MicroPNA-21 promotes proliferation of rat Schwann cells following nerve injury / 中国病理生理杂志

AIM: To investigate the molecular mechanism of microRNA-21 (miR-21) in the regulation of Schwann cell proliferation following nerve injury.METHODS:The expression of miR-2l was detected by real-time PCR. Synthetic miR-21 mimic and its control were transfected into rat Schwann cells.CCK-8 assay was performed to evaluate the influence of miR-21 on the proliferation of Schwann cells.The cell cycle distribution was determined by flow cytometry. The expression of transforming growth factorβ-induced protein ( TGFBI) and cyclin D1 were detected by Western blotting. RESULTS:The expression of miR-21 in model group was 7.87 ±0.75 and 7.75 ±0.80 times higher than that in sham operation group and blank group respectively.After transfected with miR-21 mimic, the expression of miR-21 in experimen-tal group was 2.21 ±0.14 and 2.29 ±0.21 times higher than that in negative control group and blank group respectively. Moreover, the A450 value of CCK-8 assay in experimental group at 48 h was higher than that in negative control group and blank group.The proliferation index in experimental group was higher than that in negative control group and blank group. At the same time, the expression of TGFBI obviously decreased and the cyclin D1 increased in the Schwann cells 48 h after transfection with miR-21.CONCLUSION:miR-21 promotes the proliferation activity of Schwann cells by down-regulating TGFBI expression.

MicroRNA-195 inhibits the proliferation of human glioma cells by directly targeting cyclin D1 and cyclin E1.

Glioma proliferation is a multistep process during which a sequence of genetic and epigenetic alterations randomly occur to affect the genes controlling cell proliferation, cell death and genetic stability. microRNAs are emerging as important epigenetic modulators of multiple target genes, leading to abnormal cellular signaling involving cellular proliferation in cancers.In the present study, we found that expression of miR-195 was markedly downregulated in glioma cell lines and human primary glioma tissues, compared to normal human astrocytes and matched non-tumor associated tissues. Upregulation of miR-195 dramatically reduced the proliferation of glioma cells. Flow cytometry analysis showed that ectopic expression of miR-195 significantly decreased the percentage of S phase cells and increased the percentage of G1/G0 phase cells. Overexpression of miR-195 dramatically reduced the anchorage-independent growth ability of glioma cells. Furthermore, overexpression of miR-195 downregulated the levels of phosphorylated retinoblastoma (pRb) and proliferating cell nuclear antigen (PCNA) in glioma cells. Conversely, inhibition of miR-195 promoted cell proliferation, increased the percentage of S phase cells, reduced the percentage of G1/G0 phase cells, enhanced anchorage-independent growth ability, upregulated the phosphorylation of pRb and PCNA in glioma cells. Moreover, we show that miR-195 inhibited glioma cell proliferation by downregulating expression of cyclin D1 and cyclin E1, via directly targeting the 3'-untranslated regions (3'-UTR) of cyclin D1 and cyclin E1 mRNA. Taken together, our results suggest that miR-195 plays an important role to inhibit the proliferation of glioma cells, and present a novel mechanism for direct miRNA-mediated suppression of cyclin D1 and cyclin E1 in glioma.