Thymidylate synthase disruption to limit cell proliferation in cell therapies

Mol Ther. 2024 Aug 7;32(8):2535-2548. doi: 10.1016/j.ymthe.2024.06.014. Epub 2024 Jun 12.

Abstract

Stem and progenitor cells hold great promise for regenerative medicine and gene therapy approaches. However, transplantation of living cells entails a fundamental risk of unwanted growth, potentially exacerbated by CRISPR-Cas9 or other genetic manipulations. Here, we describe a safety system to control cell proliferation while allowing robust and efficient cell manufacture, without any added genetic elements. Inactivating TYMS, a key nucleotide metabolism enzyme, in several cell lines resulted in cells that proliferate only when supplemented with exogenous thymidine. Under supplementation, TYMS-/--pluripotent stem cells proliferate, produce teratomas, and successfully differentiate into potentially therapeutic cell types such as pancreatic β cells. Our results suggest that supplementation with exogenous thymidine affects stem cell proliferation, but not the function of stem cell-derived cells. After differentiation, postmitotic cells do not require thymidine in vitro or in vivo, as shown by the production of functional human insulin in mice up to 5 months after implantation of stem cell-derived pancreatic tissue.

Keywords: DNA synthesis; TYMS; beta-cell differentiation; cell therapy; diabetes; human pluripotent stem cells; proliferation; safety switch.

MeSH terms

  • Animals
  • CRISPR-Cas Systems
  • Cell Differentiation*
  • Cell Line
  • Cell Proliferation*
  • Cell- and Tissue-Based Therapy / methods
  • Humans
  • Insulin-Secreting Cells / cytology
  • Insulin-Secreting Cells / metabolism
  • Mice
  • Pluripotent Stem Cells / cytology
  • Pluripotent Stem Cells / metabolism
  • Thymidine* / metabolism
  • Thymidylate Synthase* / genetics
  • Thymidylate Synthase* / metabolism

Substances

  • Thymidine
  • Thymidylate Synthase