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Diabetic nephropathy (DN) is one of the most common microvascular complications associated with diabetes mellitus (DM); the incidence has been predicted to reach 7.7% by 2030 on a global scale. Krüppel-like factor 5 (KLF5) is involved in numerous important biological processes; however, the potential effects of KLF5 on podocytes in patients with diabetic nephrotic (DN) have not yet been investigated. In the present study, synaptopodin expression in podocytes was investigated using an immunofluorescence assay. Following this, the proliferation of podocytes was investigated using an MTT assay. In addition, KLF5 was overexpressed in podocytes, and cell cycle arrest and apoptosis was subsequently investigated using flow cytometry. Western blotting and reverse transcription-quantitative polymerase chain reaction assays were performed to detect the expression levels of genes involved in the cell cycle and apoptosis, and the extracellular signal-regulated protein kinase (ERK)/p38 mitogen-activated protein (MAP) kinase pathway. The results demonstrated that treatment with puromycin aminonucleoside (PAN) suppressed the proliferation of podocytes in a dose- and time-dependent manner, and overexpression of KLF5 induced cell cycle arrest of podocytes regulated by PAN. Furthermore, overexpression of KLF5 was revealed to have inhibited PAN-induced apoptosis of podocytes, and that overexpression of KLF5 suppressed the ERK/p38 MAP kinase pathway in podocytes induced by PAN. Therefore, the results of the present study suggested that KLF5 may represent a potential therapeutic target for treatment of patients with DN. [ABSTRACT FROM AUTHOR]

Recently, microRNA (miR)‑590‑5p has been shown to inhibit tumorigenesis in colorectal and breast cancer; however, its function in osteosarcoma (OS) requires further investigation. In the present study miR‑590‑5p expression was poorly expressed in OS samples and cell lines when compared with that observed in normal cells. In addition, overexpression of miR‑590‑5p significantly reduced the proliferation, migration and invasion of SAOS2 and U2OS cells in vitro, as well as inhibiting tumor sizes in vivo. The results revealed that miR‑590‑5p directly targeted Kruppel‑like factor 5 (KLF5) in SAOS2 and U2OS cells. Their expression was inversely correlated with OS tissues. Finally, it was demonstrated that overexpression of KLF5 rescued the inhibitory effects of miR‑590‑5p on cell proliferation, migration and invasion. Overall, the results of the present study suggested that the miR‑590‑5p/KLF5 axis may regulate OS progression and thus, may be a novel therapeutic target for the treatment of patients with OS. [ABSTRACT FROM AUTHOR]

MicroRNAs (miRs) are important in hepatocellular carcinoma (HCC) progression. miR‑145‑5p acts as a tumor suppressor in certain malignancies, however, its role in HCC remains unclear. The present study aimed to perform a functional analysis of miR‑145‑5p in HCC in order to elucidate its role in the pathogenesis of HCC. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was performed to analyze tissue and cellular expression of miR‑145‑5p in HCC. Following miRNA mimics transfection, cell viability, apoptosis and cells migration were determined by Cell Counting kit‑8, Annexin V‑FITC/propidium iodide staining and Transwell analyses. The target of miR‑145‑5p was analyzed by luciferase reporter assay and western blot analysis. It was observed that miR‑145‑5p was significantly decreased in HCC tissues and cell lines. Overexpression of miR‑145‑5p significantly increased apoptosis, reduced cell proliferation and suppressed HCC cell migration. Kruppel‑like factor 5 (KLF5) is regarded as a target of miR‑145‑5p in HCC cells. In addition, KLF5 overexpression partially attenuated the tumor suppressive effects of miR‑145‑5p. KLF5 expression was negatively associated with levels of miR‑145‑5p in HCC tissues. The present study demonstrated that miRNA‑145‑5p may, by targeting KLF5, partially suppress HCC cell growth and motility. The results of the present study suggested that miRNA‑145‑5p alteration in HCC may serve a role in the progression of HCC. [ABSTRACT FROM AUTHOR]