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Enhanced radiosensitivity of EC109 cells by inhibition of HDAC1 expression
Bo Zhang1, Yan Wang, Xueli Pang
1Department of Medical Genetics, College of Basic Medicine, Third Military Medical University, 400038 Chongqing, China.
Abstract:
Histone deacetylase (HDAC) activity plays the role of deacetylation of histone and non-histone proteins, which can alter gene expression patterns and cell behavior potentially associated with malignant transformation. Aberrant expression of HDAC1 has been found in various types of cancers, which indicated that it might be a target for cancer therapy. In this study, overexpression of HDAC1 was found in esophageal cancer samples by real-time RT-PCR, compared with adjacent non-cancerous tissues. To further verify the possibility of anticancer treatment by silencing the increased HDAC1 in esophageal carcinoma cells, HDAC1 expression was knockdown using plasmid-based RNA interference (RNAi). Results showed the HDAC1 expression was efficiently inhibited and the acetylation of histone H3 was significantly increased by RNAi in EC109 cells. Increased apoptotic cell death was observed when HDAC1 expression was knockdown, which indicated that cells were more sensitive to radiation. Moreover, the results also showed DNA was more easily broken by radiation in EC109 cells when HDAC1 expression was knockdown, as measured by γH2AX foci and single-cell electrophoresis. Our data suggested that targeting the increased HDAC1 expression might be feasible for esophageal cancer therapy.
Insights
Targeting histone deacetylase 1 (HDAC1) in esophageal cancer may improve radiation sensitivity. Silencing HDAC1 in cancer cells increases histone acetylation and apoptosis, making them more susceptible to DNA damage from radiation therapy.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Histone deacetylase (HDAC) activity regulates gene expression and cell behavior, potentially contributing to cancer development.
- Aberrant expression of HDAC1 is observed in various cancers, suggesting its role as a therapeutic target.
- Overexpression of HDAC1 is implicated in esophageal carcinoma.
Purpose of the Study:
- To investigate the role of HDAC1 in esophageal cancer.
- To evaluate the therapeutic potential of silencing HDAC1 in esophageal carcinoma cells.
- To determine if HDAC1 inhibition enhances sensitivity to radiation therapy.
Main Methods:
- Real-time RT-PCR to quantify HDAC1 expression in esophageal cancer tissues.
- Plasmid-based RNA interference (RNAi) to knockdown HDAC1 expression in EC109 cells.
- Assays to measure histone H3 acetylation, apoptosis, DNA damage (γH2AX foci, single-cell electrophoresis).
Main Results:
- HDAC1 was overexpressed in esophageal cancer tissues compared to adjacent non-cancerous tissues.
- RNAi-mediated HDAC1 knockdown efficiently inhibited HDAC1 expression and increased histone H3 acetylation in EC109 cells.
- HDAC1 knockdown led to increased apoptotic cell death and enhanced DNA fragmentation upon radiation exposure.
Conclusions:
- Targeting the overexpressed HDAC1 in esophageal cancer is a potential therapeutic strategy.
- Silencing HDAC1 increases cancer cell sensitivity to radiation therapy.
- HDAC1 inhibition may represent a novel approach to improve esophageal cancer treatment outcomes.
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