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Rafoxanide negatively modulates STAT3 and NF-κB activity and inflammation-associated colon tumorigenesis.

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The drug rafoxanide inhibits key cancer pathways, signal transducer and activator of transcription 3 (STAT3) and nuclear factor-κB (NF-κB), to reduce inflammation-associated colorectal cancer (CRC) growth without harming healthy cells.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Drug Repurposing

Background:

  • Signal transducer and activator of transcription 3 (STAT3) and nuclear factor-κB (NF-κB) are hyperactivated in colorectal cancer (CRC), promoting tumor growth and inflammation.
  • The anthelmintic drug rafoxanide shows potential as an anticancer agent through drug repositioning.

Purpose of the Study:

  • To investigate the potential of rafoxanide in modulating STAT3/NF-κB pathways and inflammation in CRC.
  • To evaluate the antineoplastic effects of rafoxanide in preclinical CRC models.

Main Methods:

  • Utilized a murine model of colitis-associated CRC.
  • Assessed STAT3/NF-κB activation, cell proliferation, and cytokine production in CRC cells, patient-derived explants/organoids, and tumor-infiltrating leukocytes (TILs) treated with rafoxanide.
  • Evaluated the impact of rafoxanide-treated TILs on CRC cell behavior.

Main Results:

  • Rafoxanide effectively restrains STAT3/NF-κB activation and inflammation-driven colon tumorigenesis in vivo.
  • The drug reduces STAT3/NF-κB activation in CRC cells, explants, organoids, and TILs.
  • Rafoxanide impairs TILs' ability to produce pro-tumor cytokines and promote CRC cell proliferation, with no observed effects on normal intestinal cells.

Conclusions:

  • Rafoxanide exhibits a novel, multi-level inhibitory effect on STAT3/NF-κB oncogenic activity within the CRC microenvironment.
  • Rafoxanide presents a promising therapeutic candidate for inflammation-associated colorectal cancer.