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Abrogation of constitutive Stat3 activity circumvents cisplatin resistant ovarian cancer

Teng Ji1, Danni Gong, Zhiqiang Han

  • 1Cancer Biology Research Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, PR China.

Cancer Letters
|August 22, 2013
PubMed

Insights

Signal transducer and activator of transcription 3 (Stat3) plays a key role in cisplatin resistance in ovarian cancer. Inhibiting Stat3 with Stattic can restore cisplatin sensitivity in chemoresistant ovarian cancer cells and tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Cisplatin resistance is a major challenge in ovarian cancer treatment.
  • Signal transducer and activator of transcription 3 (Stat3) is implicated in various cancers, but its specific role in cisplatin resistance in ovarian cancer requires further elucidation.

Purpose of the Study:

  • To investigate the role of activated Signal transducer and activator of transcription 3 (Stat3) in the development of cisplatin resistance in ovarian cancer.
  • To evaluate the efficacy of Stat3 inhibition using Stattic in overcoming cisplatin resistance in ovarian cancer models.

Main Methods:

  • Assessed activated Stat3 levels in cisplatin-resistant ovarian cancer cell lines and clinical specimens.
  • Manipulated Stat3 expression (ectopic expression and siRNA knockdown) to assess its impact on cisplatin sensitivity.
  • Administered Stattic, a small molecular inhibitor of Stat3, to chemoresistant ovarian cancer cells and in vivo xenograft models.
  • Measured expression of apoptosis-related proteins (Bcl-2, Bcl-XL, Survivin) and phosphorylated-Akt levels.

Main Results:

  • Higher activated Stat3 levels were observed in cisplatin-resistant ovarian cancer cells and patient tumors.
  • Modulating Stat3 expression affected cisplatin sensitivity, confirming its role in resistance.
  • Stattic treatment restored cisplatin sensitivity in chemoresistant ovarian cancer cells by reducing Bcl-2, Bcl-XL, Survivin, and phosphorylated-Akt.
  • Stattic demonstrated efficacy in circumventing cisplatin resistance in an orthotopic xenograft ovarian cancer model in vivo.

Conclusions:

  • Activated Stat3 is crucial for cisplatin resistance in ovarian cancer.
  • Inhibiting Stat3 with Stattic is a promising strategy to overcome cisplatin resistance.
  • Further clinical evaluation of Stat3 inhibitors is warranted for chemoresistant ovarian cancer patients.
Keywords:
ChemoresistanceCisplatinOvarian cancerStat3Stattic

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