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• W3082203791 abstract "The forkhead family of transcription factors are highly conserved and essential during embryonic development. There have been reports showing increased expression of forkheads in various cancers, but little is known about the role of these proteins in the disease context. Analysis of 500 clear cell renal cell carcinoma (ccRCC) transcriptomes in The Cancer Genome Database revealed that FOXD1 is overexpressed in ccRCC and correlates with poor patient outcomes (median survival FOXD1-low=2830 days; FOXD1-high=1913 days). Immunohistochemistry of 46 patient tumors showed that FOXD1 is expressed the majority of tumor cells (95% CI [50.6%, 79.4%]). To understand the biological role of FOXD1, we generated FOXD1-null variants of the 786-O ccRCC cell line. Using an in vivo xenograft model, FOXD1-null cells had smaller initiating tumor sizes (parent=71.05mm3; FOXD1-null=36.39mm3) and stunted tumor growth. In vitro, FOXD1-null lines had significantly reduced growth rates compared to the parental line, and showed increased cell size. Cell cycle analysis revealed that FOXD1-null cells had an increased number of cells in G2 compared to the parental line (parent=21.1%; FOXD1-null=37.1%). After G1 synchronization, all lines progressed through G1, S, and G2 at similar rates (parent=10 hours; FOXD1-null=10 hours). However, FOXD1-null clones spent increased time in G2 compared to the parental line (parent= 4 hours; FOXD1-null= 8 hours). Western blot analysis revealed decreased levels of Cyclin B1 and p-H3, as well as increased levels of p27 10 hours post-synchronization in FOXD1-null cells compared to the parent line. Staining with yH2AX did not indicate any significant change in the number of double strand breaks at any phase. These findings suggest that FOXD1 is a mediator of the transition between G2 and M, and that its loss initializes the G2/M checkpoint. Extrapolating back to our clinical observation, we propose that increased FOXD1 expression in tumor cells accelerates the transition between G2 and M, a point that is normally critical for survey and repair of DNA damage. This could result in greater tolerance for DNA damage, accelerating tumor evolution. Citation Format: Kyle Henry Bond, Ryan Jaikaran, Suizhen Qiu, Leif Oxburgh. FOXD1 mediates G2/M transition in clear cell renal cell carcinoma [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 5812." @default.
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• W3082203791 date "2020-08-13" @default.
• W3082203791 modified "2023-10-18" @default.
• W3082203791 title "Abstract 5812: FOXD1 mediates G2/M transition in clear cell renal cell carcinoma" @default.
• W3082203791 doi "https://doi.org/10.1158/1538-7445.am2020-5812" @default.
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