Supplementary Materials

Supplementary Material for:

Obesity-dependent changes in interstitial ECM mechanics promote breast tumorigenesis

Bo Ri Seo, Priya Bhardwaj, Siyoung Choi, Jacqueline Gonzalez, Roberto C. Andresen Eguiluz, Karin Wang, Sunish Mohanan, Patrick G. Morris, Baoheng Du, Xi K. Zhou, Linda T. Vahdat, Akanksha Verma, Olivier Elemento, Clifford A. Hudis, Rebecca M. Williams, Delphine Gourdon, Andrew J. Dannenberg, Claudia Fischbach*

*Corresponding author. E-mail: cf99{at}cornell.edu

Published 19 August 2015, Sci. Transl. Med. 7, 301ra130 (2015)
DOI: 10.1126/scitranslmed.3010467

This PDF file includes:

  • Materials and Methods
  • Fig. S1. Obesity promotes interstitial fibrosis in breast adipose tissue after menopause.
  • Fig. S2. Inguinal depots of adipose tissue feature markers of interstitial fibrosis.
  • Fig. S3. The profibrotic potential of ob/ob ASCs is not due to leptin deficiency.
  • Fig. S4. Obesity-associated ASCs promote fibrotic ECM remodeling in visceral fat.
  • Fig. S5. ECMs deposited by obesity-associated ASCs promote myofibroblast differentiation.
  • Fig. S6. Physicochemical cues of ob/ob ECMs modulate MDA-MB231 behavior.
  • Fig. S7. H&E images of breast tumors with different subtypes.
  • Fig. S8. Caloric restriction decreases fibrosis in mammary fat of obese mice.
  • Fig. S9. Decellularized ECMs do not contain cellular residuals.
  • Table S1. Subtypes, demographics, and desmoplastic grade of lean and obese breast cancer samples.
  • Table S2. Gene ontology data analysis.
  • Table S3. Correlation of YAP/TAZ-regulated genes with obesity-dependent ECM remodeling/inflammation.
  • References (5458)

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