Nuclear envelope irregularity is induced by RET/PTC during interphase

Am J Pathol. 2003 Sep;163(3):1091-100. doi: 10.1016/S0002-9440(10)63468-2.

Abstract

Nuclear envelope (NE) irregularity is an important diagnostic feature of cancer, and its molecular basis is not understood. One possible cause is abnormal postmitotic NE re-assembly, such that a rounded contour is never achieved before the next mitosis. Alternatively, dynamic forces could deform the NE during interphase following an otherwise normal postmitotic NE re-assembly. To distinguish these possibilities, normal human thyroid epithelial cells were microinjected with the papillary thyroid carcinoma oncogene (RET/PTC1 short isoform, known to induce NE irregularity), an attenuated version of RET/PTC1 lacking the leucine zipper dimerization domain (RET/PTC1 Deltazip), H (V-12) RAS, and labeled dextran. Cells were fixed at 6 or 18 to 24 hours, stained for lamins and the products of microinjected plasmids, and scored blindly using previously defined criteria for NE irregularity. 6.5% of non-injected thyrocytes showed NE irregularity. Neither dextran nor RAS microinjections increased NE irregularity. In contrast, RET/PTC1 microinjection induced NE irregularity in 27% of cells at 6 hours and 37% of cells at 18 to 24 hours. RET/PTC1 Deltazip induced significantly less irregularity. Since irregularity develops quickly, and since no mitoses and only rare possible postmitotic cells were scored, postmitotic NE re-assembly does not appear necessary for RET/PTC signaling to induce an irregular NE contour.

MeSH terms

  • Cell Nucleus / drug effects
  • Cells, Cultured
  • Humans
  • Interphase / physiology*
  • Microinjections
  • Mitosis / physiology
  • Nuclear Envelope / drug effects*
  • Nuclear Envelope / ultrastructure*
  • Oncogene Proteins, Fusion / administration & dosage
  • Oncogene Proteins, Fusion / pharmacology*
  • Protein-Tyrosine Kinases
  • Thyroid Gland / drug effects
  • Time Factors

Substances

  • Oncogene Proteins, Fusion
  • Protein-Tyrosine Kinases
  • ret-PTC fusion oncoproteins, human