Heat shock protein 90 as a molecular target for therapy in oral squamous cell carcinoma: Inhibitory effects of 17‑DMAG and ganetespib on tumor cells

2020 ◽  
Vol 45 (2) ◽  
pp. 448-458
Author(s):  
Naoki Shiraishi ◽  
Takeshi Onda ◽  
Kamichika Hayashi ◽  
Kaoru Onidani ◽  
Katsuhito Watanabe ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Heat Shock ◽  
Oral Squamous Cell Carcinoma ◽  
Heat Shock Protein ◽  
Cell Carcinoma ◽  
Tumor Cells ◽  
Squamous Cell ◽  
Heat Shock Protein 90 ◽  
Molecular Target ◽  
Inhibitory Effects

scholarly journals 2-phenylethynesulfonamide inhibits growth of oral squamous cell carcinoma cells by blocking the function of heat shock protein 70

2020 ◽  
Vol 40 (3) ◽  
Author(s):  
Liang Jiang ◽  
Jing Xiao
Keyword(s):  
Cell Cycle ◽  
Squamous Cell Carcinoma ◽  
Heat Shock ◽  
Oral Squamous Cell Carcinoma ◽  
Heat Shock Protein ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Heat Shock Protein 70 ◽  
Phosphorylated Akt ◽  
Apoptosis Protein

Abstract Oral squamous cell carcinoma (OSCC) is the most common malignancy in the oral cavity, which accounts for >90% of all diagnosed oral cancers. 2-phenylethynesulfonamide (PES) was known as a selective heat shock protein 70 (Hsp70) function inhibitor, which induced cytotoxic effects on various tumor cell types, but showed to be less toxic to normal cells. However, no associated evaluation of PES on OSCC was found. In the present study, the proliferation of OSCC cells treated with PES was analyzed using a CCK-8 assay. The effects of PES on the cell cycle and apoptosis of OSCC cells were determined by flow cytometric analyses. Expression of associated protein was determined by Western blot analysis. The results of the present study showed that PES inhibited the proliferation of OSCC cell lines in vivo and in vitro. PES induced apoptosis and arrested the cell cycle of OSCC cells. PES inhibited the expression of X-linked inhibitor of apoptosis protein (XIAP), baculoviral IAP repeat containing 2 (c-IAP1), phosphorylated AKT (p-AKT), and phosphorylated extracellular signal-regulated kinase (p-ERK). Additionally, knockdown of Hsp70 enhanced the effects of PES. By contrast, overexpression of Hsp70 attenuated the inhibitory effects of PES on cell viability. PES disrupted the interaction between Hsp70 and XIAP. In conclusion, the present study demonstrated that PES suppresses the growth of OSCC cells through Hsp70-dependent mechanism.

scholarly journals Heat Shock Protein 40 (Hsp40) and Hsp70 Protein Expression in Oral Squamous Cell Carcinoma (OSCC)

2013 ◽  
Vol 04 (03) ◽  
pp. 734-741 ◽  
Author(s):  
Adi Prayitno ◽  
Elyana Asnar ◽  
Okid Parama Astirin ◽  
Dinar Rosmala ◽  
Suhartono Taat Putra
Keyword(s):  
Squamous Cell Carcinoma ◽  
Heat Shock ◽  
Oral Squamous Cell Carcinoma ◽  
Heat Shock Protein ◽  
Protein Expression ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Hsp70 Protein
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