124P - Lack of HDAC1 and HDAC2 promote breast cancer aggressiveness

Date 18 December 2016
Event ESMO Asia 2016 Congress
Session Poster lunch
Topics Breast Cancer, Metastatic
Translational Research
Presenter Nur Sabrina Kamarulzaman
Citation Annals of Oncology (2016) 27 (suppl_9): ix35-ix41. 10.1093/annonc/mdw577
Authors N.S. Kamarulzaman1, H.D. Dewadas1, N.S. Yaacob2, N.F. Mokhtar1
  • 1Institute For Research In Molecular Medicine (informm), Universiti Sains Malaysia, Health Campus, 16150 - Kota Bharu/MY
  • 2Department Of Chemical Pathology, School Of Medical Sciences, Universiti Sains Malaysia, Health Campus, 16150 - Kubang Kerian/MY



Dysregulation of histone deacetylases (HDACs) is one of the factors which affect transcriptional regulation of various genes involve in cancer progression. Owing to the discovery of HDAC inhibitors, studies on HDACs in pathological condition, particularly in various human cancers have increased in recent years. In breast cancer, HDAC1, HDAC2 and HDAC3 have been linked to cancer progression. However, the role of each HDAC in breast cancer with different metastatic potential remains unclear. This study aimed to investigate the role of HDACs in the aggressive and the less aggressive breast cancer cell types.


Basal expression of HDAC1, HDAC2 and HDAC3 were measured using quantitative real-time RT-PCR and were compared between the aggressive and the less aggressive human breast cancer cell lines, MDA-MB-231 and MCF-7 cells, respectively. MCF-7 cells were treated with a HDAC inhibitor, Trichostatin A (TSA), at several concentrations (100-10 000 ng/ml) for 24h. Cell growth and migration assays were conducted to determine the effect of TSA on metastatic behaviour of MCF-7 cells.


In comparison to MCF-7 cells, the gene expression of HDAC1, HDAC2 and HDAC3 were expressed lower in MDA-MB-231 cells. Treatment with TSA on MCF-7 cells reduced the gene expression of HDAC1, HDAC2 but not HDAC3, in a dose-dependent manner. Although the growth of MCF-7 cells was inhibited by TSA, the migration was enhanced.


This study demonstrates the important role of HDAC1 and HDAC2 in the less aggressive breast cancer in suppressing metastasis, in which both molecules are lacking in the aggressive MDA-MB-231 cells. Additionally, these findings raise concern that the application of HDAC inhibitors as cancer therapy on cancer patients may establish metastasis.

Clinical trial indentification

Legal entity responsible for the study

Institute for Research in Molecular Medicine, Universiti Sains Malaysia, Malaysia


Ministry of Higher Education (MOHE), Malaysia


All authors have declared no conflicts of interest.