Thesis Type: Postgraduate
Institution Of The Thesis: Orta Doğu Teknik Üniversitesi, Faculty of Arts and Sciences, Department of Biology, Turkey
Approval Date: 2014
Student: NİHAN ÖZDEMİRLER
Supervisor: AYŞE ELİF ERSON BENSANAbstract:
The ARID, A-T Rich Interaction Domain, is a helix-turn-helix motif based domain which binds to DNA by both sequence-specific and non-sequence specific manners. The ARID protein family is found in protozoa, green algae, higher plants, fungi and metazoans, while it is not seen in archea or eubacteria. ARID domain harboring genes are involved in variety of biological processes including embryonic development, cell lineage gene regulation, chromatin modification and cell cycle control.ARID3B, a member of ARID family, is highly conserved throughout evolution. It is homologous to retinoblastoma binding proteins, mouse Bright and Drosophila dead ringer protein. ARID3B has several roles in cellular processes; histone methylation, chromatin structure modification, transcriptional activation and possibly in development. Given its known roles, ARID3B has been linked to cellular transformation and tumor progression, and was shown to be deregulated in various different cancers. A possible link between ARID3B and breast cancer was suggested by our group. We reported miR-125b, a tumor suppressor in breast cancers to target and downregulate ARID3B mRNA. In this study, we aimed to contribute to the efforts to better understand ARID3B function in breast cancers by analyzing its expression in breast cancer cell lines. Our results confirmed the immunohistochemistry (IHC) studies performed in our lab on patient samples where a positive correlation between ARID3B expression and ER positivity was detected. Interestingly, we also detected a negative correlation between ARID3B and ERBB2 positivity, also confirming the IHC studies. Future studies will be required to mechanistically confirm these observations and their significance in terms of breast carcinogenesis.