MiR-297 inhibits tumour progression of liver cancer by targeting PTBP3.

Whereas increasing evidences demonstrate that miR-297 contributes to the tumour development and progression, the role of miR-297 and its underlying molecular mechanisms in hepatocellular carcinoma (HCC) was still unclear. Here, we reported that the expression of miR-297 increased significantly in hepG2 cells after the treatment of the conditioned medium of human amniotic epithelial cells(hAECs) which can inhibit the proliferation and migration of hepG2. And the overexpression of miR-297 inhibits the cell proliferation, migration and invasion of HCC cell lines in vitro and suppressed the tumorigenesis of HCC in vivo. Polypyrimidine tract-binding protein 3 (PTBP3) was identified as a direct target gene of miR-297 in HCC cell lines, and mediated the function of miR-297 in HCC cells. In clinical samples, miR-297 levels have a tendency to decrease, but there are no statistically significant differences. Furthermore, in vitro cell experiments confirmed that overexpression of miR-297 could inhibit the PI3K/AKT signaling pathway by down-regulating PTBP3 expression, thereby inhibiting the proliferation, migration and invasion of HCC cells. In conclusion, our results revealed that miR-297 could down-regulate the expression of PTBP3 and inhibit the activation of PI3K/AKT signaling pathway, thereby preventing HCC growth, migration and invasion.

Phenotype and biological characteristics of endometrial mesenchymal stem/stromal cells: A comparison between intrauterine adhesion patients and healthy women.

PROBLEM: Intrauterine adhesion (IUA) is a uterine disorder with partial or total obstruction of the uterine cavity and/or the cervical canal primarily caused by intrauterine operations and infections. It is the most common cause of uterine infertility and recurrent abortion. However, the reasons for endometrium repair disorders in patients with IUA are still unclear. While increasing evidence demonstrates that endometrial mesenchymal stem/stromal cells (EMSCs) contribute to the regeneration and repair of endometrium, the roles of EMSCs in the pathogenesis of IUA have not been reported. METHODS AND STUDY: We investigated the differences of phenotype and biological characteristics between EMSCs from women with IUA and healthy women. Firstly, the fibrosis of endometrium were measured by immunohistochemistry and Masson staining. Second, we used immunofluorescence to detect the location of EMSCs in endometrial tissue, and the proportion of CD146+ CD140b+ in the two groups was compared by flow cytometry. Then, plate colony formation experiment, CCK-8 assay, flow cytometry, would-healing assay, and transwell invasion experiment were used to compare the cloning ability, proliferation, cell cycle, migration and invasion capabilities respectively. Finally, we compared the potential angiogenesis and immunosuppression capabilities. RESULTS: Our results showed that there were fewer CD146+ CD140b+ cells in patients with IUA, and the clone-forming, migration, invasion, angiogenic and immunosuppressive abilities of the EMSCs of patients with IUA were significantly decreased compared with those of healthy women. CONCLUSION: There are some differences between the EMSCs of IUA patients and healthy women, which may be related to the occurrence of IUA and dysfunction of endometrium.