No abstract

Salvianolic acid B (Sal B) is the most abundant bioactive molecule from Radix Salviae Miltiorrhizae, and has recently been used for treating renal fibrosis in traditional Chinese medicine. Here we investigated the ability reversal of Sal B to reverse the transdifferentiation of human kidney proximal tubular epithelial cells that was induced by transforming growth factor-beta 1 (TGF-β1). The effects of Sal B on HK-2 cell morphology were observed by phase contrast microscopy, while alpha smooth muscle actin and E-cadherin were studied by immunocytochemistry and real-time reverse transcription polymerase chain reaction, respectively. Exposure of HK-2 cells to TGF-β1 for 72 h induced a complete conversion of the epithelial cells to myofibroblasts. When HK-2 cells were co-incubated with Sal B and TGF-β1 for a further 72 h, the morphology of myofibroblasts returned to that of proximal tubular epithelial cells, whereas the myofibroblast phenotype was maintained after exposure of cells to TGF-β1 for 144 h. Sal B reduced alpha smooth muscle actin levels and increased E-cadherin levels compared with their epithelial-to-mesenchymal transition controls. The reversal effect of Sal B was dose-dependent. That Sal B reverses the epithelial-to-mesenchymal transition in vitro suggests that it could possibly facilitate the repair of tubular epithelial structures and the regression of renal fibrosis in injured kidneys.

Cervical cancer (CC) is the most common gynecological malignancy, with high incidence and mortality rates in China. The microRNA miR‐485‐5p has previously been reported to serve as a negative regulator of tumorigenesis in breast cancer and hepatocellular carcinoma, and miR‐485‐5p has been observed to be differentially expressed between CC and normal control tissue. Here, we confirmed that miR‐485‐5p expression is lower in CC than in adjacent normal tissue and proceeded to investigate the effects of miR‐485 on tumor behavior in CC cell lines. We report that miR‐485‐5p transcription is decreased in HPV‐infected CC tissue, and levels of miR‐485 in clinical samples are positively correlated with the 5‐year overall survival rate. The Transwell assay showed that miR‐485‐5p inhibited cell invasion and migration but had no influence on apoptosis and cell proliferation. Using a luciferase reporter assay, we demonstrated that miR‐485‐5p partially abrogated cell migration and proliferation by targeting FLOT‐1 mRNA. Transfection of HPV‐infected cervical carcinoma cells with an adenovirus vector encoding human FLOT‐1 partially diminished the inhibitory effects of miR‐485 on cell invasion. Taken, together, these data demonstrated that miR‐485‐5p suppresses the invasion of cancer cells by targeting FLOT‐1 in HPV‐infected cervical carcinoma cells.