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Induction and Analysis of Epithelial to Mesenchymal Transition
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Suppression of lysyl-tRNA synthetase, KRS, causes incomplete epithelial-mesenchymal transition and ineffective

Seo Hee Nam1, Minkyung Kang2, Jihye Ryu2

  • 1Interdisciplinary Program in Genetic Engineering, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.

International Journal of Oncology
|February 20, 2016
PubMed

Insights

Lysyl-tRNA synthetase (KRS) on cancer cell membranes promotes metastasis by enhancing cell adhesion and migration. Inhibiting KRS blocks key signaling pathways, reducing cancer cell adhesion and spread.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • Cancer cell adhesion is crucial for metastasis.
  • Cytosolic lysyl-tRNA synthetase (KRS) has a known role in protein synthesis.
  • Plasma membrane-bound KRS is implicated in cancer metastasis.

Purpose of the Study:

  • To investigate the role of KRS in cell adhesion-related signal transduction for cellular migration.
  • To determine how modulating KRS protein levels affects colon cancer cell behavior.

Main Methods:

  • Colon cancer cells with altered KRS levels were analyzed.
  • Cell-cell contact and cell-substrate adhesion properties were assessed.
  • Focal adhesions, FAK, ERK, and paxillin activation were examined.

Main Results:

  • KRS suppression reduced cell-cell adhesion molecules and hindered epithelial mesenchymal transition.
  • KRS-suppressed cells showed focal adhesions but lacked laminin-mediated ERK and paxillin activation.
  • KRS interacts with p67LR and integrin α6β1 to activate ERK and paxillin signaling.
  • Inhibiting ERK or KRS blocked cell adhesion and focal adhesion formation.

Conclusions:

  • KRS promotes both cell-cell and cell-extracellular matrix (ECM) adhesion, facilitating cancer cell migration.
  • KRS is a potential therapeutic target for blocking cancer metastasis.

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