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↑, 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↑,
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.

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 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↑, 1,   NQO1↑, 1,   NRF2↑, 1,  

Core Metabolism/Glycolysis ⓘ

PKM2↓, 1,  

Cell Death ⓘ

hTERT/TERT↓, 1,   MAPK↑, 1,  

Kinase & Signal Transduction ⓘ

SOX9↓, 1,  

Protein Folding & ER Stress ⓘ

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

DNA Damage & Repair ⓘ

DNMT1↓, 1,   DNMT3A↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,   HDAC1↓, 1,   HDAC2↓, 1,   HDAC3↓, 1,   HDAC8↓, 1,  

Migration ⓘ

miR-155↓, 1,   miR-200c↑, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 2,  

Clinical Biomarkers ⓘ

hTERT/TERT↓, 1,  
Total Targets: 28

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS↓, 1,  

Cell Death ⓘ

Akt↑, 2,   Apoptosis↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,   HSP90↑, 3,  

DNA Damage & Repair ⓘ

p16↓, 1,   TP53↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

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

Migration ⓘ

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

Angiogenesis & Vasculature ⓘ

VEGF↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 2,  

Protein Aggregation ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

TP53↑, 1,  

Functional Outcomes ⓘ

cognitive↑, 2,   memory↑, 2,   neuroP↑, 2,   toxicity↓, 1,  
Total Targets: 27

Scientific Paper Hit Count for: HSP90, HSP90
2 Berberine
1 Bortezomib
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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:149  State#:%  Dir#:2
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