Epigallocatechin-3-gallate inhibits paclitaxel-induced apoptosis through the alteration of microRNA expression in human dermal papilla cells

Background Paclitaxel well known as anti-cancer drug has been shown to cause alopecia in chemotherapy. The paclitaxel chemotherapy-mediated alopecia is induced by apoptotic damage in human dermal papilla (HDP) cells. Epigallocatechin-3-gallate (EGCG) inhibits apoptosis against anti-cancer drug such as cisplatin. EGCG, one of the green tea extract ingredients, has been reported to enhance cell viability and to inhibit apoptosis. However, it is unclear that EGCG enhances cell viability and inhibits apoptosis against paclitaxel-induced apoptotic damage in HDP cells. Methods We show cell viability, cell cycle, and microRNA (miRNA) expression in EGCG-mediated rescue cell to paclitaxel-mediated cell death and growth arrest. Results EGCG promotes cell survival and cell death inhibitory effects and alteration of miRNA expression in paclitaxel-exposed HDP cells were investigated. Firstly, paclitaxel increases apoptosis and EGCG promotes cell survival and represses paclitaxel-induced apoptosis in a dose-dependent manner. Fluorescence-activated cell sorting (FACS) analysis showed that EGCG protects apoptosis in paclitaxel-exposed HDP cells. miRNA microarray analysis was performed and 48 miRNAs changed by EGCG in paclitaxel-exposed HDP cells were identified. In gene ontology analysis in silico, miRNAs regulate apoptosis and cell proliferation-regulated genes, such as BCL2L1, BCL2L2, BBC3, and MDM2. In Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, miRNAs are related to mitogen-activated protein kinase (MAPK) signaling pathway and Wnt signaling pathway, which regulate apoptosis and cell proliferation. Conclusions EGCG inhibits apoptosis through regulating miRNA expression related to apoptosis and cell proliferation in paclitaxel-treated HDP cells.