Chromosomal organization in metastatic

clear cell renal cell carcinoma

Presenter: Lexie Haralson

Presenter Status: Undergraduate student

Academic Year: 22-23

Semester: Spring

Faculty Mentor: Lisa Hua

Department: Biology

Funding Source/Sponsor: Koret Scholars Program

Screenshot URL: https://drive.google.com/uc?id=199YakJ2sB3b6ABEToLN3qe75DtskVGiv

Abstract:
Currently, there is a paucity of information for chromosomal organization in metastatic tumors. Metastatic tumors have heterogeneous cell populations and genetic instabilities (Gerlinger et al, 2012). Recently, it was shown that individual homologous chromosomes are spatially segregated, or antipaired, during mitosis in normal human cells (Hua and Mikawa, 2018). Loss of the antipairing pattern was correlated to abnormal pairing and gene mis-regulation in a metastatic renal carcinoma cell line, Caki-1 (Hua and Mikawa, 2018; Koeman et al, 2008). In particular, gene mis-regulation was observed for Chromosome 19 (Koeman et al, 2008). It is unknown whether the loss of antipairing is present for other autosomes or specific for chromosome 19 in Caki-1 cells. To test whether the loss of antipairing is limited to Chromosome 19, we performed chromosome painting for chromosomes 9 and 14 for Caki-1 cells. Using high resolution confocal microscopy, and 3D reconstruction, our preliminary analysis found that the loss of antipairing is also present for chromosomes 9 and 14. This data suggests that the loss of antipairing is shared among other autosomes in Caki-1 cells, however the increased frequency of abnormal pairing may be unique to chromosome 19. Further studies are warranted to investigate the underlying mechanism for how chromosome 19 develops increased pairing, and its significance in renal cancer metastasis. Findings of our study will aid in elucidating mechanisms of tumorigenesis, that can shed light on future cancer therapeutics.