tendency in both the BBR-L and BBR-H groups
*neuroP↑, Akt1, Ctnnb1, Tp53, and Jun were involved in the neuroprotective actions of berberine.
*Inflam↓, pharmacological effects of BBR, including anti-inflammatory
*antiOx↑, BBR has antioxidant properties as well as protective effects against neurodegenerative diseases
*p16↓, BBR reduces the expression of P16 in brain tissue of cognitive dysfunctions mice
*ER Stress↓, inhibition of endoplasmic reticulum stress
TumCP↓, implicated in cell proliferation, angiogenesis, invasion, and metastasis
angioG↓,
TumCI↓,
TumMeta↓,
TP53↑, Chrysin exhibited strong binding interactions with several key hub proteins, notably TP53, AKT1, and CASP3, suggesting its capacity to inhibit tumorigenesis in breast cancer
Akt↓,
Casp3↑,
tumCV↓, dose-dependent reduction in cell viability was observed, with an IC50 value of 67.43 and 22.55 µM for 24 and 48 h
TNF-α↓, chrysin binds strongly to TNF-α, potentially inhibiting its function.
BioAv↑, Improved bioavailability of chrysin via its interaction with HSA could enhance its therapeutic efficacy, a factor that could be further explored in future pharmacokinetic studies
BioAv↑, Albumin’s ability to bind and transport Chrysin could influence the bioavailability of the flavonoid, potentially enhancing its therapeutic effects.
AKT1↓, chrysin effectively inhibits AKT1,
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Review, |
Var, |
NA |
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Review, |
AD, |
NA |
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*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/CCND1↓,
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↑,
DNMTs↓, EGCG may competitively inhibit some epigenetic enzymes (DNMT1, DNMT3A, HDAC2, HDAC3, HDAC4, HDAC7 and EZH2).
DNMT1↓,
DNMT3A↓,
HDAC2↓,
HDAC3↓,
HDAC4↓,
EZH2↓, Interaction of EGCG with EZH2 protein indicates inhibition of activity
PI3K↓, Downregulation of key signaling moieties of PI3K, Wnt and MAPK pathways
Wnt↓,
MAPK↓,
hTERT/TERT↓, including TERT, CCNB1, CCNB2, MMP2, MMP7. PIK3C2B, PIK3CA, MAPK8 and IL6 was also observed
MMP2↓,
MMP7↓,
IL6↓,
MDM2↓, Fig 1
MMP-10↓,
TP53↑,
PTEN↑,
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in-vitro, |
GC, |
AGS |
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in-vitro, |
GC, |
SGC-7901 |
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in-vitro, |
Nor, |
GES-1 |
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TumCG↓, Lycopene specifically suppressed cell growth monitored by Real-Time Cell Analyzer, induced cell cycle arrest and cell apoptosis detected by flow cytometry, and lowered mitochondrial membrane potentials assessed by JC-1 staining of AGS and SGC-7901 ce
TumCCA↑,
Apoptosis↑,
MMP↓,
selectivity↑, while did not affect those of GES-1 cells.
cycE1↓, Lycopene decreased the high expression levels of CCNE1 and increased the levels of TP53 in AGS and SGC-7901 cells without affecting those in GES-1 cells.
TP53↑,
*antiOx↑, Lycopene has a strong antioxidant property without pro-Vitamin A function
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Review, |
NA, |
NA |
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Review, |
AD, |
NA |
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NF-kB↓, RES affects NF-kappaB activity and inhibits cytochrome P450 isoenzyme (CYP A1) drug metabolism and cyclooxygenase activity.
P450↓,
COX2↓,
Hif1a↓, RES may inhibit also the expression of hypoxia-inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) and thus may have anti-cancer properties
VEGF↓,
*SIRT1↑, RES induces sirtuins, a class of proteins involved in regulation of gene expression. RES is also considered to be a SIRT1-activating compound (STACs).
SIRT1↓, In contrast, decreased levels of SIRT1 and SIRT2 were observed after treatment of BJ cells with concentrations of RES
SIRT2↓,
ChemoSen⇅, However, the effects of RES remain controversial as it has been reported to increase as well as decrease the effects of chemotherapy.
cardioP↑, RES has been shown to protect against doxorubicin-induced cardiotoxicity via restoration of SIRT1
*memory↑, RES has been shown to inhibit memory loss and mood dysfunction which can occur during aging.
*angioG↑, RES supplementation resulted in improved learning in the rats. This has been associated with increased angiogenesis and decreased astrocytic hypertrophy and decreased microglial activation in the hippocampus.
*neuroP↑, RES may have neuroprotective roles in AD and may improve memory function in dementia.
STAT3↓, RES was determined to inhibit STAT3, induce apoptosis, suppress the stemness gene signature and induced differentiation.
CSCs↓,
RadioS↑, synergistically increased radiosensitivity. RES treatment suppressed repair of radiation-induced DNA damage
Nestin↓, RES decreased NESTIN
Nanog↓, RES was determined to suppress the expression of NANOG
TP53↑, RES treatment activated TP53 and p21Cip1.
P21↑,
CXCR4↓, RES downregulated nuclear localization and activity of NF-kappa-B which resulted in decreased expression of MMP9 and C-X-C chemokine receptor type 4 (CXCR4), two proteins associated with metastasis.
*BioAv↓, The pharmacological properties of RES can be enhanced by nanoencapsulation. Normally the solubility and stability of RES is poor.
EMT↓, RES was determined to suppress many gene products associated with EMT such as decreased vimentin and SLUG expression but increased E-cadherin expression.
Vim↓,
Slug↓,
E-cadherin↑,
AMPK↑, RES can induce AMPK which results in inhibition of the drug transporter MDR1 in oxaliplatin-resistant (L-OHP) HCT116/L-OHP CRCs.
MDR1↓,
DNAdam↑, RES induced double strand DNA breaks by interfering with type II topoisomerase.
TOP2↓, The DNA damage was determined to be due to type II topoisomerase poisoning.
PTEN↑, RES was determined to upregulate phosphatase and tensin homolog (PTEN) expression and decrease the expression of activated Akt.
Akt↓,
Wnt↓, RES was shown to decrease WNT/beta-catenin pathway activity and the downstream targets c-Myc and MMP-7 in CRC cells.
β-catenin/ZEB1↓,
cMyc↓,
MMP7↓,
MALAT1↓, RES also decreased the expression of long non-coding metastasis associated lung adenocarcinoma transcript 1 (RNA-MALAT1) in the LoVo and HCT116 CRC cells.
TCF↓, Treatment of CRC cells with RES resulted in decreased expression of transcription factor 4 (TCF4), which is a critical effector molecule of the WNT/beta-catenin pathway.
ALDH↓, RES was determined to downregulate ALDH1 and CD44 in HNC-TICs in a dose-dependent fashion.
CD44↓,
Shh↓, RES has been determined to decrease IL-6-induced Sonic hedgehog homolog (SHH) signaling in AML.
IL6↓, RES has been shown to inhibit the secretion of IL-6 and VEGF from A549 lung cancer cells
VEGF↓,
eff↑, Combined RES and MET treatment resulted in a synergistic response in terms of decreased TP53, gammaH2AX and P-Chk2 expression. Thus, the combination of RES and MET might suppress some of the aging effects elicited by UVC-induced DNA damage
HK2↓, RES treatment resulted in a decrease in HK2 and increased mitochondrial-induced apoptosis.
ROS↑, RES was determined to shut off the metabolic shift and increase ROS levels and depolarized mitochondrial membranes.
MMP↓,
Showing Research Papers: 1 to 9 of 9
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
Ferroptosis↑, 1, GCLC↑, 1, GCLM↑, 1, HO-1↑, 1, NQO1↑, 1, ROS↑, 4,
Metal & Cofactor Biology ⓘ
FTL↑, 1, STEAP3↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 1, MMP↓, 3, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
ACSL5↑, 2, AKT1↓, 1, AMPK↑, 2, cMyc↓, 2, HK2↓, 1, SAT1↑, 1, SIRT1↓, 1, SIRT2↓, 1,
Cell Death ⓘ
Akt↓, 3, Akt↑, 1, Apoptosis↑, 3, Bax:Bcl2↑, 1, Bcl-2↓, 1, Casp3↑, 2, Casp9↑, 1, Ferroptosis↑, 1, hTERT/TERT↓, 1, MAPK↓, 1, MAPK↑, 1, p‑MAPK↓, 1, MDM2↓, 1, p27↑, 1,
Kinase & Signal Transduction ⓘ
SOX9?, 1, Sp1/3/4↓, 1,
Transcription & Epigenetics ⓘ
EZH2↓, 2, miR-21↓, 1, miR-27a-3p↓, 1, tumCV↓, 1,
Autophagy & Lysosomes ⓘ
LC3II↓, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 2, DNMT1↓, 2, DNMT3A↓, 1, DNMTs↓, 1, p16↑, 1, TP53↑, 8,
Cell Cycle & Senescence ⓘ
cycD1/CCND1↓, 1, cycE1↓, 1, P21↑, 2, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
ALDH↓, 1, CD44↓, 1, CSCs↓, 2, EMT↓, 2, ERK↓, 1, p‑ERK↓, 1, HDAC2↓, 1, HDAC3↓, 1, HDAC4↓, 1, Nanog↓, 2, Nestin↓, 1, NOTCH1↓, 1, OCT4↓, 1, PI3K↓, 1, PTEN↑, 3, Shh↓, 1, SOX2↓, 1, STAT3↓, 2, TCF↓, 1, TOP2↓, 1, TumCG↓, 1, Wnt↓, 2, Wnt/(β-catenin)↓, 1,
Migration ⓘ
CXCL12↓, 1, E-cadherin↓, 1, E-cadherin↑, 1, Fibronectin↓, 1, LAMs↓, 1, MALAT1↓, 1, MMP-10↓, 1, MMP2↓, 3, MMP7↓, 2, MMP9↓, 2, Slug↓, 1, TGF-β↓, 1, TumCI↓, 1, TumCP↓, 1, TumMeta↓, 1, Vim↓, 1, α-SMA↓, 1, β-catenin/ZEB1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1, Hif1a↓, 2, VEGF↓, 4, VEGFR2↓, 1, ZBTB10↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, CXCR4↓, 1, IL6↓, 3, IL8↑, 1, JAK2↓, 1, NF-kB↓, 2, TNF-α↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 3, ChemoSen↑, 3, ChemoSen⇅, 1, eff↑, 2, MDR1↓, 1, P450↓, 1, RadioS↑, 1, selectivity↑, 1,
Clinical Biomarkers ⓘ
EZH2↓, 2, hTERT/TERT↓, 1, IL6↓, 3, TP53↑, 8,
Functional Outcomes ⓘ
cardioP↑, 1,
Total Targets: 117
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 3, MDA↓, 1, ROS↓, 2, SOD↑, 1,
Core Metabolism/Glycolysis ⓘ
SIRT1↑, 1,
Cell Death ⓘ
Akt↑, 1,
Protein Folding & ER Stress ⓘ
ER Stress↓, 1, HSP90↑, 1,
DNA Damage & Repair ⓘ
p16↓, 1, TP53↑, 1,
Proliferation, Differentiation & Cell State ⓘ
Jun↓, 1, PI3K↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↑, 1, NO↑, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 2,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1,
Clinical Biomarkers ⓘ
TP53↑, 1,
Functional Outcomes ⓘ
cognitive↑, 2, memory↑, 3, neuroP↑, 2,
Total Targets: 20
Scientific Paper Hit Count for: TP53, tumor protein p53
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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