Inhibition of heat shock protein 90 exerts an antitumour effect in angiosarcoma: involvement of the vascular endothelial growth factor signalling pathway

Yamada‐Kanazawa, Saori; Kajihara, Ikko; Fukushima, Satoshi; Jinnin, Masatoshi; Masuzawa, Mikio; Amoh, Yasuyuki; Hoshina, Daichi; Abe, Riichiro; Ihn, Hironobu

doi:10.1111/bjd.15303

Cited by 16 publications

(19 citation statements)

References 47 publications

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“…Ito et al [ 10 ] found that forkhead box M1 (FOXM1) serves as a prognostic marker for patients with cAS, and is a candidate drug target. Yamada-Kanazawa et al [ 11 ] highlighted the role of heat shock protein (HSP) 90 in cAS. They used various cAS cell lines to show that HSP90 inhibition suppresses the proliferation, migration, and invasion of cAS cells.…”

Section: Biologymentioning

confidence: 99%

Cutaneous angiosarcoma: update on biology and latest treatment

Ishida

Otsuka

Kabashima

2018

Current Opinion in Oncology

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Purpose of reviewThe present review aims to provide readers with the latest updates on the biology and clinical management of cutaneous angiosarcoma (cAS).Recent findingsThe genomic alteration of cAS is heterogeneous. Mutations are enriched in the mitosis-activated kinase (MAPK) pathway. Functional analysis has identified molecules that may serve as potential markers and therapeutic targets of angiosarcoma. These molecules include survivin, HSP90, FOXM1, miR-497-5p, KCa3.1, and miR210.This body of knowledge has not yet transferred to clinical practice. The mainstay of treatment for cAS remains surgery followed by postoperative radiotherapy. The efficacy of paclitaxel as an adjuvant chemotherapy is suggested.For patients with advanced cAS, paclitaxel is the treatment of choice. There are also second-line treatment options that are supported by evidence of varying strength. A multikinase inhibitor, pazopanib, has been assessed in several studies, most of which support its efficacy for angiosarcoma. Bevacizumab monotherapy may be effective for angiosarcoma. The efficacy of eribulin mesylate and trabectedin for angiosarcoma is currently being assessed. Recent publications highlighted the role of the immune system in the biology of cAS.SummaryFuture research efforts should focus on the following aspects of cAS: drug development directed at recent molecular targets, clinical trials designed specifically for patients with cAS, and the role of immunotherapy for cAS.

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Section: Biologymentioning

confidence: 99%

Cutaneous angiosarcoma: update on biology and latest treatment

Ishida

Otsuka

Kabashima

2018

Current Opinion in Oncology

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“…In addition, HSP90 has been considered to be a potent target for cancer therapy, and various HSP90 inhibitors have been developed as anti-cancer agents since HSP90 stabilizes proteins necessary for progression of cancer cells (20). It has been reported that knock-down of HSP90 suppresses the migration and proliferation of angiosarcoma cells (25). Accumulating evidence indicates that HSP90 is involved also in various physiological cellular functions such as regulation of glucocorticoid receptors (20).…”

Section: Discussionmentioning

confidence: 99%

HSP90 inhibitors diminish PDGF-BB-induced migration of osteoblasts via suppression of p44/p42 MAP kinase

et al. 2019

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Migration of osteoblasts to the sites resorbed by osteoclasts is an essential step in bone remodeling. However, the exact mechanism of osteoblast migration is still not known. We have shown that platelet-derived growth factor (PDGF)-BB induces the migration of osteoblast-like MC3T3-E1 cells through the activation of p38 mitogen-activated protein (MAP) kinase, c-Jun N-terminal kinase (JNK) and p44/p42 MAP kinase. Evidence is accumulating that heat shock protein 90 (HSP90) acts as a central regulator of proteostasis under stress conditions and physiological cell functions. In the present study, using transwell cell migration assay and wound-healing assay, we investigated the involvement of HSP90 in the PDGF-BB-stimulated migration of MC3T3-E1 cells, and the underlying signaling mechanism estimated by Western blot analyses. Onalespib, an HSP90 inhibitor, significantly reduced the PDGF-BB-stimulated migration evaluated by the two types of migration assays. The cell migration was also suppressed by geldanamycin, another type of HSP90 inhibitor. Onalespib markedly attenuated the PDGF-BB-elicited phosphorylation of p44/ p42 MAP kinase without affecting that of p38 MAP kinase or JNK. In addition, the phosphorylation of p44/p42 MAP kinase by PDGF-BB was reduced by geldanamycin. Taken together, these results strongly suggest that HSP90 inhibitors suppress the PDGF-BB-induced osteoblast migration through the attenuation of p44/p42 MAP kinase activity.

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“…Patients with angiosarcoma often present with high‐grade histology and multifocal disease, and the prognosis of advanced angiosarcoma is poor, often because of highly developed resistance to standard chemotherapy. New treatment strategies are critically needed to overcome treatment resistance and provide long‐term tumour control of this aggressive disease …”

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confidence: 99%

“…In this issue of the BJD , Yamada‐Kanazawa et al . describe the interesting observation of characteristic heat shock protein 90 (HSP90) overexpression in angiosarcomas, thus opening up inhibition of HSP90 as a new potentially useful approach in the management of patients with angiosarcoma . HSP90 is a critical molecular chaperone regulating various cancer‐related proteins, hence involved in virtually all ‘hallmarks of cancer’ .…”

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confidence: 99%