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A Novel Therapeutic Strategy Targeting BACH1 For Triple-Negative Breast Cancer

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Technical Report,01 Jul 2017,30 Jun 2018

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University of Chicago Chicago United States

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Currently women have a 12 chance of developing breast cancer during their lifetime. The most aggressive and lethal subtype of breast cancer is triple negative breast cancer TNBC, yet no approved targeted therapy for this group of patients. My research proposal addresses overarching challenges 1 to develop therapeutic intervention with the approved drugs that are less toxic. 2 to maximize the efficacy of the approved drug with a combinational treatment that targets a metabolic regulator. With these questions, I will characterize breast tumor metabolism, identify molecular mechanisms beyond, and establish their roles for a novel therapeutic intervention. The goal of this research is to provide a novel therapeutic regimen to give benefits to the patients with breast cancer. My research accomplishment during the first year 2017-2018 identifiedBACH1 regulates mitochondrial genes at the transcriptional levels by direct binding on the promoter regions in breast cancer cells. These regulations altered metabolic phenotypes such as oxygen consumption rates OCR and extracellular acidification rates ECAR, as well as increasing NADNADH ratio, ATP levels, and mitochondrial ROS levels when BACH1 is depleted. Taken together, my research during the Year 1 from DOD clearly elucidated metabolic pathway regulation by BACH1 as a transcriptional regulator in TNBC cells.

Subject Categories:

  • Medicine and Medical Research
  • Anatomy and Physiology

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