Xingxiang Liu1, Wei Zhao2, Wei Wang3, Sen Lin4, Liu Yang5. 1. Inspection Center, Huai'an No 4 People's Hospital, Huai'an 223002, China. 2. Department of Laboratory, Nanjing Maternity and Child Health Care Hospital, Nanjing 210000, China. 3. Department of Pathology, Nanjing Maternity and Child Health Care Hospital, Nanjing 210000, China. 4. Department of Laboratory, Huai'an Hospital, Xuzhou Medical University, Huai'an 223002, China. Electronic address: linsenls2016@126.com. 5. Department of General Surgery, Jiangsu Cancer Hospital, Nanjing 210000, China. Electronic address: yl19810412@163.com.
Abstract
BACKGROUND: Chronic inflammation is a major risk factor for the development and metastatic progression of breast cancer. Puerarin has long been used as traditional Chinese medicine, which possesses manifold physiological activities, including anti-inflammation and anti-cancer activities. However, its anti-cancer metastasis activity in breast cancer cell inflammation-mediated have not been studied. METHODS: Cell viability was detected with Cell Counting Kit (CCK)-8. Transwell migration and invasion assay were performed to evaluate cell migration and invasion, respectively. Enzyme-linked immunosorbent assay (ELISA) was conducted to analysis the expression of inflammatory factor. In addition, mRNA and protein levels of related cytokines were determined by qRT- PCR assay and western blot analysis, respectively. RESULTS: In this study, puerarin significantly inhibited lipopolysaccharide (LPS)-induced MCF-7 and MDA-MB-231 cell migration, invasion and adhesion. The mRNA and protein levels revealed that puerarin treatment effectively negated the expression of CCR7, CXCR4, MMP-2, MMP-9, ICAM and VCAM in LPS- activated MCF-7 and MDA-MB-231 cells. Further, the expression of inflammatory factor TNF-α and IL-6 in cell culture supernatant remarkably reduced. Finally, the result indicated that puerarin abrogated the NF-κB activation in breast cancer cells stimulated by LPS, which is mediated through inhibition of phosphorylation of p65 and IκBα. Also, puerarin inhibited phosphorylation of Erk in breast cancer cells LPS-induced. CONCLUSIONS: This present study revealed that puerarin might be a novel therapeutic drug for breast cancer treatment.
BACKGROUND:Chronic inflammation is a major risk factor for the development and metastatic progression of breast cancer. Puerarin has long been used as traditional Chinese medicine, which possesses manifold physiological activities, including anti-inflammation and anti-cancer activities. However, its anti-cancer metastasis activity in breast cancer cell inflammation-mediated have not been studied. METHODS: Cell viability was detected with Cell Counting Kit (CCK)-8. Transwell migration and invasion assay were performed to evaluate cell migration and invasion, respectively. Enzyme-linked immunosorbent assay (ELISA) was conducted to analysis the expression of inflammatory factor. In addition, mRNA and protein levels of related cytokines were determined by qRT- PCR assay and western blot analysis, respectively. RESULTS: In this study, puerarin significantly inhibited lipopolysaccharide (LPS)-induced MCF-7 and MDA-MB-231 cell migration, invasion and adhesion. The mRNA and protein levels revealed that puerarin treatment effectively negated the expression of CCR7, CXCR4, MMP-2, MMP-9, ICAM and VCAM in LPS- activated MCF-7 and MDA-MB-231 cells. Further, the expression of inflammatory factor TNF-α and IL-6 in cell culture supernatant remarkably reduced. Finally, the result indicated that puerarin abrogated the NF-κB activation in breast cancer cells stimulated by LPS, which is mediated through inhibition of phosphorylation of p65 and IκBα. Also, puerarin inhibited phosphorylation of Erk in breast cancer cells LPS-induced. CONCLUSIONS: This present study revealed that puerarin might be a novel therapeutic drug for breast cancer treatment.