Role of arid3A in the regulation of LNCRNA Ericd

ERICD (E2F1-Regulated Inhibitor of Cell Death) is a newly found lncRNA located on chromosome 8. ERICD is regulated by E2F1. ARID3A/DRIL1/Bright is a family member of the AT rich interaction domain (ARID) DNA-binding proteins that are involved in diverse biological processes. ARID3A binds to the E2F transcription factor and activates E2F-dependent transcription. I have found putative binding sites of ARID3A on ERICD. I think that ARID3A and ERICD might be regulated by each other for several biological processes in cancer. The other hypothesis for selecting these two in our study is that both of them have just opposite roles in apoptosis in case of DNA damage indicating a probability of reciprocal interaction between each other. To explore if ARID3A regulates expression of lncRNA ERICD, I took advantage of a human osteosarcoma cell line (U2OS) that each express conditionally active ARID3A and ERICD. Overexpression and knockdown experiments were carried out for ARID3A and knockdown experiment was done for ERICD. Migration assay and colony formation assays were also performed in U2OS. siRNA-mediated knockdown of ARID3A and ERICD inhibited cell migration and reduced the formation of colonies in U2OS cells to a considerable degree. On the other side overexpression of ARID3A confirmed a significant induction in wound closure and increased colony forming ability of U2OS cells. In summary, the obtained data in my thesis suggest that ARID3A and ERICD interact with each other indirectly via E2F1. Moreover, ARID3A and lncRNA ERICD have oncogenic functions in osteosarcoma. The interaction that has been found between ARID3A and lncRNA ERICD is novel and adds a further milestone regarding lncRNAs targeting DNA binding proteins.