Exploration of the Effects of Two Inflammatory Cytokines in Triple Negative and ER+/PR+/HER2- Breast Cancer
Abstract
Triple negative breast cancer (TNBC) is characterized by cells lacking estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), and is an aggressive, metastatic, and treatment-resistant cancer. An ER+PR+HER2- breast cancer phenotype is more pervasive in the population, less aggressive, and susceptible to hormone therapies. In this study, we employed MDA-MB-231 (triple negative) and T47D (ER+PR+HER2-) human breast cancer cell lines to explore the effects of inflammatory cytokines on the expression of genes known to promote cancer metastasis and growth. The aim of this series of experiments was to use quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) to quantify changes in gene expression of several receptors and signaling molecules known to promote cancer in response to two separate cytokines. Trials were also conducted using both cytokines in concert in an attempt to observe a suspected synergistic effect. Results suggest inflammatory cytokines as a potential target for varied breast cancer subtypes, and further investigation may elucidate novel therapies for preventing breast cancer growth and metastasis.
Exploration of the Effects of Two Inflammatory Cytokines in Triple Negative and ER+/PR+/HER2- Breast Cancer
Triple negative breast cancer (TNBC) is characterized by cells lacking estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), and is an aggressive, metastatic, and treatment-resistant cancer. An ER+PR+HER2- breast cancer phenotype is more pervasive in the population, less aggressive, and susceptible to hormone therapies. In this study, we employed MDA-MB-231 (triple negative) and T47D (ER+PR+HER2-) human breast cancer cell lines to explore the effects of inflammatory cytokines on the expression of genes known to promote cancer metastasis and growth. The aim of this series of experiments was to use quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) to quantify changes in gene expression of several receptors and signaling molecules known to promote cancer in response to two separate cytokines. Trials were also conducted using both cytokines in concert in an attempt to observe a suspected synergistic effect. Results suggest inflammatory cytokines as a potential target for varied breast cancer subtypes, and further investigation may elucidate novel therapies for preventing breast cancer growth and metastasis.