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Enhanced Gαq Signaling in TSC2-Deficient Cells Is Required for Their Neoplastic Behavior.

Aurélie Tréfier1, Nihad Tousson-Abouelazm1,2, Lama Yamani3

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American Journal of Respiratory Cell and Molecular Biology
|November 8, 2024
PubMed
Summary

Loss of the TSC2 gene causes LAM, a lung disease driven by mTORC1-independent signaling. Urotensin-II receptor (UT) and Gαq signaling are key drivers, offering new therapeutic targets for LAM tumors.

Keywords:
Gαqlymphangioleiomyomatosismechanistic target of rapamycintuberous sclerosis complexurotensin-II receptor

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Area of Science:

  • Cell Biology
  • Oncology
  • Genetics

Background:

  • Loss of the TSC2 gene causes pulmonary lymphangioleiomyomatosis (LAM), a rare cystic lung disease.
  • Aberrant growth of LAM cells is linked to increased mechanistic target of rapamycin complex 1 (mTORC1) activity.
  • Rapamycin, an mTORC1 inhibitor, slows LAM progression but does not eradicate it, suggesting mTORC1-independent mechanisms.

Purpose of the Study:

  • To investigate the role of G protein-coupled urotensin-II receptor (UT) signaling in TSC2-deficient LAM pathogenesis.
  • To elucidate the mTORC1-independent mechanisms driving LAM cell migration and oncogenic signaling.

Main Methods:

  • Utilized a human pluripotent stem cell-derived in vitro model of LAM.
  • Performed bioluminescence resonance energy transfer (BRET) assays in TSC2-deficient HEK 293T cells.
  • Conducted co-immunoprecipitation assays to assess protein interactions.

Main Results:

  • Demonstrated hyperactivation of UT signaling in TSC2-deficient LAM cells, driving enhanced migration and proneoplastic signaling via Gαq.
  • Showcased selective and enhanced activation of Gαq and its RhoA-associated effectors in TSC2-deficient cells.
  • Confirmed physical association between recombinant UT and Gαq/TSC2, and identified increased endosomal targeting of p63RhoGEF.

Conclusions:

  • Identified UT and Gαq signaling as critical mTORC1-independent drivers of LAM pathogenesis.
  • Highlighted potential therapeutic targets for preventing or eradicating pulmonary and extrapulmonary LAM tumors.