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Our study was intended to provide evidence for whether long noncoding RNA (lncRNA) SNHG1 would accelerate the epithelial-mesenchymal transition (EMT) course intrinsic in colorectal cancer (CRC) by sponging downstream miR-497-5p and miR-195-5p. We altogether collected 338 pairs of CRC and noncancerous tissues, and meanwhile purchased five CRC cell lines (i.e., SW480, HCT116, Lovo, CaCO-2, and HT29) and human embryo intestinal mucosal tissue-sourced cell line (i.e., CCC-HIE-2). The CRC cells as mentioned above were appraised regarding their potencies in proliferation, migration, and invasion, after being transfected with pcDNA3.1-SNHG1, si-SNHG1, miR-195-5p mimic/inhibitor, and miR-497-5p mimic/inhibitor. Eventually, we depended on reverse transcription-polymerase chain reaction to assess SNHG1, miR-497-5p, and miR-195-5p expressions, and the protein levels of EMT-specific molecules were determined on the strength of western blotting. It seemed that there was a high potential for highly expressed SNHG1 and lowly expressed miR-497/miR-195 to symbolize CRC patients' unfavorable prognosis (p < .05). Concurrently, CRC cells were detected with higher SNHG1 expression and lower miR-497/miR-195 expression than CCC-HIE-2 cells (p < .05). In addition, the EMT process of CRC cells was facilitated markedly against the contexts of overexpressed SNHG1 and underexpressed miR-497-5p/miR-195-5p. Intriguingly, the strength of miR-195-5p collaborating with miR-497-5p in affecting the activity of CRC cells seemed to overweigh that of miR-497/miR-195-5p alone. Besides, both miR-195-5p and miR-497-5p were subjected to in vivo and in vitro modification of SNHG1 (p < .05). Conclusively, application of lncRNA SNHG1 for treating CRC might be promising, given its dual modulation of miR-497 and miR-195 underlying CRC pathogenesis.

MiR-30 family plays an important role in the tumorigenesis of human cancers. The aim of the study is to investigate the role of miR-30d in human colon cancer cell lines and explore the molecular mechanism in the proliferation of colon cancer cells. The expression of miR-30d was determined by real-time polymerase chain reaction assay in colon cancer cell lines (HCT15, HCT116, HT-29, DLD-1, and SW480) and the results demonstrated that miR-30d level was significantly decreased in human colon cancer cell lines, compared with normal colon epithelial cell line. Transfection with miR-30d mimics inhibited cell proliferation, and transfection with miR-30d inhibitors significantly promoted cell viability of colon cancer cells. Furthermore, TargetScan analysis predicted that miR-30d interacted with messenger RNA on its 3' untranslated region of ATG5, phosphoinositide 3-kinase, and Beclin1 to negatively regulate cell autophagy in colon cancer cells. Moreover, transfection with miR-30d induced cell arrest at G2/M phase of HT-29 cells. Overexpression of miR-30d mimics inhibited cell viability probably due to the inhibition of cell autophagy and promotion of cell apoptosis. Thus, MiR-30d inhibited cell autophagy by directly targeting messenger RNA of ATG5, phosphoinositide 3-kinase, and Beclin1 and promoted cell apoptosis of human colon cancer cells. It is helpful to clarify the function of miR-30d in tumorigenesis of human cancers.

To investigate the protective effect of Rosuvastatin on myocardial cells in rats with acute myocardial infarction and its possible mechanism.Rats were randomly assigned to four groups: Control group, Sham group, AMI and Rosuvastatin group. The levels of lactate dehydrogenase (LDH) and creatine jubase (CK), the vitality of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were detected by assay kits and the levels of C-reactive protein (CRP), tumor necrosis factor (TNF) alpha and interleukin (IL)-6 expression were detected by enzyme linked immunosorbent assay (ELISA). TTC/Evans blue staining was used to determine the relative myocardial infarction area, HE staining was used to detect pathologic changes and myocardial apoptosis was detected by terminal-deoxynucleoitidyl transferase mediated nick end labeling (TUNEL). What's more, Western blot was used to detect the protein expression of B-cell lymphoma-2 (Bcl-2), Bax, cleaved-Caspase-3, Rock1, Rock2, I-κB and NF-κBp65.The model of acute myocardial infarction rats was established. Compared with Sham group, the myocardial pathological changes were more severe, and the apoptosis number, the production of inflammatory factors and oxidative damage were significantly increased in AMI group. Compared with AMI group, the relative area of infarction myocardium (43% ± 4% vs 31% ± 8%, P=0.004 3) was dramatically reduced, the levels of LDH (2 545.45 ± 613.67 U/L vs 1 573.43 ± 373.72 U/L, P=0.02) and CK (7.49 ± 1.75 U/ml vs 4.42 ± 1.28 U/ml, P=0.04) in serum were significantly lower (P0.01), the myocardial pathological damage degree was relieved, the apoptosis number (41% ± 8% vs 23% ± 6%, P=0.014 7) was significantly decreased, the expression of Bax (1.17 ± 0.10 vs 0.57 ± 0.08, P=0.003) and cleaved-Caspase-3 (1.31 ± 0.07 vs 0.70 ± 0.01, P=0.004) were dramatically reduced, and the expression of Bcl-2 (0.19 ± 0.01 vs 0.32 ± 0.01, P=0.003) was enhanced in Rosuvastatin group. Furthermore, the production of inflammatory factors and oxidative damage were effectively alleviated (P0.05), the protein expression of Rock1, Rock2 and NF-κBp65 were declined in Rosuvastatin group (P0.01).Rosuvastatin can effectively alleviate the cardiomyocyte apoptosis induced by acute ischemia, and its main mechanism may be the inhibition on RhoA/ROCK activation and the oxidative stress and inflammation reaction mediated by it.