Stable maintenance of genetic information is essential for cell viability. Genetic instability, a condition in which the genome is not properly maintained, causes numerous pathologies including cancer and aging. Transposable elements (TEs) comprise ~45% of our genome and mobilize to other genomic loci, termed transposition. TEs destabilize genetic information and cause various diseases-associated phenotypes including cancer. It has also been reported that TE expression is associated with aging and inflammation. We are interested in the mechanisms of how TEs mobilize in our genome and result in disease-associated phenotypes.
Aging can be defined as the accumulation of damaged cells caused by various stresses. Stress is generally considered to be non-adaptive. However, low-dose stress can act in an adaptive role by fostering cell resistance to prospective lethal stresses. This process is termed acquired tolerance (or hormesis) and its molecular mechanisms remain largely unknown. We are trying to understand how acquired tolerance is induced molecularly. Arguably, cancer cells in vivo acquire stress resistance through experiencing ever-lasting environmental changes. As such, inhibiting the acquired tolerance in cancer cells may lead to fragility of cancers to various stresses, including iatrogenic ones.

• Mechanisms of retrotransposition and its impact on genomic instability in the mammalian genome.
• Host defense mechanisms that inhibit retrotransposition.
• Development of therapeutic strategies for cancer by elucidating the mechanisms of cellular senescence.
• Functional roles of acquired tolerance in various physiological and pathological conditions.