NOXA Cancer Research Results

NOXA, Phorbol-12-myristate-13-acetate-induced protein 1 (PMAIP1): Click to Expand ⟱
Source:
Type:
NOXA is a pro-apoptotic protein that plays a crucial role in the regulation of apoptosis, or programmed cell death, in cancer cells. NOXA is a member of the BCL-2 family of proteins, which are key regulators of apoptosis.

Low NOXA expression has been associated with poor prognosis and reduced overall survival.
Scientific Papers found: Click to Expand⟱
742- Bor,    In Vitro Effects of Boric Acid on Cell Cycle, Apoptosis, and miRNAs in Medullary Thyroid Cancer Cells
- in-vitro, Thyroid, NA
NOXA↑,
APAF1↑,
BAX↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
Bcl-xL↓,
miR-21↓,

4826- CUR,    The Bright Side of Curcumin: A Narrative Review of Its Therapeutic Potential in Cancer Management
- Review, Var, NA
*antiOx↑, Curcumin demonstrates strong antioxidant and anti-inflammatory properties, contributing to its ability to neutralize free radicals and inhibit inflammatory mediators
*Inflam↑,
*ROS↓,
Apoptosis↑, Its anticancer effects are mediated by inducing apoptosis, inhibiting cell proliferation, and interfering with tumor growth pathways in various colon, pancreatic, and breast cancers
TumCP↓,
BioAv↓, application is limited by its poor bioavailability due to its rapid metabolism and low absorption.
Half-Life↓,
eff↑, curcumin-loaded hydrogels and nanoparticles, have shown promise in improving curcumin bioavailability and therapeutic efficacy.
TumCCA↑, Studies have demonstrated that curcumin can suppress the proliferation of cancer cells by interfering with the cell cycle [21,22]
BAX↑, Curcumin enhances the expression of pro-apoptotic proteins such as Bax, Bak, PUMA, Bim, and Noxa and death receptors such as TRAIL-R1/DR4 and TRAIL-R2/DR5
Bak↑,
PUMA↑,
BIM↑,
NOXA↑,
TRAIL↑,
Bcl-2↓, curcumin decreases the levels of anti-apoptotic proteins like Bcl-2, Bcl-XL, survin, and XIAP
Bcl-xL↓,
survivin↓,
XIAP↓,
cMyc↓, This shift in the balance of apoptotic regulators facilitates the release of cytochrome c from mitochondria [33,35] and activates caspases
Casp↑,
NF-kB↓, Curcumin suppresses the activity of key transcription factors like NF-κB, STAT3, and AP-1 and interferes with critical signal transduction pathways such as PI3K/Akt/mTOR and MAPK/ERK.
STAT3↓,
AP-1↓,
angioG↓, curcumin inhibits angiogenesis and metastasis by downregulating VEGF, VEGFR2, and matrix metalloproteinases (MMPs).
TumMeta↑,
VEGF↓,
MMPs↓,
DNMTs↓, Epigenetic modifications through the inhibition of DNA methyltransferases (DNMTs) and histone deacetylases (HDACs) further contribute to its anticancer properties.
HDAC↓,
ROS↑, curcumin-loaded nanoparticles showed significant cytotoxicity in the SCC25, MDA-MB-231, and A549 cell lines, with a decrease in tumor cell proliferation, an increase in ROS, and an increase in apoptosis.

1605- EA,    Ellagic Acid and Cancer Hallmarks: Insights from Experimental Evidence
- Review, Var, NA
*BioAv↓, Within the gastrointestinal tract, EA has restricted bioavailability, primarily due to its hydrophobic nature and very low water solubility.
antiOx↓, strong antioxidant properties [12,13], anti-inflammatory effects
Inflam↓,
TumCP↓, numerous studies indicate that EA possesses properties that can inhibit cell proliferation
TumCCA↑, achieved this by causing cell cycle arrest at the G1 phase
cycD1/CCND1↓, reduction of cyclin D1 and E levels, as well as to the upregulation of p53 and p21 proteins
cycE/CCNE↓,
P53↑,
P21↑,
COX2/PTGS2↓, notable reduction in the protein expression of COX-2 and NF-κB as a result of this treatment
NF-kB↓,
Akt↑, suppressing Akt and Notch signaling pathways
NOTCH↓,
CDK2↓,
CDK6↓,
JAK↓, suppression of the JAK/STAT3 pathway
STAT3↓,
EGFR↓, decreased expression of epidermal growth factor receptor (EGFR)
p‑ERK↓, downregulated the expression of phosphorylated ERK1/2, AKT, and STAT3
p‑Akt↓,
p‑STAT3↓,
TGF-β↓, downregulation of the TGF-β/Smad3
SMAD3↓,
CDK6↓, EA demonstrated the capacity to bind to CDK6 and effectively inhibit its activity
Wnt/(β-catenin)↓, ability of EA to inhibit phosphorylation of EGFR
Myc↓, Myc, cyclin D1, and survivin, exhibited decreased levels
survivin↓,
CDK8↓, diminished CDK8 level
PKCδ↓, EA has demonstrated a notable downregulatory impact on the expression of classical isoenzymes of the PKC family (PKCα, PKCβ, and PKCγ).
tumCV↓, EA decreased cell viability
RadioS↑, further intensified when EA was combined with gamma irradiation.
eff↑, EA additionally potentiated the impact of quercetin in promoting the phosphorylation of p53 at Ser 15 and increasing p21 protein levels in the human leukemia cell line (MOLT-4)
MDM2↓, finding points to the ability of reduced MDM2 levels
XIAP↓, downregulation of X-linked inhibitor of apoptosis protein (XIAP).
p‑RB1↓, EA exerted a decrease in phosphorylation of pRB
PTEN↑, EA enhances the protein phosphatase activity of PTEN in melanoma cells (B16F10)
p‑FAK↓, reduced phosphorylation of focal adhesion kinase (FAK)
Bax:Bcl2↑, EA significantly increases the Bax/Bcl-2 rati
Bcl-xL↓, downregulates Bcl-xL and Mcl-1
Mcl-1↓,
PUMA↑, EA also increases the expression of Bcl-2 inhibitory proapoptotic proteins PUMA and Noxa in prostate cancer cells
NOXA↑,
MMP↓, addition to the reduction in MMP, the release of cytochrome c into the cytosol occurs in pancreatic cancer cells
Cyt‑c↑,
ROS↑, induction of ROS production
Ca+2↝, changes in intracellular calcium concentration, leading to increased levels of EndoG, Smac/DIABLO, AIF, cytochrome c, and APAF1 in the cytosol
Endoglin↑,
Diablo↑,
AIF↑,
iNOS↓, decreased expression of Bcl-2, NF-кB, and iNOS were observed after exposure to EA at concentrations of 15 and 30 µg/mL
Casp9↑, increase in caspase 9 activity in EA-treated pancreatic cancer cells PANC-1
Casp3↑, EA-induced caspase 3 activation and PARP cleavage in a dose-dependent manner (10–100 µmol/L)
cl‑PARP↑,
RadioS↑, EA sensitizes and reduces the resistance of breast cancer MCF-7 cells to apoptosis induced by γ-radiation
Hif1a↓, EA reduced the expression of HIF-1α
HO-1↓, EA significantly reduced the levels of two isoforms of this enzyme, HO-1, and HO-2, and increased the levels of sEH (Soluble epoxide hydrolase) in LnCap
HO-2↓,
SIRT1↓, EA-induced apoptosis was associated with reduced expression of HuR and Sirt1
selectivity↑, A significant advantage of EA as a potential chemopreventive, anti-tumor, or adjuvant therapeutic agent in cancer treatment is its relative selectivity
Dose∅, EA significantly reduced the viability of cancer cells at a concentration of 10 µmol/L, while in healthy cells, this effect was observed only at a concentration of 200 µmol/L
NHE1↓, EA had the capacity to regulate cytosolic pH by downregulating the expression of the Na+/H+ exchanger (NHE1)
Glycolysis↓, led to intracellular acidification with subsequent impairment of glycolysis
GlucoseCon↓, associated with a decrease in the cellular uptake of glucose
lactateProd↓, notable reduction in lactate levels in supernatant
PDK1?, inhibit pyruvate dehydrogenase kinase (PDK) -bind and inhibit PDK3
PDK1?,
ECAR↝, EA has been shown to influence extracellular acidosis
COX1↓, downregulation of cancer-related genes, including COX1, COX2, snail, twist1, and c-Myc.
Snail↓,
Twist↓,
cMyc↓,
Telomerase↓, EA, might dose-dependently inhibit telomerase activity
angioG↓, EA may inhibit angiogenesis
MMP2↓, EA demonstrated a notable reduction in the secretion of matrix metalloproteinase (MMP)-2 and MMP-9.
MMP9↓,
VEGF↓, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
Dose↝, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
PD-L1↓, EA downregulated the expression of the immune checkpoint PD-L1 in tumor cells
eff↑, EA might potentially enhance the efficacy of anti-PD-L1 treatment
SIRT6↑, EA exhibited statistically significant upregulation of sirtuin 6 at the protein level in Caco2 cells
DNAdam↓, increase in DNA damage

7513- FA,    Anti-proliferative and anti-invasive effects of ferulic acid in TT medullary thyroid cancer cells interacting with URG4/URGCP
- in-vitro, Thyroid, NA
cycD1/CCND1↓, FA caused a decrease in the expression of novel gene URG4/URGCP, CCND1, CDK4, CDK6, BCL2, MMP2, and MMP9
URGCP/URG4↓,
CDK4↓,
CDK6↓,
Bcl-2↓,
MMP2↓,
MMP9↓,
P53↑, a significant increase in the expression of p53, PARP, PUMA, NOXA, BAX, BID, CASP3, CASP9, and TIMP1 genes in TT human thyroid cancer cell line
PARP↑,
PUMA↑,
NOXA↑,
BAX↑,
Casp3↑,
Casp9↑,
TIMP1↑,
TumCI↓, FA in TT cells suppressed invasion, migration, and colony formation
TumCMig↓,
TumCCA↑, FA indicates anticarcinogenesis activity by affecting cell cycle arrest, apoptosis, invasion, migration, and colony formation on TT cells.
Apoptosis↑,

1656- FA,    Ferulic Acid: A Natural Phenol That Inhibits Neoplastic Events through Modulation of Oncogenic Signaling
- Review, Var, NA
tyrosinase↓,
CK2↓,
TumCP↓,
TumCMig↓,
FGF↓,
FGFR1↓,
PI3K↓,
Akt↓,
VEGF↓,
FGFR1↓,
FGFR2↓,
PDGF↓,
ALAT↓,
AST↓,
TumCCA↑, G0/G1 phase arrest
CDK2↓,
CDK4↓,
CDK6↓,
BAX↓,
Bcl-2↓,
MMP2↓,
MMP9↓,
P53↑,
PARP↑,
PUMA↑,
NOXA↑,
Casp3↑,
Casp9↑,
TIMP1↑,
lipid-P↑,
mtDam↑,
EMT↓,
Vim↓,
E-cadherin↓,
p‑STAT3↓,
COX2/PTGS2↓,
CDC25↓,
RadioS↑,
ROS↑,
DNAdam↑,
γH2AX↑,
PTEN↑,
LC3II↓,
Beclin-1↓,
SOD↓,
Catalase↓,
GPx↓,
Fas↑,
*BioAv↓, ferulic acid stability and limited solubility in aqueous media continue to be key obstacles to its bioavailability, preclinical efficacy, and clinical use.
cMyc↓,
Beclin-1↑, ferulic acid by elevating the levels of the apoptosis and autophagy biomarkers, including beclin-1, Light chain (LC3-I/LC3-II), PTEN-induced putative kinase 1 (PINK-1), and Parkin
LC3‑Ⅱ/LC3‑Ⅰ↓,

2496- FBZ,    Impairment of the Ubiquitin-Proteasome Pathway by Methyl N-(6-Phenylsulfanyl-1H-benzimidazol-2-yl)carbamate Leads to a Potent Cytotoxic Effect in Tumor Cells
- in-vitro, NSCLC, A549 - in-vitro, NSCLC, H460
TumCG↓, We report that fenbendazole (FZ) (methyl N-(6-phenylsulfanyl-1H-benzimidazol-2-yl)carbamate) exhibits a potent growth-inhibitory activity against cancer cell lines but not normal cells.
selectivity↑, but not normal cells
P53↑, A number of apoptosis regulatory proteins that are normally degraded by the ubiquitin-proteasome pathway like cyclins, p53, and IκBα were found to be accumulated in FZ-treated cells.
IKKα↑,
ER Stress↑, FZ induced distinct ER stress-associated genes like GRP78, GADD153, ATF3, IRE1α, and NOXA in these cells.
GRP78/BiP↑,
CHOP/DDIT3↑,
ATF3↑,
IRE1↑,
NOXA↑,
ROS↑, fenbendazole induced endoplasmic reticulum stress, reactive oxygen species production, decreased mitochondrial membrane potential, and cytochrome c release that eventually led to cancer cell death.
MMP↓,
Cyt‑c↑,
selectivity↑, treatment of human lung cancer cell lines with fenbendazole (FZ)3 induces apoptotic cell death, whereas primary normal cells in culture remain widely unaffected.
eff↝, The growth-inhibitory action of FZ in H460 and A549 cells was also compared with the Food and Drug Administration-approved proteasomal inhibitor bortezomib, and the results showed that the activities of both of the compounds were comparable

7321- Gos,    The potential roles of gossypol as anticancer agent: advances and future directions
- Review, Var, NA
other↝, Except in China, where gossypol is available on the drug market as an adjuvant used for tumour treatment [85], in the rest of the world, gossypol is still under clinical trials investigation.
BioAv↑, To improve the water solubility and bioavailability of gossypol, Wang et al. [76] used gossypol-loaded pluronic F127 nanoparticles (GLPFNs), which increased bioavailability several times and exhibited higher organ uptake of the drug compared to using
Bcl-2↓, The main mechanism of gossypol-anticancer activity is inducing apoptosis through suppressing anti-apoptotic proteins of the Bcl-2 family.
Casp3↑, The caspase-dependent anti-tumour effect of gossypol is led by activation of caspase-3 and caspase-9.
Casp9↑,
MOMP↑, Apoptosis induced by independent pathways is made by alternations on the mitochondrial outer membrane permeabilisation
ROS↑, Gossypol treatment has been demonstrated to induce the production of reactive oxygen species (ROS) in tumour cell
ATP↓, 80 μmol/L gossypol resulted in a significant increase in cellular ROS levels, leading to ATP depletion, which induces mitochondrial dysfunction
mtDam↑,
Apoptosis↑, The impaired function of mitochondria further contributes to the activation of apoptosis
hTERT/TERT↓, ↓ decrease, telomerase reverse transcriptase (TERT)
Akt↓, ↓ decrease, telomerase reverse transcriptase (TERT), Adenosine triphosphate (ATP), Cellular myelocytomatosis oncogene (c-MyC), serine/threonine protein kinase (Akt)
TumAuto↑, Induction of autophagy as a complementary process of apoptosis
LC3‑Ⅱ/LC3‑Ⅰ↑, gossypol in colorectal cancer cells increased the LC3-II/LC3-I ratio and induced autophagy
NRF2↓, gossypol reduced Nrf2 protein stability, leading to the inhibition of the Nrf2/ARE pathway, resulting in a significant decrease of cell viability in human cancer cells
ARE↓,
ICAM-1↓, Treating breast cancer cells with gossypol has been shown to block the binding of NF-κB to the promoter regions of ICAM-1, suppressing TNF-α-induced ICAM-1 expression.
CX43/GJA1↓, It down-regulates the expression of CX43, nuclear NF-κB, TNF-α, toll-like receptor 4 (TLR4), and interleukin-6 (IL-6) in these cells, indicating its potential anti-inflammatory and anti-apoptotic effects
NF-kB↓,
TLR4↓,
IL6↓,
Inflam↓,
CUL5↝, gossypol has been found to block the neddylation of cullin enzymes (CUL5 and CUL1) by directly binding to the SAG-CUL5 or RBX1-CUL1 complex.
CUL1↝,
NOXA↑, This leads to the accumulation of both the pro-apoptotic protein NOXA
TumCI↓, gossypol significantly reduced the invasion, migration, and adhesion of these cancer cells by suppressing the FAK pathway and ETM
TumCMig↓,
TumCA↓,
FAK↓,
MDM2↓, gossypol, the binding between the MDM2 protein and VEGF mRNA was disrupted in breast cancer cells [78]. As a result, the expression of MDM2 and VEGF proteins is significantly decreased.
VEGF↓,
angioG↓, anti-angiogenic mechanism of gossypol in cancer cells (Fig. 7).
HLA-I/II↑, gossypol has been found to increase the expression of HLA-I/II molecules
Imm↑, This immune modulation may contribute to its anti-cancer activity by enhancing immune recognition and response against tumour cells
Dose↝, phase III clinical trial performed between January 2014 and February 2017, gossypol acetate tablets (20 mg/tablet) produced by Xi’an Northern Pharmaceutical Co., Ltd were tested with a placebo in 102 patients with NSCLC
Glycolysis↓, Moreover, the treatment of boars with gossypol inhibited glycolysis and the respiratory chain, leading to a decrease in oxidative phosphorylation and adenosine triphosphate (ATP) synthesis, causing a decrease in energy supply and inhibition of sperm
OXPHOS↓,

7317- Gos,    A phase II study of AT-101 (gossypol) in chemotherapy-sensitive recurrent extensive stage small cell lung cancer (ES-SCLC)
- Trial, Lung, NA
Bcl-2↓, AT-101 is an oral inhibitor of the anti-apoptotic Bcl proteins (Bcl-2, Bcl-XL, Bcl-W, and Mcl-1) and an inducer of the pro-apoptotic proteins noxa and puma.
Bcl-xL↓,
Mcl-1↓,
NOXA↑,
PUMA↑,
Dose↝, AT-101 was administered 20 mg orally daily for 21 out of 28 days each cycle for up to 6 cycles.
eff↓, At the time of planned interim evaluation, none of the 14 evaluable patients enrolled in the first stage had any response to therapy and the study was closed permanently for further accrual.

7588- I3C,    Indole-3-carbinol suppresses NF-κB activity and stimulates the p53 pathway in pre-B acute lymphoblastic leukemia cells
- in-vitro, AML, NA
TumCG↓, I3C induced cell growth inhibition by G1 cell cycle arrest and triggered apoptosis in a dose- and time-dependent manner.
TumCCA↑,
Apoptosis↑,
P53↑, p53, p21, and Bax proteins showed increased expression after I3C treatment
P21↑,
BAX↑,
PUMA↑, up-regulation of PUMA, NOXA, and Apaf-1.
NOXA↑,
APAF1↑,
NF-kB↓, I3C also suppressed constitutive nuclear factor-κB (NF-κB) activation and inhibited the protein expression of NF-kappa B-regulated antiapoptotic (IAP1, Bcl-xL, Bcl-2, XIAP) and proliferative (c-Myc) gene products.
IAP1↓,
Bcl-xL↓,
Bcl-2↓,
XIAP↓,
Myc↓,
ChemoSen↑, Coadministration of I3C with the topoisomerase II inhibitor, doxorubicin, potentiates cytotoxic effects compared with either agent alone
Casp9↑, enhanced caspase-9 activation and PARP cleavage
cl‑PARP↑,
eff↑, Overall, our results indicated that using nontoxic agents, such as I3C, in combination with anthracyclines might provide a new insight into the development of novel combination therapies in childhood BCP-ALL.

1469- SFN,    Sulforaphane enhances the therapeutic potential of TRAIL in prostate cancer orthotopic model through regulation of apoptosis, metastasis, and angiogenesis
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vivo, Pca, NA
eff↑, Sulforaphane enhanced the therapeutic potential of TRAIL in PC-3 cells and sensitized TRAIL-resistant LNCaP cells.
ROS↑,
MMP↓,
Casp3↑,
Casp9↑,
DR4↑,
DR5↑,
BAX↑,
Bak↑,
BIM↑,
NOXA↑,
Bcl-2↓,
Bcl-xL↓,
Mcl-1↓,
eff↓, quenching of ROS generation with antioxidant N-acetyl-L-cysteine conferred significant protection against sulforaphane-induced ROS generation, mitochondrial membrane potential disruption, caspase-3 activation, and apoptosis.
TumCG↓,
TumCP↓,
eff↑, enhanced the antitumor activity of TRAIL.
NF-kB↓,
PI3K↓,
Akt↓,
MEK↓,
ERK↓,
angioG↓, combination of sulforaphane and TRAIL was more effective in inhibiting markers of angiogenesis and metastasis and activating FOXO3a transcription factor than single agent alone.
FOXO3↑,

1002- SSE,  Osi,  Adag,    Selenite as a dual apoptotic and ferroptotic agent synergizes with EGFR and KRAS inhibitors with epigenetic interference
- in-vitro, Lung, H1975 - in-vitro, Lung, H385
Apoptosis↑,
Ferroptosis↑,
DNMT1↓,
TET1↑,
TumCCA↑, G2/M arrest
cl‑PARP↑,
cl‑Casp3↑, H1975 cells only
Cyt‑c↑,
BIM↑,
NOXA↑,
Apoptosis↑,
ROS↑, Selenite is associated with oxidative stress
ER Stress↑, H1975 cells only
UPR↑, H1975 cells only

4839- Uro,    Urolithin A induces prostate cancer cell death in p53-dependent and in p53-independent manner
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, LNCaP
tumCV↓, We found UA inhibited CaP cells' viability and induced apoptosis.
Apoptosis↓,
P53↑, we found UA increased p53 protein expression and its main target protein, p21, and MDM2, forming an autoregulatory feedback loop
P21↑,
PUMA↑, UA increased the p53 proapoptotic proteins PUMA and NOXA
NOXA↑,
MDM2↓, UA downregulated MDM2 and XIAP protein expression in PC3 cells and upregulated p21 and p14ARF in a p53-independent manner.
XIAP↓,


Showing Research Papers: 1 to 12 of 12

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

CUL1↝, 1,   CUL5↝, 1,   CX43/GJA1↓, 1,   HLA-I/II↑, 1,   URGCP/URG4↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↓, 1,   ARE↓, 1,   ATF3↑, 1,   Catalase↓, 1,   Ferroptosis↑, 1,   GPx↓, 1,   HO-1↓, 1,   HO-2↓, 1,   lipid-P↑, 1,   NRF2↓, 1,   OXPHOS↓, 1,   ROS↑, 7,   SOD↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 1,   ATP↓, 1,   CDC25↓, 1,   FGFR1↓, 2,   MEK↓, 1,   MMP↓, 3,   mtDam↑, 2,   XIAP↓, 4,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   cMyc↓, 3,   ECAR↝, 1,   GlucoseCon↓, 1,   Glycolysis↓, 2,   lactateProd↓, 1,   PDK1?, 2,   SIRT1↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 3,   Akt↑, 1,   p‑Akt↓, 1,   APAF1↑, 2,   Apoptosis↓, 1,   Apoptosis↑, 6,   Bak↑, 2,   BAX↓, 1,   BAX↑, 5,   Bax:Bcl2↑, 1,   Bcl-2↓, 8,   Bcl-xL↓, 6,   BIM↑, 3,   Casp↑, 1,   Casp3↑, 6,   cl‑Casp3↑, 1,   Casp9↑, 7,   CK2↓, 1,   Cyt‑c↑, 3,   Diablo↑, 1,   DR4↑, 1,   DR5↑, 1,   Fas↑, 1,   Ferroptosis↑, 1,   hTERT/TERT↓, 1,   IAP1↓, 1,   iNOS↓, 1,   Mcl-1↓, 3,   MDM2↓, 3,   MOMP↑, 1,   Myc↓, 2,   NOXA↑, 12,   PUMA↑, 7,   survivin↓, 2,   Telomerase↓, 1,   TRAIL↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

miR-21↓, 1,   other↝, 1,   tumCV↓, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   ER Stress↑, 2,   GRP78/BiP↑, 1,   IRE1↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 1,   Beclin-1↑, 1,   LC3‑Ⅱ/LC3‑Ⅰ↓, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   LC3II↓, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,   DNAdam↑, 1,   DNMT1↓, 1,   DNMTs↓, 1,   P53↑, 6,   PARP↑, 2,   cl‑PARP↑, 3,   SIRT6↑, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 2,   CDK4↓, 2,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 1,   P21↑, 3,   p‑RB1↓, 1,   TumCCA↑, 6,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CDK8↓, 1,   EMT↓, 1,   ERK↓, 1,   p‑ERK↓, 1,   FGF↓, 1,   FGFR2↓, 1,   FOXO3↑, 1,   HDAC↓, 1,   NOTCH↓, 1,   PI3K↓, 2,   PTEN↑, 2,   STAT3↓, 2,   p‑STAT3↓, 2,   TumCG↓, 3,   tyrosinase↓, 1,   Wnt/(β-catenin)↓, 1,  

Migration(tgid=13) ⓘ

AP-1↓, 1,   Ca+2↝, 1,   E-cadherin↓, 1,   FAK↓, 1,   p‑FAK↓, 1,   MMP2↓, 3,   MMP9↓, 3,   MMPs↓, 1,   PDGF↓, 1,   PKCδ↓, 1,   SMAD3↓, 1,   Snail↓, 1,   TET1↑, 1,   TGF-β↓, 1,   TIMP1↑, 2,   TumCA↓, 1,   TumCI↓, 2,   TumCMig↓, 3,   TumCP↓, 4,   TumMeta↑, 1,   Twist↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 4,   EGFR↓, 1,   Endoglin↑, 1,   Hif1a↓, 1,   VEGF↓, 4,  

Barriers & Transport(tgid=15) ⓘ

NHE1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX1↓, 1,   COX2/PTGS2↓, 2,   ICAM-1↓, 1,   IKKα↑, 1,   IL6↓, 1,   Imm↑, 1,   Inflam↓, 2,   JAK↓, 1,   NF-kB↓, 5,   PD-L1↓, 1,   TLR4↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 4,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   ChemoSen↑, 1,   Dose↝, 3,   Dose∅, 1,   eff↓, 2,   eff↑, 6,   eff↝, 1,   Half-Life↓, 1,   RadioS↑, 3,   selectivity↑, 3,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   EGFR↓, 1,   hTERT/TERT↓, 1,   IL6↓, 1,   Myc↓, 2,   PD-L1↓, 1,  
Total Targets: 174

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   ROS↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2,  
Total Targets: 4

Scientific Paper Hit Count for: NOXA, Phorbol-12-myristate-13-acetate-induced protein 1 (PMAIP1)
2 Ferulic acid
2 Gossypol/AT-101
1 Boron
1 Curcumin
1 Ellagic acid
1 Fenbendazole
1 Indole-3-carbinol
1 Sulforaphane (mainly Broccoli)
1 Selenite (Sodium)
1 Osimertinib
1 Adagrasib
1 Urolithin
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#:%  Target#:874  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

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