ArticleOncotarget2012
Heat Shock Protein 90 is overexpressed in high-risk myelodysplastic syndromes and associated with higher expression and activation of Focal Adhesion Kinase.
Article in Oncotarget, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Peripheral blood mononuclear cell proteome changes in patients with myelodysplastic syndrome.BioMed research international · 2015Trial
- TP53 in Myelodysplastic Syndromes.Cancers · 2021Review
- Combination of HDE and BIIB021 efficiently inhibits cell proliferation and induces apoptosis via downregulating hTERT in myelodysplastic syndromes.Experimental and therapeutic medicine · 2021Article
- Heat shock protein 90-targeted photodynamic therapy enables treatment of subcutaneous and visceral tumors.Communications biology · 2020Article
- Integrated bioinformatic analysis of microarray data reveals shared gene signature between MDS and AML.Oncology letters · 2018Article
- Impaired Expression of Focal Adhesion Kinase in Mesenchymal Stromal Cells from Low-Risk Myelodysplastic Syndrome Patients.Frontiers in oncology · 2017Article
- MicroRNA-223 is a novel negative regulator of HSP90B1 in CLL.BMC cancer · 2015Article
- Heat shock protein 90β stabilizes focal adhesion kinase and enhances cell migration and invasion in breast cancer cells.Experimental cell research · 2014Article
- BIIB021, an Hsp90 inhibitor, effectively kills a myelodysplastic syndrome cell line via the activation of caspases and inhibition of PI3K/Akt and NF-κB pathway proteins.Experimental and therapeutic medicine · 2014Article
- PTK2 and PTPN11 expression in myelodysplastic syndromes.Clinics (Sao Paulo, Brazil) · 2013Article
- Targeting HSF1 sensitizes cancer cells to HSP90 inhibition.Oncotarget · 2013Article
- Inhibiting the molecular evolution of cancer through HSP90.Oncotarget · 2012Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myelodysplastic syndromes are characterized by a high risk of evolution into acute myeloid leukaemia which can involve activation of signalling pathways. As the chaperone heat shock protein 90 (HSP90) has a key role in signal transduction, we investigated its role in the pathogenesis and evolution of myelodysplastic syndromes. Expressions of HSP90 and signalling proteins clients (phosphorylated-AKT (pAKT), Focal Adhesion Kinase (FAK) and phosphorylated-FAK (pFAK)), were assessed in bone marrow mononuclear and CD34-positive (CD34+) cells from 177 patients with myelodysplasia. Effects of HSP90 inhibition were also evaluated in 39 samples. The levels of all proteins studied were significantly higher in patients with high grade disease, than those with low grade myelodysplastic syndrome or chronic myelomonocytic leukaemia. High levels of HSP90, FAK, pFAK and pAKT were associated with shorter survival and increased risk of progression into acute leukaemia. A down regulation of pFAK and pAKT and increased apoptosis was observed in mononuclear and CD34+ cells after 12 hours of incubation with 17-AAG. In conclusion, our data suggest the implication of HSP90 and FAK and AKT activation in the pathogenesis of myelodysplastic syndromes with excess of blasts and evolution to leukaemia. Moreover this signalling network could be a therapeutic target through HSP90 inhibition.
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