Aims/Introduction The aim of the present study was to identify candidate differentially expressed genes ( DEG s) and pathways using bioinformatics analysis, and to improve our understanding of the cause and potential molecular events of diabetic nephropathy. Materials and Methods Two cohort profile datasets ( GSE 30528 and GSE 33744) were integrated and used for deep analysis. We sorted DEG s and analyzed differential pathway enrichment. DEG ‐associated ingenuity pathway analysis was carried out. The screened gene expression feature was verified in the db / db mouse kidney cortex. Then, rat mesangial cells cultured with high‐concentration glucose were used for verification. The target genes of transcriptional factor E26 transformation‐specific‐1 (ETS1) were predicted with online tools and validated using chromatin immunoprecipitation assay quantitative polymerase chain reaction . Results The two GSE datasets identified 89 shared DEG s; 51 were upregulated; and 38 were downregulated. Most of the DEG s were significantly enriched in cell adhesion, the plasma membrane, the extracellular matrix and the extracellular region. Quantitative reverse transcription polymerase chain reaction analysis validated the upregulated expression of Itgb2 , Cd44 , Sell , Fn1 , Tgfbi and Il7r , and the downregulated expression of Igfbp2 and Cd55 in the db / db mouse kidney cortex. Chromatin immunoprecipitation assay quantitative polymerase chain reaction showed that Itgb2 was the target gene of transcription factor Ets1. ETS 1 knockdown in rat mesangial cells decreased integrin subunit beta 2 expression. Conclusion We found that EST 1 functioned as an important transcription factor in diabetic nephropathy development through the promotion of integrin subunit beta 2 expression. EST 1 might be a drug target for diabetic nephropathy treatment.

Objective To investigate the effect of microRNA‐137 (miR‐137) on the migration and invasion of melanoma cells and its mechanism. Methods Quantitative real‐time polymerase chain reaction (qRT‐PCR) was used to detect the expression of miR‐137 in melanoma tissues and cells. miR‐137 mimics, phosphoinositide‐3‐kinase regulatory subunit 3 (PIK3R3) small interfering RNA and corresponding controls were transfected into A375 and WM451 cells by lipofection. The expression of PIK3R3 was examined by qRT‐PCR and Western blot analysis. The Trans‐well assay was conducted to measure cell migration and invasion. Dual luciferase reporter assay was used to detect the interaction between miR‐137 and PIK3R3. Results Compared with normal pigmented nevus tissue, miR‐137 expression was significantly reduced in melanoma tissues. Compared with keratinous HaCaT cells, the level of miR‐137 was significantly decreased in melanoma SK‐MEL‐1, A375, and WM451 cells. Knockdown of miR‐137 significantly reduced the migrated and invasive abilities of melanoma A375 and WM451 cells. Moreover, inhibition of PIK3R3 obviously suppressed the migration and invasion abilities of melanoma A375 and WM451 cells. Luciferase activity assay showed that PIK3R3 was a direct target of miR‐137. In addition, overexpression of miR‐137‐inhibited PIK3R3 expression, while knockdown of miR‐137‐enhanced PIK3R3 abundance. Restoration of PIK3R3 reversed the regulatory effect of miR‐137 on cell migration and invasive in melanoma A375 and WM451 cells. Conclusion miR‐137 inhibited melanoma cell migration and invasion by targeting PIK3R3 gene.