miR-653 Induces Bone Marrow Mesenchymal Stem Cells Proliferation via Activating Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma

This study intends to assess miR-653’s expression in MSCs and OSCC and discuss molecular biological mechanism of changes of EMT in MSCs through activating miR-653 in OSCC. miR-653 expression in MSCs and OSCC was detected. si-miR-653 was transfected into MSCs followed by analysis of cell proliferation by CCK-8 and clone formation assay, cell apoptosis and cycle by FCM, and the changes of transcription factor as ZEB1 and Snail by qRT-PCR. miR-653 expression in OSCC cell was up-regulated significantly from the result of q-RT-PCR detection. The proliferation of MSCs induced by miR-653 was restrained and apoptotic rate was increased after treatment with si-miR-653 along with stagnated cycle of G1/G0 staging cell. The expression of transcription factor of EMT type as ZEB1 and Snail was elevated significantly after intervention using si-miR-653. In conclusion, the proliferation of OSCC could be induced by MSCs through activation with miR-653 which might be through regulation of EMT process.

Extracellular Vesicles from Esophageal Squamous Cell Carcinoma Promote Angiogenesis and Tumor Growth

Angiogenesis is a prerequisite for tumor development and metastasis. Emerging evidence shows that tumor-derived extracellular vesicles (EVs) are an important component of tumor microenvironment, which participate in the communication between normal cells and tumor cells. In this study, we aimed to investigate the role of EVs derived from esophageal squamous cell carcinoma (ESCC) on tumor angiogenesis. We found that ESCC cell-derived EVs promoted the proliferation, migration, and tubule formation of human umbilical vein endothelial cells in vitro, and enhanced angiogenesis and tumor growth in vivo. Our results suggest that ESCC cell-derived EVs could promote angio-genesis and tumor growth, which also indicated the application of EVs as a valuable therapeutic strategy of ESCC.