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Assays for Validating Histone Acetyltransferase Inhibitors
Published on: August 6, 2020
Histone deacetylase 8 as a novel therapeutic target in oral squamous cell carcinoma
Mee-Young Ahn1, Jung-Hoon Yoon2
1College of Medical and Life Sciences, Division of Bio-industry, Major in Pharmaceutical Engineering, Silla University, Busan 46958, Republic of Korea.
Abstract:
The overexpression of histone deacetylases (HDACs) has been observed in many cancers and inhibition of specific HDAC has emerged as a new target for cancer therapy. The present study examined the expression of HDAC8 and the inhibitory effect of HDAC8 in oral squamous cell carcinoma (OSCC). The expression of HDAC8 was measured in human OSCC tissues and OSCC cell lines using immunohistochemistry and immunoblotting. HDAC8 was knocked down in OSCC cells by transfection with HDAC8 siRNAs and cell proliferation was quantified. Apoptosis and autophagy were measured using flow cytometry and immunoblotting. HDAC8 were overexpressed in OSCC tissues and OSCC cells, mainly localized in the cytoplasm. HDAC8 siRNAs effectively reduced the level of HDAC8 expression and HDAC8 silencing significantly inhibited the proliferation of OSCC cells. HDAC8 knockdown induced apoptotic cell death through caspases activation and pro-survival autophagy in OSCC cells. Combination with HDAC silencing and autophagy inhibition enhanced cell death by increasing apoptosis in OSCC cells. This study suggests that inhibition of HDAC8 might become a novel therapeutic strategy for OSCC.
Insights
Histone deacetylase 8 (HDAC8) is overexpressed in oral squamous cell carcinoma (OSCC). Inhibiting HDAC8 reduces cancer cell proliferation and induces apoptosis, suggesting HDAC8 as a potential therapeutic target for OSCC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Therapeutics
Background:
- Overexpression of histone deacetylases (HDACs) is implicated in various cancers.
- Targeting specific HDACs presents a promising avenue for cancer therapy.
Purpose of the Study:
- To investigate the expression of HDAC8 in oral squamous cell carcinoma (OSCC).
- To evaluate the therapeutic potential of HDAC8 inhibition in OSCC.
Main Methods:
- Immunohistochemistry and immunoblotting were used to measure HDAC8 expression in OSCC tissues and cell lines.
- HDAC8 was silenced using siRNAs in OSCC cells.
- Cell proliferation, apoptosis, and autophagy were quantified using flow cytometry and immunoblotting.
Main Results:
- HDAC8 was found to be overexpressed in OSCC tissues and cell lines, primarily localized in the cytoplasm.
- HDAC8 silencing significantly inhibited OSCC cell proliferation.
- HDAC8 knockdown induced apoptosis via caspase activation and promoted pro-survival autophagy.
Conclusions:
- HDAC8 is overexpressed in OSCC and its inhibition suppresses cancer cell proliferation.
- Combined inhibition of HDAC8 and autophagy enhances cancer cell death.
- HDAC8 inhibition represents a potential novel therapeutic strategy for OSCC.
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