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Molecular changes have a substantial impact on the onset of colorectal cancer (CRC). Complexes of HOTAIR and miRNAs disrupt several cellular functions during carcinogenesis, primarily by disrupting several carcinogenic signaling pathways. In the present study, the relationships between the serum levels of transforming growth factor-β1 (TGF-β1), sirtuin-1 (SIRT1) and E-cadherin and those of HOX transcript antisense intergenic RNA (HOTAIR) and microRNA-130a (miR-130a) in individuals with CRC were analyzed, including their correlations and diagnostic potential. Patients with colon cancer and healthy volunteers were enrolled in the study. Blood samples were collected from 70 patients with CRC and 30 age-matched healthy control volunteers and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to determine the serum levels of HOTAIR and miR-130a. In addition, the levels of TGF-β1, SIRT1 and E-cadherin were determined utilizing enzyme-linked immunosorbent assays. Patients with CRC were found to have significantly higher TGF-β1, SIRT1, HOTAIR and miR-130a serum levels than those of healthy participants. In addition, patients with high-grade CRC had significantly higher levels of TGF-β1, SIRT1, HOTAIR and miR-130a compared with those of patients with low-grade CRC. A significant reduction in the serum levels of E-cadherin was observed in participants with CRC compared with healthy participants, but no significant difference was detected according to the grade of CRC. Positive correlations were found between HOTAIR and miR-130a, as well as TGF-β1 and SIRT1. By contrast, negative correlations were noted between E-cadherin and HOTAIR, miR-130a, TGF-β1 and SIRT1. Therefore, it may be concluded that the miR-130a/HOTAIR and TGF-β1/SIRT1/E-cadherin axes may serve as novel biomarkers for the early diagnosis of CRC. [ABSTRACT FROM AUTHOR]

Effect of micro ribonucleic acid (miR)-130a on neuronal apoptosis in rats with cerebral infarction (CI) was studied to explore whether phosphatase and tensin homolog deleted on chromosome ten (PTEN)/phosphatidylinositol 3-hydroxy kinase (PI3K)/protein kinase B (Akt) is involved in the regulation of neuronal apoptosis. Thirty-six Sprague-Dawley (SD) rats were randomly divided into blank control group, model group and miR-130a low-expression group. miR-130a was determined by quantitative polymerase chain reaction (qPCR), the content of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-10 was detected using the enzyme-linked immunosorbent assay (ELISA) kits, and the neuronal apoptosis level in each group was determined through terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. The neurobehavioral score was significantly lower in model group than that in blank control group (P<0.01), while it was significantly higher in miR-130a low-expression group than that in model group (P<0.01). Compared with blank control group, the model group had obviously increased content of TNF-α and IL-6 (P<0.01), decreased content of IL-10 (P<0.01), more apoptotic neurons (P<0.01), higher expression of caspase-3 (P<0.01), and obviously lower Bcl-2/Bax (P<0.01). Moreover, expression of phosphorylated (p)-PTEN, PI3K and p-Akt in brain tissues was remarkably lower in the model group than those in the blank control group (P<0.01). The expression level of miR-130a in brain tissues of CI rats is significantly increased. miR-130a promotes the release of inflammatory factors and facilitates neuronal apoptosis through suppressing the PTEN/PI3K/Akt signaling pathway. [ABSTRACT FROM AUTHOR]

MicroRNA-130a (miR-130a) has been reported to be downregulated in hepatocellular carcinoma (HCC). However, the roles and underlying tumor-suppressive mechanisms of miR-130a in the pathogenesis of HCC remain unclear. In the current study, reduced expression of miR-130a was observed in tumor tissues of patients with HCC in addition to in four HCC cell lines, BEL-7402, MHCC97H, HepG2 and Huh7. Results of methyl thiazolyl tetrazolium (MTT) assays identified decreased growth rates of MHCC97H and HepG2 cells transfected with miR-130a mimics. The in vitro colony formation assays demonstrated that the number of colonies formed by cells transfected with miR-130a mimics and cells transfected with miR-130a inhibitors was lower and higher, respectively, than that formed by the cells transfected with miR-negative control. In addition, it was identified that overexpression of miR-130a reduced the migration and invasiveness of MHCC97H and HepG2 cells. Luciferase reporter assays demonstrated that miR-130a directly targeted the 3′-untranslated region of Rho-kinase 2 (ROCK2) mRNA. Northern and western blot analyses indicated that miR-130a could modulate the mRNA and protein expression of ROCK2. Additionally, small-interfering RNA-mediated knockdown of ROCK2 decreased the proliferation, migration and invasiveness of MHCC97H and HepG2 cells. Overall, these observation suggest that miR-130a is a regulator of ROCK2 and can inhibit proliferation, migration and invasive ability of HCC cells, at least in part, by suppressing the expression of ROCK2. The current study provides further insight into the molecular mechanisms of HCC pathogenesis and suggests a new potential biotarget for HCC treatment. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the role of microRNA (miR)-130a in the pathogenesis of myocardial hypoxia/reoxygenation (H/R) injury. Primary rat cardiomyocytes were cultured and subjected to H/R treatment. Reverse transcription-quantitative polymerase chain reaction was performed to detect the levels of miR-130a, western blot analysis was used to determine the expression of various proteins, and CCK-8 assay was performed to determine cell viability. In addition, flow cytometry was used to assess apoptosis. The cell viability was significantly decreased and the apoptosis rate was significantly increased in H/R-treated primary cardiomyocytes, and the expression level of miR-130a was also elevated in these model cells. Transfection with miR-130a inhibitor significantly elevated the cell viability and reduced the apoptosis rate in H/R-treated cardiomyocytes. Bioinformatics analysis indicated that autophagy-related gene 14 (ATG14) is the target for miR-130a, which was confirmed by dual-luciferase reporter assay and western blot analysis. When the H/R model cells were co-transfected with miR-130a inhibitor and small interfering RNA against ATG14, the cell viability was significantly reduced and the apoptosis rate was significantly elevated, compared with that of cells transfected with miR-130a inhibitor alone. miR-130a inhibitor transfection significantly elevated the levels of ATG14 and phosphorylated (p-)Beclin 1, increased the LC3II/LC3I ratio, and decreased the expression levels of P62 and cleaved caspase-3, while the co-transfection of miR-130a inhibitor and siR-ATG14 attenuated these effects in H/R-induced primary cardiomyocytes. These results indicate that miR-130a is involved in H/R-induced injuries in primary cardiomyocytes, and that the inhibition of miR-130a increases the levels of ATG14 and p-Beclin 1, thereby increasing autophagy and inhibiting apoptosis in these cells. [ABSTRACT FROM AUTHOR]