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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Nat Genet. 2015 Oct 12;47(11):1346–1351. doi: 10.1038/ng.3419

Fig. 4. HOXB13 and FOXA1 are sufficient for reprogramming AR in LHSAR cells and are essential for prostate cancer cell survival.

Fig. 4

A. AR binding intensity in LHSAR cells transduced with HOXB13 and FOXA1, HOXB13 alone, FOXA1 alone or with LacZ at T-ARBS and N-ARBS. The joint effects of FOXA1 and HOXB13 recapitulate AR binding patterns in tumor. B. Cluster analysis of all human specimens and LHSAR-modified cell lines supervised by T-ARBS and N-ARBS. C. Top, dependency of LNCaP on HOXB13 and FOXA1 as measured by proliferation upon knockdown of HOXB13 and FOXA1 shRNAs. ShRNAs targeting GFP (shGFP) were used as negative controls. All knockdowns were performed in triplicate. Error bars represent 95% confidence intervals (at Day 6: shHOXB13 vs. controls, p=2.2×10–7; shFOXA1 vs. controls, p=3.8×10−7). Knockdown of the transcription factors were confirmed by Western blot analysis (lower graphs). D. Dependency of 102 cell lines of multiple cancer types on HOXB13 (top) and FOXA1 (below). Lower ATARiS values represent increased dependency. The LNCaP cell line is in red. Data are part of the Broad Institute Project Achilles.