Supplementary Figures S1-S10 from ZNF397 Deficiency Triggers TET2-Driven Lineage Plasticity and AR-Targeted Therapy Resistance in Prostate Cancer

作者：Yaru Xu, Yuqiu Yang, Zhaoning Wang, Martin Sjöström, Yuyin Jiang, Yitao Tang, Siyuan Cheng, Su Deng, Choushi Wang, Julisa Gonzalez, Nickolas A. Johnson, Xiang Li, Xiaoling Li, Lauren A. Metang, Atreyi Mukherji, Quanhui Xu, Carla R. Tirado, Garrett Wainwright, Xinzhe Yu, Spencer Barnes, Mia Hofstad, Yu Chen, Hong Zhu, Ariella B. Hanker, Ganesh V. Raj, Guanghui Zhu, Housheng Hansen He, Zhao Wang, Carlos L. Arteaga, Han Liang, Felix Y. Feng, Yunguan Wang, Tao Wang, Ping Mu · 年份：2026 · DOI：10.1158/2159-8290.32698305 · 研究领域：Epigenetics and DNA Methylation、Protein Degradation and Inhibitors、Prostate Cancer Treatment and Research

<p>Figure S1. ZNF397-deficiency has bifurcated effects on PCa with or without AR inhibition. Figure S2. The impact of ZNF397-deficiency on AR protein and AR cistrome. Figure S3. ZNF397 is required for the activation of canonical AR transcriptional program. Figure S4. ZNF397-KO impairs DHT-induced AR signaling activation. Figure S5. ZNF397-KO promotes multilineage and lineage plastic gene expression. Figure S6. ZNF397-KO promotes stem-like and EMT-like transcriptional programs. Figure S7. ZNF397-KO led to induction of TET2 downstream genes. Figure S8. ZNF397-KO promotes transcriptional activation of TET2 downstream genes. Figure S9. ZNF397-deficiency has bifurcated effects on AR-dependent vs AR-independent PCas. Figure S10. Targeting TET2-driven epigenetic rewiring to overcome resistance.</p>