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RICTOR Affects Melanoma Tumorigenesis and Its Resistance to Targeted Therapy

Ahlem Jebali1,2, Maxime Battistella1,2,3, Céleste Lebbé1,2,4

  • 1INSERM, U976, Team 1, Human Immunology Pathophysiology & Immunotherapy (HIPI), F-75010 Paris, France.

Biomedicines
|October 23, 2021
PubMed

Insights

Rapamycin-insensitive companion of mTOR (RICTOR) drives melanoma growth and BRAF inhibitor resistance. Targeting RICTOR shows promise for treating resistant melanoma by disrupting key signaling pathways.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The PI3K/AKT/mTOR pathway is crucial in melanoma development and BRAF inhibitor resistance.
  • RICTOR, a key component of mTORC2, has an emerging but not fully understood role in this context.

Purpose of the Study:

  • To investigate the role of mTORC2/RICTOR in BRAF-mutated melanomas.
  • To determine the impact of RICTOR on melanoma-initiating cells and resistance to BRAF inhibitors.

Main Methods:

  • Assessed RICTOR expression in melanoma tissues.
  • Investigated the effects of RICTOR overexpression on melanoma-initiating cells.
  • Evaluated the sensitivity of resistant melanoma cells to mTORC2 inhibition.
  • Analyzed interactions between RICTOR, STAT3, and RAS in resistant melanoma.

Main Results:

  • RICTOR was overexpressed in melanoma and linked to poor prognosis.
  • RICTOR overexpression promoted melanoma-initiating cells with stemness properties.
  • RICTOR contributed to BRAF inhibitor resistance and sensitivity to mTORC2 inhibition.
  • Disruption of RAS-RICTOR interaction inhibited resistant cell proliferation.

Conclusions:

  • RICTOR is a significant signaling node in BRAF-dependent melanoma.
  • RICTOR plays a key role in melanoma development and therapeutic resistance.
  • RICTOR represents a promising therapeutic target for melanoma treatment.
Keywords:
BRAFBRAF inhibitorsmTORmTOR inhibitorsmTORC2melanomaresistance

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