Estrogen Regulates Tumor Growth Through a Nonclassical Pathway that Includes the Transcription Factors ERβ and KLF5

Yuka Nakajima, Kensuke Akaogi, Takashi Suzuki, Asami Osakabe, Chie Yamaguchi, Nanae Sunahara, Junji Ishida, Koichiro Kako, Sonoko Ogawa, Tetsuya Fujimura, Yukio Homma, Akiyoshi Fukamizu, Akiko Murayama, Keiji Kimura, Satoshi Inoue, Junn Yanagisawa*

*To whom correspondence should be addressed. E-mail: junny{at}agbi.tsukuba.ac.jp

This PDF file includes:

• Materials and Methods
• Fig. S1. Efficiency of ERβ (ESR2), KLF5, FOXO1, and WWP1 knockdown or overexpression in prostate cancer cells.
• Fig. S2. GS-1405 antagonizes the transcriptional activity of ERs.
• Fig. S3. ER ligands modulate colony formation of prostate cancer cells through ERβ.
• Fig. S4. ER ligands modulate colony formation of prostate cancer cells through KLF5, which acts as a prostate tumor suppressor.
• Fig. S5. FOXO1 mRNA abundance is regulated by ER ligands through KLF5 and ERβ.
• Fig. S6. FOXO1 regulates apoptosis of PC-3 cells under detached conditions.
• Fig. S7. Effects of GPR30 (GPER) or ERα (ESR1) knockdown on the alteration of FOXO1 mRNA abundance by ER ligands.
• Fig. S8. ER ligands regulate FOXO1 expression through KLF5 and ERβ (ESR2).
• Fig. S9. ERβ and KLF5 recruit CBP in an ER ligand–dependent manner.
• Fig. S10. E₂ induces ubiquitination and degradation of KLF5 in prostate cancer cells.
• Fig. S11. Binding between ERβ and KLF5 is necessary for E₂-dependent KLF5 degradation and suppression of KLF5-mediated transcription.
• Table S1. Relationship between KLF5 and ERβ immunoreactivity and clinicopathologic findings in human prostatic carcinomas (n = 102).
• References

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© 2011 American Association for the Advancement of Science