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Soft drug-resistant ovarian cancer cells migrate via two distinct mechanisms utilizing myosin II-based contractility

Aastha Kapoor1, Amlan Barai1, Bhushan Thakur2

  • 1Department of Biosciences and Bioengineering, IIT Bombay, India.

Biochimica Et Biophysica Acta. Molecular Cell Research
|November 28, 2017
PubMed

Insights

Drug-resistant ovarian cancer cells exhibit altered biophysical properties, migrating via distinct protease-dependent or -independent pathways. Myosin II is identified as a key regulator and potential therapeutic target for these resistant cells.

Area of Science:

  • Biophysics
  • Cancer Biology
  • Cell Migration

Background:

  • Chemotherapeutic drug resistance is a major challenge in cancer treatment.
  • The migration mechanisms of drug-resistant cancer cells are not fully understood.

Purpose of the Study:

  • To investigate the biophysical properties and migration mechanisms of drug-resistant ovarian cancer cells (OCCs).
  • To identify potential therapeutic targets for overcoming drug resistance in ovarian cancer.

Main Methods:

  • Phenotypic characterization of cisplatin-resistant (CisR), paclitaxel-resistant (PacR), and dual drug-resistant OCCs.
  • Assessment of cell contractility, softness, and invasion.
  • Analysis of migration modes using protease inhibition.
  • Investigation of the RhoA-ROCK2-Myosin II signaling pathway.
  • Confined migration experiments to study nuclear translocation and proteolytic activity.

Main Results:

  • Drug-resistant OCCs are more contractile and softer than drug-sensitive cells.
  • CisR cells exhibit protease-dependent migration, while PacR cells show protease-independent migration.
  • Actomyosin contractility via the RhoA-ROCK2-Myosin II pathway regulates both migration modes.
  • Myosin IIA and IIB are crucial for nuclear translocation and proteolytic activity during migration.

Conclusions:

  • Ovarian cancer cell migration is modulated by drug resistance and involves distinct biophysical mechanisms.
  • Myosin II plays a critical role in the migration of drug-resistant ovarian cancer cells.
  • Myosin II represents a promising therapeutic target for treating drug-resistant ovarian cancer.
Keywords:
Amoeboid mode of invasionCisplatin resistanceMatrix metalloproteinases (MMPs)Mesenchymal mode of invasionMyosin IIAMyosin IIBOvarian cancer cells (OCCs)Paclitaxel resistanceROCKRho

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