HSP27 Cancer Research Results

HSP27, Heat shock protein 27: Click to Expand ⟱
Source:
Type: Protein
Heat Shock Protein 27 (Hsp27), also known as HSPB1, is a small heat shock protein that plays a crucial role in cellular stress responses, protein folding, and protection against apoptosis.
Hsp27 is involved in various cellular processes, including the stabilization of proteins, regulation of the cytoskeleton, and modulation of signaling pathways.
Acts as a protein chaperone and an antioxidant and plays a role in the inhibition of apoptosis and actin cytoskeletal remodeling. Plays a key role in anti-cancer treatment resistance, inhibition of apoptosis and tumor progression. HSP27 is upregulated in many cancers and is associated with a poor prognosis.

Expression in Cancers: Hsp27 is often overexpressed in various types of cancers, including breast, prostate, lung, and colorectal cancers. Its expression can be induced by stressors such as heat shock, oxidative stress, and exposure to certain chemotherapeutic agents.
Prognostic Implications: The expression levels of Hsp27 have been associated with cancer prognosis. In many studies, high levels of Hsp27 expression correlate with poor prognosis, increased tumor aggressiveness, and resistance to chemotherapy.
Scientific Papers found: Click to Expand⟱
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↓,

2028- PB,    Potential of Phenylbutyrate as Adjuvant Chemotherapy: An Overview of Cellular and Molecular Anticancer Mechanisms
- Review, Var, NA
HDAC↓, Phenylbutyrate is one of the first drugs encountered in cancer therapy as a histone deacetylase inhibitor (HDACI).
TumCCA↑, phenylbutyrate treatment that results in reduced proliferation and cell-cycle arrest in G1 or G2 phases.
P21↑, common sequela of phenylbutyrate treatment is the upregulation of p21,
Dose↝, In prostate cancer, phenylbutyrate at clinically achievable concentrations (0.1 mM-8 mM),
Telomerase↓, butyrate or its derivatives was also evident in several other types of cancers and was associated with loss of telomerase activity
IGFBP3↑, Upregulation of insulin-like growth factor binding protein 3 (IGFBP-3) is another unique antiproliferative mechanism of sodium butyrate in breast cancer cells
p‑p38↑, Phenylbutyrate and its derivatives upregulated p21, gelsolin, phosphorylated p38, JNK, and ERK (MAPK pathway members), Bax, caspases-3,
JNK↑,
ERK↑,
BAX↑,
Casp3↑,
Bcl-2↓, downregulated Bcl-X L , Bcl-2, cytochrome c, FAK, and survivin
Cyt‑c↝,
FAK↓,
survivin↓,
VEGF↓, Butyrate treatment reduced the level of vascular endothelial growth factor (VEGF)
angioG↓,
DNArepair↓, Inhibition of DNA Repair.
TumMeta↓,
HSP27↑, Moreover, butyrate treatment in colorectal cancer cells resulted in an acute stress response that was associated with HSP27 activation, activation of ASK1 (MAP3K) and p38 MAPK pathway consequently.
ASK1↑,
ROS↑, Also it resulted in elevated cellular levels of reactive oxygen species (ROS) in oral and tongue cancer cells.
eff↑, phenylbutyrate enhanced the cytotoxicity of temozolamide in malignant glioma cells via suppression of the endoplasmic reticulum stress revealed by the decreased expression of GRP78 and GADD153.
ER Stress↓,
GRP78/BiP↓,
CHOP↑, GADD153
AR↓, Sodium butyrate treatment of prostate cancer cells was associated with downregulation of androgen receptor
other?, lots of references in this paper.

3192- SFN,    Transcriptome analysis reveals a dynamic and differential transcriptional response to sulforaphane in normal and prostate cancer cells and suggests a role for Sp1 in chemoprevention
- in-vitro, Pca, PC3
Sp1/3/4↓, Sp1 protein was significantly decreased by SFN treatment in prostate cancer cells . Because SFN decreased the expression of Sp1, and to a lesser extent Sp3
selectivity↑, SFN alters gene expression differentially in normal and cancer cells with key targets in chemopreventive processes, making it a promising dietary anti-cancer agent.
NRF2↑, through the induction of phase 2 enzymes via Keap1-Nrf2 signaling
HDAC↓, SFN also inhibits the activity and/or expression of genes that regulate epigenetic mechanisms including histone deactylases (HDACs) and DNA methyltransferases (DNMTs) in cancer cells
DNMTs↓,
TumCCA↑, 15 μM SFN treatment induces cell cycle arrest at the G1 phase and only modestly increases apoptosis
selectivity↑, Normal prostate epithelial cells (PREC) do not undergo cell cycle arrest or apoptosis in response to this SFN treatment
HO-1↑, In all cell lines and time points, HO1 and NQO1 were identified as significantly upregulated by SFN
NQO1↑,
CDK2↓, MX non-receptor tyrosine kinase (BMX), cyclin-dependent kinase 2 (CDK2), and polo-like kinase 1 (PLK1) had decreased expression with SFN treatment
TumCP↓, suppression of Sp1 expression decreased prostate cancer cells proliferation.
BID↑, SFN treatment produced a significant increase in the expression of the apoptosis related genes Bid, Smac/Diablo, and ICAD only in PC-3 cells (
Smad1↑,
Diablo↑,
ICAD↑,
Cyt‑c↑, It also increased the expression of cytochrome c, c-IAP1, and HSP27 in PC-3 cells while it decreased expression in PREC cells.
IAP1↑,
HSP27↑,
*Cyt‑c↓,
*IAP1↓,
*HSP27↓,
survivin↓, In these studies, inhibition of Sp1 is associated with inhibition of the cancer promoting genes survivin, CDK4, VEGF and the androgen receptor.
CDK4↓,
VEGF↓,
AR↓,

3648- SIL,    Silymarin/Silybin and Chronic Liver Disease: A Marriage of Many Years
- Review, NA, NA
*antiOx↑, antioxidant, anti-inflammatory and antifibrotic power
*Inflam↓,
*lipid-P↓, reduce both lipid peroxidation and cellular necrosis.
*necrosis↓,
*hepatoP↑, silybin use in chronic liver diseases, cirrhosis and hepatocellular carcinoma.
*IL1↓, figure 1
*IL6↓,
*TNF-α↓,
*IFN-γ↓,
MAPK↓,
Apoptosis↑,
Cyt‑c↑,
Casp3↑,
Casp9↑,
*PPARγ↑,
*GLUT4↑,
*HSPs↓,
*HSP27↑,
*Trx↑,
*SIRT1↑,
*ALAT↓, as well as prevent ALT increase, Glutathione (GSH) decrease, lipid peroxidation and TNF-α increase
*GSH↑,
*lipid-P↓,
*TNF-α↓,
TumCG↓, silybin significantly reduces HuH7, HepG2, Hep3B, and PLC/PRF/5 human hepatoma cells growth by increasing cyclin-dependent kinase inhibitor p21 and p27/cyclin-dependent kinase (CDK) 4 complexes, by reducing retinoblastoma protein (Rb)-phosphorylatio
P21↑,
CDK4↑,


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GPx1↓, 1,   GPx4↓, 1,   HO-1↑, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↑, 2,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 2,   ASK1↑, 1,   BAD↑, 1,   p‑BAD↓, 1,   BAX↑, 1,   Bcl-2↓, 2,   BID↑, 1,   Casp3↑, 2,   Casp9↑, 1,   Cyt‑c↑, 2,   Cyt‑c↝, 1,   Diablo↑, 1,   IAP1↑, 1,   ICAD↑, 1,   JNK↑, 1,   MAPK↓, 1,   p‑p38↑, 1,   survivin↓, 2,   Telomerase↓, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

other?, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↓, 1,   GRP78/BiP↓, 1,   HSP27↑, 3,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   p62↑, 1,  

DNA Damage & Repair ⓘ

DNArepair↓, 1,   DNMTs↓, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   CDK4↑, 1,   P21↑, 2,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,   HDAC↓, 2,   IGFBP3↑, 1,   TumCG↓, 1,  

Migration ⓘ

FAK↓, 1,   Smad1↑, 1,   TumCP↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 2,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 2,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,   eff↑, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

AR↓, 2,  
Total Targets: 58

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GSH↑, 1,   lipid-P↓, 2,   Trx↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   PPARγ↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Cyt‑c↓, 1,   IAP1↓, 1,   necrosis↓, 1,  

Protein Folding & ER Stress ⓘ

HSP27↓, 1,   HSP27↑, 1,   HSPs↓, 1,  

Barriers & Transport ⓘ

GLUT4↑, 1,  

Immune & Inflammatory Signaling ⓘ

IFN-γ↓, 1,   IL1↓, 1,   IL6↓, 1,   Inflam↓, 1,   TNF-α↓, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   IL6↓, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,  
Total Targets: 22

Scientific Paper Hit Count for: HSP27, Heat shock protein 27
1 Curcumin
1 Phenylbutyrate
1 Sulforaphane (mainly Broccoli)
1 Silymarin (Milk Thistle) silibinin
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#:386  State#:%  Dir#:2
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