p53 and MicroRNA-34 Are Suppressors of Canonical Wnt Signaling

Nam Hee Kim, Hyun Sil Kim, Nam-Gyun Kim, Inhan Lee, Hyung-Seok Choi, Xiao-Yan Li, Shi Eun Kang, So Young Cha, Joo Kyung Ryu, Jung Min Na, Changbum Park, Kunhong Kim, Sanghyuk Lee, Barry M. Gumbiner, Jong In Yook,* Stephen J. Weiss

*To whom correspondence should be addressed. E-mail: jiyook{at}yuhs.ac

This PDF file includes:

• Fig. S1. Loss of p53 function increases Wnt activity.
• Fig. S2. Loss of p53 function increases TCF/LEF target gene expression.
• Fig. S3. miR-34 transactivated by p53 suppresses Wnt activity.
• Fig. S4. miR-34 targets UTRs of Wnt genes.
• Fig. S5. Loss of p53 function potentiates Wnt UTR activity.
• Fig. S6. Gain of p53 function attenuates Wnt activity.
• Fig. S7. Loss of p53/miR-34 potentiates Wnt activity in colorectal cancer cells.
• Fig. S8. Interactions between miR-34 and β-catenin UTR are functional during in vivo invasion.
• Table S1. hsa–miR-34a match sites on Wnt genes.
• Table S2. hsa–miR-34b* and hsa–miR-34c-5p match sites on Wnt genes.
• Table S3. Highly conserved miR-34a sequences in vertebrates.
• Table S4. Conserved miR-34a match sites in vertebrate Wnt genes.
• Table S5. List of TCF/LEF and miR-34 signature genes using hierarchical clustering analysis.
• Table S6. Primer oligonucleotide sequences for qPCR analysis.
  

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© 2011 American Association for the Advancement of Science