ArticleBioscience reports2020
2-phenylethynesulfonamide inhibits growth of oral squamous cell carcinoma cells by blocking the function of heat shock protein 70.
Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Heat shock proteins as hallmarks of cancer: insights from molecular mechanisms to therapeutic strategies.Journal of hematology & oncology · 2024Review
- The Multiple Roles of CD147 in the Development and Progression of Oral Squamous Cell Carcinoma: An Overview.International journal of molecular sciences · 2022Review
- Study on the mechanism of SALL4 down-regulation in promoting the invasion and migration of oral squamous cell carcinoma and influencing the survival and prognosis of patients.Annals of translational medicine · 2022Article
- Advances in the study of HSP70 inhibitors to enhance the sensitivity of tumor cells to radiotherapy.Frontiers in cell and developmental biology · 2022Review
- Inhibition ofFrontiers in molecular biosciences · 2022Article
- Curcumin suppresses the proliferation of oral squamous cell carcinoma through a specificity protein 1/nuclear factor-κB-dependent pathway.Experimental and therapeutic medicine · 2021Article
- Anlotinib Suppresses Oral Squamous Cell Carcinoma Growth and Metastasis by Targeting the RAS Protein to Inhibit the PI3K/Akt Signalling Pathway.Analytical cellular pathology (Amsterdam) · 2021Article
- The role of heat shock proteins in neoplastic processes and the research on their importance in the diagnosis and treatment of cancer.Contemporary oncology (Poznan, Poland) · 2021Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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