Supplementary Materials

Supplementary Material for:

Metarrestin, a perinucleolar compartment inhibitor, effectively suppresses metastasis

Kevin J. Frankowski, Chen Wang, Samarjit Patnaik, Frank J. Schoenen, Noel Southall, Dandan Li, Yaroslav Teper, Wei Sun, Irawati Kandela, Deqing Hu, Christopher Dextras, Zachary Knotts, Yansong Bian, John Norton, Steve Titus, Marzena A. Lewandowska, Yiping Wen, Katherine I. Farley, Lesley Mathews Griner, Jamey Sultan, Zhaojing Meng, Ming Zhou, Tomas Vilimas, Astin S. Powers, Serguei Kozlov, Kunio Nagashima, Humair S. Quadri, Min Fang, Charles Long, Ojus Khanolkar, Warren Chen, Jinsol Kang, Helen Huang, Eric Chow, Esthermanya Goldberg, Coral Feldman, Romi Xi, Hye Rim Kim, Gary Sahagian, Susan J. Baserga, Andrew Mazar, Marc Ferrer, Wei Zheng, Ali Shilatifard, Jeffrey Aubé, Udo Rudloff,* Juan Jose Marugan,* Sui Huang*

*Corresponding author. Email: s-huang2{at} (S.H.); maruganj{at} (J.J.M.); rudloffu{at} (U.R.)

Published 16 May 2018, Sci. Transl. Med. 10, eaap8307 (2018)
DOI: 10.1126/scitranslmed.aap8307

This PDF file includes:

  • Materials and Methods
  • Fig. S1. Synthetic scheme for metarrestin.
  • Fig. S2. Drug response of PANC1 cells treated with metarrestin.
  • Fig. S3. Metastatic cancer progression in PANC1 NSG mice.
  • Fig. S4. Metarrestin plasma and tumor PKs.
  • Fig. S5. Metarrestin-induced nucleolar structure changes as observed by EM.
  • Fig. S6. Changes of nucleolar structure in metarrestin-treated cells.
  • Fig. S7. Capping structure of Pol I transcription factors in metarrestin-treated cells.
  • Fig. S8. No impact of metarrestin treatment on Pol II transcription, translation, or cytoplasmic-nuclear trafficking in metarrestin-treated cells.
  • Fig. S9. No impact on DNA damage response, cell cycle, or Pol II transcription in metarrestin-treated cells.
  • Fig. S10. Effectiveness of biotin-metarrestin in disassembling PNCs.
  • Fig. S11. Expression of eEF1A2-HA in transfected cells.
  • Fig. S12. Synthesis of 2-amino-1-benzyl-4,5-diphenyl-1H-pyrrole-3-carbonitrile.
  • Fig. S13. Synthesis of (E)-ethyl N-(1-benzyl-3-cyano-4,5-diphenyl-1H-pyrrol-2-yl)formimidate.
  • Fig. S14. Synthesis of trans-4-(7-benzyl-4-imino-5,6-diphenyl-4,7-dihydro-3H-pyrrolo[2,3-d]pyrimidin-3-yl)cyclohexanol (metarrestin).
  • Fig. S15. Synthesis of 2-amino-1-(3-bromobenzyl)-4,5-diphenyl-1H-pyrrole-3-carbonitrile.
  • Fig. S16. Synthesis of (E)-ethyl N-(1-(3-bromobenzyl)-3-cyano-4,5-diphenyl-1H-pyrrol-2-yl)formimidate.
  • Fig. S17. Synthesis of trans-4-(7-(3-bromobenzyl)-4-imino-5,6-diphenyl-4,7-dihydro-3H-pyrrolo[2,3-d]pyrimidin-3-yl)cyclohexanol.
  • Fig. S18. Synthesis of N-(6-(3-((3-(trans-4-hydroxycyclohexyl)-4-imino-5,6-diphenyl-3,4-dihydro-7H-pyrrolo[2,3-d]pyrimidin-7-yl)methyl)phenyl)hex-5-yn-1-yl)-5-((3aS,4S,6aR)-2-oxohexahydro-1H-thieno[3,4-d]imidazol-4-yl)pentanamide (biotin-metarrestin, P1).
  • Table S1. Cancer cell lines examined for PNC prevalence with or without metarrestin treatment (from Fig. 1C).
  • Table S2. Pancreatic cancer cell lines evaluated for PNC prevalence in Fig. 2A.
  • Table S3. Veterinary pathology read of the organs in KPC mice treated with metarrestin.
  • Table S4. Hematology and blood biochemistry assessment of metarrestin toxicity in tumor-bearing KPC and wild-type mice.
  • References (7482)

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