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Recently, the role of gut microbiota in the development of obesity and type 2 diabetes mellitus (T2DM) has been highlighted. We performed an 8-week administration protocol on T2DM (C57BL/6J db-/db-) mice and fecal samples were collected. Comparisons of fecal bacterial communities were performed between db-/db- mice and normal mice (DB/DB) and between the db-/db mice treated and untreated with AOE using next-generation sequencing technology. Our results showed that the db-/db-AOE group had improved glycemic control and renal function compared with the db-/db-H2O group. Compared with the db-/db-H2O group, AOE administration resulted in significantly increased ratio of Bacteroidetes-to-Firmicutes in db-/db- mice. In addition, the abundance of Akkermansia was significantly increased, while Helicobacter was significantly suppressed in the db-/db-AOE group compared with the db-/db-H2O group. Our data suggest that AOE treatment decreased blood glucose levels and significantly reduced damage of renal pathology in the T2DM mice by modulating gut microbiota composition.

MiR-223-5p has been demonstrated to regulate the development and progression of various cancers, such as hepatocellularcarcinoma, breast cancer and gastric carcinoma. However, the role of miR-223-5p in non-small cell lung cancer (NSCLC) requires further investigation. In this study, we found that the expression of miR-223-5p was significantly down-regulated in NSCLC tissues and cell lines. Moreover, the expression level of miR223-5p is negatively correlated with the malignance of NSCLC. Besides, we found that overexpression of miR-223-5p remarkably suppressed the proliferation of NSCLC cells and. MiR-223-5p overexpression also led to reduced migration and invasion in NSCLC cells. Mechanistically, we found that E2F8, a key transcription factor involved in many kinds of biological processes, was a direct target gene of miR-223-5p. Overexpression of miR-223-5p significantly decreased the mRNA and protein levels of E2F8 in NSCLC cells. What's more, we showed that restoration of E2F8 rescued the proliferation, migration and invasion of miR-223-5p-overexpressing NSCLC cells. Taken together, our findings demonstrated that miR-223-5p suppressed NSCLC progression through targeting E2F8.

Background/Aims: The purpose of our experiments was to investigate the targeting relationship of linc00515, miR-140-5p and ATG14 and to explore the roles of linc00515, miR-140-5p and ATG14 in autophagy and chemoresistance of melphalan-resistant multiple myeloma cells. Methods: Plasmids that could interfere with the expression of linc00515 and ATG14 were loaded into myeloma cells, which were cultured with melphalan. MTT assay and flow cytometry analysis were utilized to investigate the effect of linc00515, miR-140-5p and ATG14 on the resistance of myeloma cells. QRT-PCR was used to determine the levels of mRNAs. Western blot was utilized to explore the level of ATG14 and autophagy-related proteins. Dual luciferase assay was utilized to explore the targeting relationship between linc00515, miR-140-5p and ATG14. GFP LC3 fluorescence assay was conducted to study the autophagy of cells. Results: The expression of linc00515 and ATG14 were significantly higher in melphalan-resistant myeloma cells. Knockdown of linc00515 and ATG14 led to decreased autophagy and chemoresistance of melphalan-resistant myeloma cells. The forced expression of miR-140-5p suppressed autophagy and chemoresistance of melphalan-resistant myeloma cells. Conclusion: Linc00515 enhanced autophagy and chemoresistance of melphalan-resistant myeloma by directly inhibiting miR-140-5p, which elevated ATG14 level.

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