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Rab1A is an mTORC1 activator and a colorectal oncogene.

Janice D Thomas1, Yan-Jie Zhang2, Yue-Hua Wei3

  • 1Rutgers Cancer Institute of New Jersey, Rutgers, The State University of New Jersey, 195 Little Albany Street, New Brunswick, NJ 08903, USA; Department of Pharmacology, Robert Wood Johnson Medical School, Rutgers, The State University of New Jersey, 675 Hoes Lane, Piscataway, NJ 08854, USA.

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Amino acids regulate cell growth via Rab1, a newly identified mTORC1 activator. Rab1A overexpression drives cancer growth and poor prognosis in colorectal cancer, suggesting it as a therapeutic target.

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Area of Science:

  • Cellular Biology
  • Molecular Oncology
  • Cancer Research

Background:

  • Amino acids (AA) are critical regulators of cell growth and metabolism.
  • The mechanistic target of rapamycin complex 1 (mTORC1) pathway is central to nutrient sensing and cell growth.
  • Dysregulation of AA signaling and mTORC1 is implicated in various cancers.

Purpose of the Study:

  • To identify novel regulators of amino acid signaling to mTORC1.
  • To investigate the role of Rab1 in mTORC1 activation and oncogenesis.
  • To explore the therapeutic potential of targeting Rab1 in colorectal cancer (CRC).

Main Methods:

  • Identification of Rab1 as a regulator of AA-mTORC1 signaling.
  • Analysis of Rab1A GTP binding and its interaction with mTORC1 and Rheb.
  • Overexpression and knockdown studies in cancer cell models.
  • Correlation analysis of Rab1A expression with clinical parameters in CRC patient cohorts.

Main Results:

  • Rab1 was identified as a conserved regulator of AA signaling to mTORC1.
  • AA stimulation promotes Rab1A GTP binding and its interaction with mTORC1 and Rheb in the Golgi.
  • Rab1A overexpression enhances mTORC1 signaling and oncogenic growth in an AA- and mTORC1-dependent manner.
  • Rab1A knockdown attenuates the growth of Rab1-overexpressing cancer cells.
  • Rab1A is overexpressed in CRC, correlating with elevated mTORC1 signaling, invasion, progression, and poor prognosis.

Conclusions:

  • Rab1 acts as an mTORC1 activator and an oncogene.
  • Hyperactive AA signaling through Rab1A overexpression drives oncogenesis.
  • Rab1A overexpression sensitizes cancer cells to mTORC1-targeted therapies, presenting a potential therapeutic strategy for CRC.