Activation of the mTOR/ Akt pathway in thymic epithelial cells derived from thymomas

PLoS One. 2019 Mar 21;14(3):e0197655. doi: 10.1371/journal.pone.0197655. eCollection 2019.

Abstract

The pathogenesis of thymic epithelial tumors remains poorly elucidated. The PIK3/Akt/mTOR pathway plays a key role in various cancers; interestingly, several phase I/II studies have reported a positive effect of mTOR inhibitors in disease control in thymoma patients. A major limit for deciphering cellular and molecular events leading to the transformation of thymic epithelial cells or for testing drug candidates is the lack of reliable in vitro cell system. We analyzed protein expression and activation of key players of the Akt/ mTOR pathway namely Akt, mTOR, and P70S6K in eleven A, B and AB thymomas as well as in normal thymuses. While only Akt and phospho-Akt were expressed in normal thymuses, both Akt and mTOR were activated in thymomas. Phospho-P70S6K was expressed in all thymic tumors whatever their subtypes, and absent in normal thymus. Interestingly, we report the activation of Akt, mTOR and P70S6 proteins in primary thymic epithelial cells maintained for short period of time after their derivation from seven AB and B thymomas. Finally, we showed that rapamycin (100 nM) significantly reduced proliferation of thymoma- derived epithelial cells without inducing cell death. Our results suggest that the activation of the Akt/ mTOR pathway might participate to the cell proliferation associated with tumor growth. Ultimately, our data enhance the potential role of thymic epithelial cells derived from tissue specimens for in vitro exploration of molecular abnormalities in rare thymic tumors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • Cell Proliferation / drug effects
  • Class I Phosphatidylinositol 3-Kinases / genetics
  • Female
  • Humans
  • Male
  • Middle Aged
  • Mutation
  • Neoplasms, Glandular and Epithelial / genetics
  • Neoplasms, Glandular and Epithelial / metabolism*
  • Neoplasms, Glandular and Epithelial / pathology
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Ribosomal Protein S6 Kinases, 70-kDa / metabolism
  • Signal Transduction
  • Sirolimus / pharmacology
  • TOR Serine-Threonine Kinases / metabolism*
  • Thymoma / genetics
  • Thymoma / metabolism*
  • Thymoma / pathology
  • Thymus Gland / metabolism
  • Thymus Gland / pathology
  • Thymus Neoplasms / genetics
  • Thymus Neoplasms / metabolism*
  • Thymus Neoplasms / pathology
  • Transcription Factors, TFII / genetics
  • Tumor Cells, Cultured

Substances

  • GTF2I protein, human
  • Transcription Factors, TFII
  • MTOR protein, human
  • Class I Phosphatidylinositol 3-Kinases
  • PIK3CA protein, human
  • Proto-Oncogene Proteins c-akt
  • Ribosomal Protein S6 Kinases, 70-kDa
  • TOR Serine-Threonine Kinases
  • Sirolimus

Supplementary concepts

  • Thymic epithelial tumor

Grants and funding

This work was supported by SIRIC LYric Grant INCa-DGOS-4664, anonymous donation to research and Aristot association. CMDV was the recipient of a HCL (Hospices Civils de Lyon) grant.