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Ovarian Cancer Susceptibility and Chemosensitivity to KRAS Modulation.

Alexandra Maria Psaras1, Steven J McKay1, Janelle Vasquez Vilela1

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Targeting KRAS (Kirsten rat sarcoma viral oncogene homolog) can overcome chemotherapy resistance in ovarian cancer. Inhibiting KRAS enhances the effectiveness of drugs like paclitaxel, offering new therapeutic strategies.

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3D spheroidsKRASchemosensitizationcisplatincombination therapydrug resistanceovarian cancerpaclitaxel

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • KRAS amplification/overexpression is common in ovarian cancer, contributing to chemoresistance.
  • KRAS is a potential therapeutic target for improving treatment outcomes.

Purpose of the Study:

  • To investigate if modulating KRAS enhances chemotherapeutic efficacy in ovarian cancer models.
  • To evaluate different KRAS inhibition strategies, including gene editing and pharmacological inhibition.

Main Methods:

  • CRISPR/Cas9 gene editing for KRAS knockdown.
  • Tet-ON inducible knockdown system.
  • Polypurine reverse Hoogsteen hairpin (PPRH) oligonucleotides.
  • Pan-KRAS inhibitor BI2865 treatment.
  • Ovarian cancer cell lines (SKOV-3, Kuramochi) in 2D and 3D cultures.

Main Results:

  • CRISPR-mediated KRAS knockdown altered spheroid morphology and enhanced sensitivity to cisplatin and paclitaxel.
  • Tet-ON system showed dose-dependent chemosensitization, with optimal effects at ~50-60% knockdown.
  • PPRH oligonucleotides reduced IC50 values for cisplatin and paclitaxel by ~50% in 2D cultures.
  • BI2865 demonstrated significant synergy with paclitaxel, reversing chemoresistance in 3D cultures.
  • BI2865 enhanced paclitaxel efficacy in KRAS-amplified cells.

Conclusions:

  • KRAS is a viable target for chemosensitization in ovarian cancer.
  • Combination therapy with KRAS inhibitors and taxanes shows significant promise.
  • Targeting KRAS offers a strategy to overcome chemoresistance, particularly with paclitaxel.