| Name | Gargi Pal |
| Institution | Hunter College |
| Research Field | Basic Cancer Research |
| Role at Institution | Post-Doctoral Fellow |
| Presenter(s) | Gargi Pal, Lia Di, Akintunde Orunmuyi, E. Oluwabunmi Olapade-Olaopa, Weigang Qiu, and Olorunseun O. Ogunwobi |
Population-Level Genetic Differentiation at the PVT1 Gene Locus: Implications for Prostate Cancer
Gargi Pal1, Lia Di1, Akintunde Orunmuyi2, E. Oluwabunmi Olapade-Olaopa2, Weigang Qiu1, and Olorunseun O. Ogunwobi1,3,4
1Department of Biological Sciences, Hunter College of The City University of New York, New York, NY; 2University of Ibadan, Ibadan, Nigeria; 3Hunter College Center for Cancer Health Disparities Research (CCHDR), New York, NY; 4Joan and Sanford I. Weill Department of Medicine, Cornell University, New York, NY.
The incidence and mortality rate of prostate cancer (PCa) is highest in males of African ancestry. PCa is a multi-factorial, complex disease, but the exact mechanisms for its development and progression are unclear. Analysis of data from the one thousand genomes project revealed that a 26-kb region spanning PVT1 exons 4A and 4B shows a run of 75 SNPs with distinct allelic frequencies between African and non-African populations. The gene desert located on chromosome 8q24 is associated with aggressiveness of PCa in males of African ancestry. Interestingly, the non-protein coding gene locus Plasmacytoma Variant Translocation (PVT1) present at 8q24 is overexpressed in PCa. PVT1 gives rise to multiple transcripts with potentially different functions. To investigate if our observed population-level differences at the PVT1 gene locus have implications for PCa, we determined the expression of PVT1 exons 4A and 4B in histologically confirmed normal prostate (n=22), benign tumor prostate (n=35), and malignant tumor prostate tissue (n=28) samples obtained from males who had undergone prostatectomy or transrectal ultrasound-guided biopsy in Nigeria, a sub-Saharan Black African population. We have observed that PVT1 exons 4A and 4B are significantly overexpressed in PCa tissues in comparison to benign prostatic hyperplasia and normal prostate tissues obtained from males of African ancestry (moAA). Transient and stable overexpression of PVT1 exons 4A and 4B significantly induce greater prostate epithelial cell migration and proliferation. We anticipate that further exploration of the role of PVT1 exons 4A and 4B may lead to the possibility of exploiting them for diagnosis, therapy, and other clinical applications in PCa.
Email questions and comments about this abstract to gargi.genetics@gmail.com.