AI Article Synopsis
- The study aims to understand how ionizing radiation (IR) influences matrix metalloproteinase (MMP) activity and cancer cell invasion, and whether this process can be altered by inhibiting histone deacetylases (HDAC).
- Human breast cancer cell lines (MDA-MB-231 and MCF-7) were used to analyze their invasion capabilities and gene expression after IR exposure, both with and without HDAC inhibitors.
- Results indicated that IR significantly increased invasion and MMP expression in MDA-MB-231 cells, but not in MCF-7, and that inhibition with valproic acid reduced these effects, highlighting a potential strategy for modifying cancer cell behavior post-radiation.
Article Abstract
Purpose: To evaluate matrix metalloproteinase (MMP) activity and invasion after ionizing radiation (IR) exposure and to determine whether MMP could be epigenetically modulated by histone deacetylase (HDAC) inhibition.
Material And Methods: Two human breast cancer cell lines (MDA-MB-231 and MCF-7) were cultured in monolayer (2D) and in laminin-rich extracellular matrix (3D). Invasion capability, collagenolytic and gelatinolytic activity, MMP and TIMP protein and mRNA expression and clonogenic survival were analyzed after IR exposure, with and without a HDAC inhibition treatment [1.5 mM valproic acid (VA) or 1 μM trichostatin-A (TSA)].
Results: IR exposure resulted in cell line-dependent stimulation of invasion capacity. In contrast to MCF-7 cells, irradiated MDA-MB-231 showed significantly enhanced mRNA expression of mmp-1, mmp-3 and mmp-13 and of their regulators timp-1 and timp-2 relative to unirradiated controls. This translated into increased collagenolytic and gelatinolytic activity and could be reduced after valproic acid (VA) treatment. Additionally, VA also mitigated IR-enhanced mmp and timp mRNA expression as well as IR-increased invasion capability. Finally, our data confirm the radiosensitizing effect of VA.
Conclusion: These results suggest that IR cell line-dependently induces upregulation of MMP mRNA expression, which appears to be mechanistically linked to a higher invasion capability that is modifiable by HDAC inhibition.
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| http://dx.doi.org/10.3109/09553002.2015.1087067 | DOI Listing |
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