mTOR Signaling and Neural Stem Cells: The Tuberous Sclerosis Complex Model

Int J Mol Sci. 2018 May 16;19(5):1474. doi: 10.3390/ijms19051474.

Abstract

The mechanistic target of rapamycin (mTOR), a serine-threonine kinase, plays a pivotal role in regulating cell growth and proliferation. Notably, a great deal of evidence indicates that mTOR signaling is also crucial in controlling proliferation and differentiation of several stem cell compartments. Consequently, dysregulation of the mTOR pathway is often associated with a variety of disease, such as cancer and metabolic and genetic disorders. For instance, hyperactivation of mTORC1 in neural stem cells (NSCs) is associated with the insurgence of neurological manifestation characterizing tuberous sclerosis complex (TSC). In this review, we survey the recent contributions of TSC physiopathology studies to understand the role of mTOR signaling in both neurogenesis and tumorigenesis and discuss how these new insights can contribute to developing new therapeutic strategies for neurological diseases and cancer.

Keywords: mTOR signaling; neural stem cells; tuberous sclerosis complex.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Proliferation
  • Disease Susceptibility
  • Energy Metabolism
  • Humans
  • Mechanistic Target of Rapamycin Complex 1 / metabolism
  • Neural Stem Cells / metabolism*
  • Signal Transduction* / drug effects
  • TOR Serine-Threonine Kinases / metabolism*
  • Tuberous Sclerosis / drug therapy
  • Tuberous Sclerosis / metabolism*

Substances

  • Mechanistic Target of Rapamycin Complex 1
  • TOR Serine-Threonine Kinases