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Updated: Jul 7, 2026
Assays for Validating Histone Acetyltransferase Inhibitors
Published on: August 6, 2020
Histone deacetylase (HDAC) encoding gene expression in pancreatic cancer cell lines and cell sensitivity to HDAC
M Ouaïssi1, S Cabral, J Tavares
1Service de chirurgie Digestive et Oncologique, Hôpital Timone, Marseille, France.
Purpose:
Multiple biochemical and molecular alterations occur in pancreatic cancer cells. In the present study, attempts were made for the first time, to explore the level of expression of members of histone deacetylase encoding genes (HDACs) in four pancreatic tumor cell lines: Panc-1, BxPC-3, SOJ-6 and MiaPaCa-2; and two non-related tumor cells: Jurkat and HeLa. Furthermore, we examined the possible relationship between the levels of HDACs expression and the sensitivity/resistance to HDAC inhibitors (TSA, Nicotinamide and Sirtinol).
Results:
We have found that although a slight variation in the profiles of gene expression among cell lines could be evidenced, HDACs protein synthesis seem to be similar. Furthermore, the cells were equally sensitive to inhibition by Sirtinol whereas some variation in the IC(50) could be seen in the case of TSA. We also demonstrate that the drugs had the capacity to induce the death of cells by apoptosis.
Methods:
We have used four human pancreatic tumor cell lines and two-non related tumor cells, to evaluate the expression of HDAC encoding genes by RT-PCR and Western blot analysis. We also measured the effect of certain HDAC inhibitors (HDIs) on cell growth, cell cycle alteration, membrane phosphatidyl-serine exposure, DNA fragmentation and mitochondrial membrane potential loss.
Conclusions:
Taken together, our data support the notion that the level of cell sensitivity to the HDIs might be related to the level of expression of genes such as those encoding proteins playing a role in cell cycle checkpoints control but not HDAC per se.
Insights
Histone deacetylase (HDAC) gene expression in pancreatic cancer cells was analyzed. Cell sensitivity to HDAC inhibitors may relate to cell cycle checkpoint genes, not HDACs themselves.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Pancreatic cancer exhibits numerous biochemical and molecular alterations.
- Understanding gene expression patterns in pancreatic cancer is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the expression levels of histone deacetylase (HDAC) encoding genes in human pancreatic tumor cell lines.
- To determine the relationship between HDAC expression and sensitivity to HDAC inhibitors (TSA, Nicotinamide, Sirtinol).
Main Methods:
- Utilized RT-PCR and Western blot analysis to assess HDAC gene and protein expression in four pancreatic cell lines (Panc-1, BxPC-3, SOJ-6, MiaPaCa-2) and two non-related cell lines (Jurkat, HeLa).
- Evaluated the impact of HDAC inhibitors on cell growth, cell cycle, apoptosis (membrane phosphatidyl-serine exposure, DNA fragmentation), and mitochondrial membrane potential.
Main Results:
- HDAC protein synthesis appeared similar across cell lines, despite slight variations in gene expression profiles.
- Cells showed equal sensitivity to Sirtinol, with some variation in IC50 for TSA.
- HDAC inhibitors induced cell death through apoptosis.
Conclusions:
- Cellular sensitivity to HDAC inhibitors may be linked to the expression of genes involved in cell cycle checkpoints.
- The study suggests that HDAC expression levels alone may not be the sole determinant of sensitivity to HDAC inhibitors in pancreatic cancer.
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