Student Profile: Roy Kim
About my path to academic dentistryI was born in Seoul, South Korea and came to the Unites States when I was 3 years old. I attended University of California at Riverside where I received my Bachelor of Science degree in Biology and tutored math and science where I developed a passion for teaching. I continued to teach while I worked at Physician's Formula for 5 years. In 2006, I enrolled at UCLA to obtain a Master of Science degree in Oral Biology and I successfully defended my thesis on October 28th 2010 as a third year dental student.
At UCLA I worked in a lab with many talented scientists as part of my research to earn my degree. I was introduced to the lab by Dr. Ki-Hyuk Shin and after a few months I started working under the guidance of Dr. Mo Kang. During my time in the lab I also had the opportunity to observe Dr. Reuben Kim complete his Ph.D. and become a new faculty member. I was very fortunate to complete my thesis under the guidance of my mentors, Dr. No-Hee Park and Dr. Mo Kang.
The great thing about the R25 Academic Track Program is that it provides us with guidance in the things we need as students who are interested in teaching as a future career. Before the R25, I was very limited with the knowledge I possessed about a possible future in academics, but I have learned a great deal about the different avenues available to me. One of the most valuable aspects of the Academic Track is that it provides opportunities to learn and interact with a vast array of faculty members and to learn how they were able to get to their respective positions.
About my research
Radioprotection of Oral Mucosa Cells by Bmi-1
Bmi-1 is a polycomb group protein necessary for cellular proliferation and maintenance of stem cell phenotype. The current study was undertaken to determine the role of Bmi-1 in protecting the human oral and cutaneous epithelial cells from the growth inhibitory and cytotoxic effects of ionizing radiation (IR). Primary normal human keratinocytes (NHK) from skin or oral mucosa were infected with retroviruses expressing Bmi-1(RV-Bmi-1) or empty vector (RV-B0). The infected cells were exposed to 0, 5, or 10 Gy IR and assayed for phenotypic alterations, i.e., clonogenic efficiency, cell morphology, and expression of senescence-associated beta-galactosidase (SA β-Gal) activity. NHK infected with RV-B0 (NHK/B0) rapidly underwent premature senescence upon exposure to 5 or 10 Gy IR. However, the cells overexpressing Bmi-1 (NHK/Bmi-1) continued to replicate post-IR and demonstrated significantly higher clonogenic efficiency than did the NHK/B0 cells. To determine whether the observed radioresistance of the NHK/Bmi-1 cells was associated with enhanced DNA repair, we compared the in vitro and in vivo DNA repair activities for double stranded breaks (DSBs) in cells with or without Bmi-1 overexpression. In vitro DNA end joining (EJ) activity was notably induced in NHK/Bmi-1 compared with the NHK/EV cells, especially for blunt-ended DSBs. Chromosomal DSB repair activity was also compared between cells expressing Bmi-1 and the controls by pulse-field gel electrophoresis after exposure to 60 Gy IR. Bmi-1 expression led to significant increase in the kinetics of DSB repair in vivo for the IR-induced chromosomal DSBs. These data indicate that Bmi-1 enhances radioresistance of NHK and suggest possible therapeutic use of this pathway for protection of oral and cutaneous tissues from radiation damage. Therefore, we performed a screening for possible compounds that upregulate the Bmi-1 promoter activity by high throughput screening of chemical libraries and identified a set of compounds for future studies.