Differential response to apigenin in African American triple‐negative breast cancer in reducing TNF‐α mediated rise in CXCL1

Triple‐negative breast cancer (TNBC) is characterized by the absence of estrogen, progesterone and HER2 receptors. African Americans have higher death rates from TNBC attributable to inadequate preventative health care, late‐stage detection worsened by this being an inherent aggressive malignancy with limited treatment options with the exclusion of hormone receptor‐based chemotherapies. This health disparity may equally be a function of phenotype, where breast cancer can evade the immune system by sequestering tumor‐associated neutrophils and macrophages, in an environment rich in TNF‐α. In this study, we investigated the effects of apigenin, a natural compound from parsley to reduce TNF‐α mediated rise in chemokine (C‐X‐C motif) ligand 1 (CXCL1) in TNBC cell lines of ethnic origin: Caucasian (MDA‐MB‐231) and African American (MDA‐MB‐468). CXCL1 is a known key mediator in neutrophil recruitment and degranulation. The data obtained show that TNF‐α induced greater CXCL1 transcript and protein levels, which were attenuated by apigenin only in the MDA‐MB‐468 cell line. The implications of this warrant further investigation as to the capacity of natural or anti‐cancer agents to act differentially based on the ethnic phenotype of TNBC. Support or Funding Information Supported by the National Institutes of Health, National Institute on Minority Health and Health Disparities, RCMI grant (8G12MD007582‐28.) and COE grant (P20 MD006738). This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .