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  • 1Affiliations of authors: Houston Methodist Cancer Center, Houston, TX (BD, DDG, ZBL, HW, SG, DHS, JEE, JCC); Division of Basic Science Research, Department of Systems Biology (NEE, AKE, GBM), and Division of Pathology/Lab Medicine, Department of Pathology (MZG), The University of Texas MD Anderson Cancer Center, Houston, TX; Department of Breast Surgery, Shanghai Cancer Center and Cancer Institute of Fudan University, Shanghai, China (ZBL); Department of Pathology and Laboratory Medicine, Emory University, Atlanta, GA (XL); Department of Physiology and Biophysics, Institute for Computational Biomedicine, Weill Cornell Medical College, New York, NY (OE); Joan and Sanford I. Weill Medical School of Cornell University, New York, NY (SSG); Department of Medicine, Indiana University Medical School, Indianapolis, IN (KDM); Departments of Surgery and Medical and Molecular Genetics, IU Center for Computational Biology and Bioinformatics, Indianapolis, IN (MR).

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Metaplastic breast cancer often harbors the RPL39 A14V mutation, driving tumor growth and chemoresistance via iNOS signaling. Inhibiting iNOS or modulating RNA editing may offer new therapeutic strategies for this challenging cancer.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Metaplastic breast cancer (MBC) presents significant therapeutic challenges due to its heterogeneity and chemoresistance.
  • Previous research identified oncogenic activity of ribosomal protein L39 (RPL39) and its A14V mutation in triple-negative breast cancer, potentially mediated by inducible nitric oxide synthase (iNOS).
  • The role of RPL39 and its A14V mutation in MBC remained unexplored.

Purpose of the Study:

  • To investigate the role and mechanism of action of RPL39 in metaplastic breast cancer.
  • To determine the prevalence of the RPL39 A14V mutation in MBC patient samples.
  • To assess the association between RPL39/iNOS expression and patient survival.

Main Methods:

  • Determined RPL39 A14V mutation rate using competitive allele-specific and droplet digital PCR.
  • Analyzed the impact of RPL39 and iNOS expression on overall survival via Kaplan-Meier method.
  • Utilized co-immunoprecipitation and immunoblot analyses for mechanistic evaluation.

Main Results:

  • The RPL39 A14V mutation was highly prevalent (97.5%) in MBC samples.
  • High RPL39 and iNOS expression correlated with reduced patient overall survival.
  • iNOS inhibition decreased tumor proliferation, migration, growth in xenograft models, and chemoresistance, mediated by RPL39 via adenosine deaminase acting on RNA 1.

Conclusions:

  • RPL39 plays a significant role in MBC progression through iNOS signaling.
  • iNOS inhibition demonstrates therapeutic potential against MBC.
  • Targeting RNA editing enzymes could offer novel treatment avenues for MBC.