Triple negative breast cancer (TNBC) is subtype of breast disease devoid of the estrogen, progesterone, and Her2/neu receptors which are targets for pharmacological intervention. There is a need for novel anti-breast cancer agents that target TNBC. Therefore, novel isochalcone DJ52 was evaluated using the alamar blue dye exclusion assay, the luciferase colony assay, and xenograft models to determine its efficacy and potency. DJ52 significantly decreased proliferation of cells measured by using the alamar blue dye method and produced IC50 values of DJ52, DJ56, and DJ82 at 10-6M, 10-5M, and 10-5M, respectively. In vivo studies were conducted by injecting MDA-MB-231 cells into SCID mice to determine tumor regression was measured over 20 days. DJ52 at 50mg/kg caused significant decrease in tumor volume (p value <.05) by nearly 50% compared with the control with vehicle alone. These data suggest that DJ52 has merit for further evaluation as a novel anticancer agent.
Patients who present with the subtype of breast cancer called triple negative breast cancer (TNBC) have poorer outcomes than patients with less aggressive subtypes of breast cancer. To better understand the proliferation, migration, and invasion associated with TNBC, we evaluated the microenviroment of the TNBC cells using noncancerous breast epithelial cell line MCF‐10A. Exosomes secreted from MCF‐10A when in crisis cells enhances growth, motility, and invasion by promotion signals and prepares metastatic niches both in vitro and in vivo. Our laboratory investigated this phenomenon using TNBC cell lines MDA‐MB‐231 and MDA‐MB‐468. Preliminary data suggests that this exosomal media contains biomolecules that enhance proliferation, migration, and invasion of TNBC cells. Here we will report our findings on exosomal media promoting the proliferation, migration, and invasion in both MDA‐MB‐231 and MDA‐MB‐468 cells. Gene expression is modified when these cells are exposed to exosomal media, and finally, we demonstrate that exosomal media has a significant impact in enhancing the growth of both MDA‐MB‐231 and MDA‐MB‐468 cells in vivo over 90 days. Better understanding the microenvironment of the TNBC cells will aid us in identifying novel targets for pharmacological intervention.
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