HSP90 Cancer Research Results

HSP90, HSP90: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
Heat shock protein 90 (Hsp90) is a molecular chaperone that plays a critical role in the proper folding, stabilization, and function of many proteins, including those involved in cell signaling, cell cycle regulation, and stress responses.
-Hsp90 interacts with a variety of client proteins that are often mutated or overexpressed in cancer. These include oncogenes (like HER2, BRAF, and AKT) and tumor suppressor proteins (like p53).
-Hsp90 is often overexpressed in cancer cells, which can help them survive under stressful conditions, such as those found in the tumor microenvironment. This overexpression is associated with poor prognosis in several types of cancer.
-HSPs, particularly HSP90, are known to stabilize many proteins that drive cancer progression (oncoproteins).
Scientific Papers found: Click to Expand⟱
3680- BBR,    Network pharmacology reveals that Berberine may function against Alzheimer’s disease via the AKT signaling pathway
- in-vivo, AD, NA
*Akt↑, Akt1 mRNA expression levels were significantly decreased in AD mice and significantly increased after BBR treatment (p < 0.05).
*neuroP↑, BBR may exert a neuroprotective effect by modulating the ERK and AKT signaling pathways.
*p‑ERK↑, Besides, AKT and ERK phosphorylation decreased in the model group, and BBR significantly increased their phosphorylation levels.
*Aβ↓, BBR has therapeutic potential in the treatment of AD by targeting amyloid beta plaques, neurofibrillary tangles, neuroinflammation, and oxidative stress
*Inflam↓,
*ROS↓,
*BioAv↑, oral bioavailability (OB) = 36.86%, drug-likeness (DL) = 0.78,
*BBB↑, blood brain barrier (BBB) = 0.57,
*Half-Life↝, half-life (HL) = 6.57. BBR half-life (t1/2) is in the mid-elimination group.
*memory↑, BBR improves the performance of memory and recognition tasks in AD mice
*cognitive↑,
*HSP90↑, Among the core targets, Akt1 (t = −5.01, p = 0.002), Hsp90aa1 (t = −3.66, p = 0.011), Hras (t = −2.99, p = 0.024) and Igf1 (t = 3.75, p = 0.019) mRNA levels were significantly increased after BBR treatment
*APP↓, BBR reduces Aβ levels by modulating APP processing and ameliorates Aβ pathology by inhibiting the mTOR/p70S6K signaling pathway
*mTOR↓,
*P70S6K↓,
*CD31/PECAM-1↑, it promotes the formation of brain microvessels by enhancing CD31, VEGF, N-cadherin, Ang-1 and inhibits neuronal apoptosis (Ye et al., 2021).
*VEGF↑,
*N-cadherin↑,
*Apoptosis↓,

3681- BBR,    The efficacy and mechanism of berberine in improving aging-related cognitive dysfunction: A study based on network pharmacology
- in-vivo, AD, NA
*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

5674- BTZ,    Bortezomib-induced unfolded protein response increases oncolytic HSV-1 replication resulting in synergistic, anti-tumor effects
- in-vivo, GBM, NA - in-vivo, HNSCC, NA
ER Stress↑, Bortezomib treatment induced ER stress, evident by strong induction of Grp78, CHOP, PERK and IRE1α
GRP78/BiP↑,
CHOP/DDIT3↑,
PERK↑,
IRE1↑,
UPR↑, and the UPR (induction of hsp40, 70 and 90)
HSP70/HSPA5↑,
HSP90↑,
eff↑, combination of bortezomib and 34.5ENVE significantly enhanced anti-tumor efficacy in multiple different tumor models in vivo.

7816- ISQ,    Isoquercitrin Induces Endoplasmic Reticulum Stress and Immunogenic Cell Death in Gastric Cancer Cells
- in-vitro, GC, AGS - in-vitro, GC, HGC27
TumCP↑, Isoquercitrin at doses greater than 20 μM had significant inhibitory effects on the survival of GC cell lines, including HGC-27, AGS, MKN-45, and SNU-1.
Bcl-2↓, downregulation of BCL-2 and upregulation of BAX, cleaved caspase-3, and caspase-12.
BAX↑,
cl‑Casp3↑,
Casp12↑,
MMP↓, isoquercitrin promoted the disruption of mitochondrial membrane potential in GC cells.
CRT↑, GC cell surface levels of calreticulin (CRT) and extracellular levels of CRT, ATP, and HMGB1 were enhanced by treatment with isoquercitrin.
e-ATP↑,
HMGB1↑,
HSP70/HSPA5↑, The protein levels of HMGB1, HSP70, and HSP90 were upregulated by isoquercitrin in a dose-dependent manner.
HSP90↑,
ER Stress↑, isoquercitrin induces ER stress and ICD in GC cells.

7896- IVT,  VT,    Molecular targets of vitexin and isovitexin in cancer therapy: a critical review
- Review, Var, NA
chemoPv↑, Both in vitro and in vivo studies suggest that vitexin and isovitexin are chemopreventive compounds with activity against various cancers through proapoptotic processes and/or autophagy.
Dose↝, Vitexin and isovitexin are the main constituents of the fruits of Cucurbitaceae, mung beans (Vigna radiata), pigeon pea leaves (Cajanus cajan Millsp.), bamboo leave
ACE/ACE1↓, Experimental studies showed that flavone C-glycosides act as angiotensin-converting enzyme (ACE) inhibitors and have vasodilatory, -blocking, and/ or Ca 2+ channel-blocking activities.
Ca+2↓,
*iNOS↓, C-glycosides reduced lipopolysaccharide-induced proinflammatory cytokine secretion, inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 expression
*COX2/PTGS2↓,
*ROS↓, and reactive oxygen species (ROS) generation
*Stroke↓, provide protective effects against myocardial ischemia–reperfusion injury.
Apoptosis↑, Vitexin-triggered apoptosis was generally accompanied by a decrease in mitochondrial membrane potential and Bcl-2 protein levels, as well as an increase in caspase-3 and caspase-9 protein expression.
MMP↓,
Bcl-2↓,
Casp3↑,
Casp9↑,
TumAuto↑, In heat stress–related research, vitexin promoted autophagy through the upregulation of Hsp90 expression and subsequent activation of endoplasmic reticulum stress.
HSP90↑,
ER Stress↑,
Hif1a↓, vitexin and isovitexin was found in PC12 and CORL-23 cells by inhibiting hypoxia-inducible factor 1 (HIF-1a)
TumMeta↓, resulting in the reduction of the metastatic prospective of PC12 and CORL-23 cells and angiogenesis.
angioG↓, They are prominent antiangiogenic potential agents
Tf↓, Isovitexin and vitexin were found to bind to transferrin (TF), 38 one type of iron-binding glycoprotein that is highly expressed in fast-growing cells, including cancer cells
MAPK↓, Molecular targets for flavone C-glycosides comprise the mitogenactivated protein kinase (MAPK), protein kinase C (PKC), PI3K-Akt, and -catenin pathways
PI3K↓,
Akt↓,
β-catenin/ZEB1↓,
TumCCA↑, Vitexin inhibited growth and induced cell cycle arrest at G1 /G0 by regulating the Akt/FOXO3a pathway
FOXO3↓,
mTOR↓, Vitexin inhibits choriocarcinoma via inducing cell apoptosis and suppressing the mTOR pathway

2429- PB,    Impact of butyrate on PKM2 and HSP90β expression in human colon tissues of different transformation stages: a comparison of gene and protein data
- in-vitro, Colon, NA
PKM2↓, amount of PKM2 transcripts decreased in all three tissue types with the strongest effects observed in tumors (median fold decrease 45%
*HSP90↑, expression of HSP90β in normal tissue was found 1.38-fold increased by butyrate (P < 0.05), but not the corresponding protein level.
HSP90∅, HSP90β expression in adenomas and tumors remained generally insensitive

1437- SFN,    Dietary Sulforaphane in Cancer Chemoprevention: The Role of Epigenetic Regulation and HDAC Inhibition
- Review, NA, NA
HDAC↓, 15 μM
HDAC1↓,
HDAC2↓,
HDAC3↓,
HDAC8↓,
eff↑, this evidence suggests that sulforaphane may also compromise DNA repair mechanisms in cancer cells with selectivity.
ac‑HSP90↑,
DNMT1↓, 10 μM sulforaphane in 6 days inhibited DNMT1 and DNMT3a expression by 48% and 78%, respectively
DNMT3A↓,
hTERT/TERT↓,
NRF2↑, enhance nuclear translocation of Nrf2 and increase expression of Nrf2-target antioxidant genes, including HO-1, NQO1, and UGT1A1
HO-1↑,
NQO1↑,
miR-155↓,
miR-200c↑,
SOX9↓,
*toxicity↓, broccoli sprout-infused beverage containing 400 μM glucoraphanin nightly for 2 weeks causing no adverse effects and being well tolerated in 200 subjects


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

ACE/ACE1↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

HO-1↑, 1,   NQO1↑, 1,   NRF2↑, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

Tf↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

e-ATP↑, 1,   MMP↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

PKM2↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 2,   Casp12↑, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp9↑, 1,   hTERT/TERT↓, 1,   MAPK↓, 1,   MAPK↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

SOX9↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   CRT↑, 1,   ER Stress↑, 3,   GRP78/BiP↑, 1,   HSP70/HSPA5↑, 2,   HSP90↑, 3,   HSP90∅, 1,   ac‑HSP90↑, 1,   IRE1↑, 1,   PERK↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNMT1↓, 1,   DNMT3A↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

FOXO3↓, 1,   HDAC↓, 1,   HDAC1↓, 1,   HDAC2↓, 1,   HDAC3↓, 1,   HDAC8↓, 1,   mTOR↓, 1,   PI3K↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 1,   miR-155↓, 1,   miR-200c↑, 1,   TumCP↑, 1,   TumMeta↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

HMGB1↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,   eff↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

hTERT/TERT↓, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoPv↑, 1,  
Total Targets: 56

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   ROS↓, 2,  

Cell Death(tgid=5) ⓘ

Akt↑, 2,   Apoptosis↓, 1,   iNOS↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↓, 1,   HSP90↑, 3,  

DNA Damage & Repair(tgid=10) ⓘ

p16↓, 1,   TP53↑, 1,  

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

p‑ERK↑, 1,   Jun↓, 1,   mTOR↓, 1,   P70S6K↓, 1,   PI3K↑, 1,  

Migration(tgid=13) ⓘ

APP↓, 1,   CD31/PECAM-1↑, 1,   N-cadherin↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

VEGF↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   Inflam↓, 2,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   Half-Life↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

TP53↑, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 2,   memory↑, 2,   neuroP↑, 2,   toxicity↓, 1,  
Total Targets: 30

Scientific Paper Hit Count for: HSP90, HSP90
2 Berberine
1 Bortezomib
1 isoquercitrin
1 Isovitexin
1 Vitexin
1 Phenylbutyrate
1 Sulforaphane (mainly Broccoli)
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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