Supplementary Materials

Supplementary Material for:

Epigenetic Reprogramming of HOXC10 in Endocrine-Resistant Breast Cancer

Thushangi N. Pathiraja, Shweta R. Nayak, Yuanxin Xi, Shiming Jiang, Jason P. Garee, Dean P. Edwards, Adrian V. Lee, Jian Chen, Martin J. Shea, Richard J. Santen, Frank Gannon, Sara Kangaspeska, Jaroslav Jelinek, Jean-Pierre J. Issa, Jennifer K. Richer, Anthony Elias, Marie McIlroy, Leonie S. Young, Nancy E. Davidson, Rachel Schiff, Wei Li, Steffi Oesterreich*

*Corresponding author. E-mail: oesterreichs@upmc.edu

Published 26 March 2014, Sci. Transl. Med. 6, 229ra41 (2014)
DOI: 10.1126/scitranslmed.3008326

This PDF file includes:

  • Materials and Methods
  • Fig. S1. Characterization of C4-12 and LTED cells.
  • Fig. S2. E2 response in MCF-7, MDA-MB-134-VI, and HCC1395.
  • Fig. S3. ER ChIP for LTED cells.
  • Fig. S4. E2 regulation of classical ER target genes in LTED cells.
  • Fig. S5. Loss of E2 response and associated modest changes in EZH2 recruitment and trimethylation of H3K27 and H3K4 at HOXC10 proximal promoter region.
  • Fig. S6. Different effects of HOXC10 knockdown on growth in breast cancer cell lines.
  • Fig. S7. Tamoxifen resistance mediated by loss of HOXC10.
  • Fig. S8. In vivo growth of HOXC10 knockdown clone sh-H2.
  • Legend for table S1
  • Table S2. Significant GO terms for hypermethylated genes in C4-12 and LTED.
  • Legends for tables S3 and S4
  • Table S5. List of qPCR primers.
  • Table S6. List of bisulfite sequencing primers.

[Download PDF]

Other Supplementary Material for this manuscript includes the following:

  • Table S1. Differentially methylated genes in C4-12 and LTED compared to MCF-7 (see Excel file).
  • Table S3. Original data for graphs that show composite results (see Excel file).
  • Table S4. Exact P values for statistical analyses (see Excel file).

[Tables S1, S3 and S4]