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Quantitation of Endothelial Cell Adhesiveness In Vitro
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Quantitative Proteomics Implicates Rictor/mTORC2 in Cell Adhesion

Hao Wang1, Xianfeng Shao2, Qian He3

  • 1Department of Genetics, School of Basic Medical Sciences , Tianjin Medical University , Tianjin 300070 , P.R. China.

Journal of Proteome Research
|August 30, 2018
PubMed

Insights

Mammalian target of rapamycin complex 2 (mTORC2) regulates cell adhesion and invasion. Reducing Rictor, an mTORC2 component, alters proteome, impacting cell adhesion molecules and promoting renal cancer cell invasion.

Area of Science:

  • Cellular Biology
  • Molecular Oncology
  • Proteomics

Background:

  • Mammalian target of rapamycin complex 2 (mTORC2) is crucial for cellular functions.
  • Rictor is a specific component of mTORC2, essential for its activity.

Purpose of the Study:

  • To investigate the proteomic changes and functional roles of mTORC2 by reducing Rictor expression.
  • To elucidate the molecular mechanisms by which mTORC2 influences renal cancer cell behavior.

Main Methods:

  • Established a stable Rictor knockdown cell line.
  • Performed quantitative proteomic analysis to identify differentially expressed proteins.
  • Constructed a protein-protein interaction network.
  • Utilized gene ontology analysis for functional enrichment.
  • Investigated the role of AKT signaling pathway.

Main Results:

  • Identified 101 downregulated and 50 upregulated proteins in Rictor knockdown cells.
  • Established a Rictor/mTORC2-regulated protein-protein interaction network.
  • Demonstrated significant involvement of Rictor/mTORC2 in cell adhesion processes.
  • Observed altered expression of key cell adhesion molecules, including ITGA5, TGFB1I1, and LOXL2.
  • Showed that Rictor/mTORC2 modulates cell adhesion and invasion via AKT signaling.

Conclusions:

  • Rictor/mTORC2 regulates a significant portion of the cellular proteome.
  • Rictor/mTORC2 plays a critical role in cell adhesion and renal cancer cell invasion.
  • Modulation of cell adhesion molecules by Rictor/mTORC2, potentially through AKT, drives cancer cell migration and invasion.
Keywords:
AktRictorTMT labelingcell adhesioncell migrationgene expressionmTORC2mass spectrometryquantitative proteomicsrenal cancer

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