PUBLICATION

Sulfopin is a covalent inhibitor of Pin1 that blocks Myc-driven tumors in vivo

Authors
Dubiella, C., Pinch, B.J., Koikawa, K., Zaidman, D., Poon, E., Manz, T.D., Nabet, B., He, S., Resnick, E., Rogel, A., Langer, E.M., Daniel, C.J., Seo, H.S., Chen, Y., Adelmant, G., Sharifzadeh, S., Ficarro, S.B., Jamin, Y., Martins da Costa, B., Zimmerman, M.W., Lian, X., Kibe, S., Kozono, S., Doctor, Z.M., Browne, C.M., Yang, A., Stoler-Barak, L., Shah, R.B., Vangos, N.E., Geffken, E.A., Oren, R., Koide, E., Sidi, S., Shulman, Z., Wang, C., Marto, J.A., Dhe-Paganon, S., Look, T., Zhou, X.Z., Lu, K.P., Sears, R.C., Chesler, L., Gray, N.S., London, N.
ID
ZDB-PUB-210512-7
Date
2021
Source
Nature Chemical Biology   17(9): 954-963 (Journal)
Registered Authors
He, Shuning
Keywords
none
MeSH Terms
  • Animals
  • Antineoplastic Agents/chemical synthesis
  • Antineoplastic Agents/chemistry
  • Antineoplastic Agents/pharmacology*
  • Apoptosis/drug effects
  • Cell Proliferation/drug effects
  • Cell Survival/drug effects
  • Dose-Response Relationship, Drug
  • Drug Screening Assays, Antitumor
  • Enzyme Inhibitors/chemical synthesis
  • Enzyme Inhibitors/chemistry
  • Enzyme Inhibitors/pharmacology*
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Molecular Structure
  • NIMA-Interacting Peptidylprolyl Isomerase/antagonists & inhibitors*
  • NIMA-Interacting Peptidylprolyl Isomerase/metabolism
  • Neoplasms, Experimental/drug therapy
  • Neoplasms, Experimental/metabolism
  • Neoplasms, Experimental/pathology
  • Proto-Oncogene Proteins c-myc/antagonists & inhibitors*
  • Proto-Oncogene Proteins c-myc/metabolism
  • Structure-Activity Relationship
  • Tumor Cells, Cultured
PubMed
33972797 Full text @ Nat. Chem. Biol.
Abstract
The peptidyl-prolyl isomerase, Pin1, is exploited in cancer to activate oncogenes and inactivate tumor suppressors. However, despite considerable efforts, Pin1 has remained an elusive drug target. Here, we screened an electrophilic fragment library to identify covalent inhibitors targeting Pin1's active site Cys113, leading to the development of Sulfopin, a nanomolar Pin1 inhibitor. Sulfopin is highly selective, as validated by two independent chemoproteomics methods, achieves potent cellular and in vivo target engagement and phenocopies Pin1 genetic knockout. Pin1 inhibition had only a modest effect on cancer cell line viability. Nevertheless, Sulfopin induced downregulation of c-Myc target genes, reduced tumor progression and conferred survival benefit in murine and zebrafish models of MYCN-driven neuroblastoma, and in a murine model of pancreatic cancer. Our results demonstrate that Sulfopin is a chemical probe suitable for assessment of Pin1-dependent pharmacology in cells and in vivo, and that Pin1 warrants further investigation as a potential cancer drug target.
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