Hepatocellular carcinoma (HCC) remains the fifth most frequent cancer with high mortality rate worldwide. However, the underlying molecular mechanisms of HCC progression are still barely known. Long noncoding RNAs (lncRNAs) have been recognized as significant therapeutic targets for HCC. Recently, the biological role of LINC00857 in several cancer types has been reported. Our present study was aimed to investigate the role of LINC00857 in HCC progression. We observed that LINC00857 was overexpressed in HCC cell lines (Huh7, Hep3B, HepG2, MHCC‐97H, and SNU449). Knockdown of LINC00857 significantly repressed Hep‐3B and SNU449 cell proliferation and inhibited the HCC cell colony formation. In addition, cell apoptosis was induced by the silence of LINC00857 and cell cycle progression was blocked in G1 phase. Besides these, downregulation of LINC00857 was able to restrain HCC cell migration and invasion capacity via enhancing epithelial‐mesenchymal transition (EMT) process. As displayed, E‐cadherin protein expression was increased by LINC00857 silence, while N‐cadherin protein level was repressed by LV‐shLINC00857 in HCC cells. Finally, the in vivo assays were used and the data indicated that LINC00857 could also obviously suppress the HCC tumor growth in vivo. In conclusion, our study revealed that LINC00857 might provide a novel perspective for the HCC treatment.

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Colon cancer is one of the most common malignant tumors worldwide, and the molecular mechanisms involved in the oncogenesis and progression of colon cancer remain unclear. Early growth response 1 (Egr-1) is a transcription factor that is closely associated with several tumor processes; however, its role in colon cancer is unknown. The present study aimed to explore the function and mechanism of transcription factor Egr-1 in colon cancer progression. The association between Egr-1 expression and the survival of patients with colon cancer was analyzed. Transwell assay was used to measure the migration and invasion of colon cancer cells. Cell Counting Kit-8 assay was used to evaluate the cell proliferative ability. Reverse transcription-quantitative PCR and western blot assays were used to identify whether Egr-1 could regulate cyclin-dependent kinase-like 1 (CDKL1). Luciferase and chromatin immunoprecipitation assays were used to detect the mechanism by which Egr-1 regulated CDKL1. Based on The Cancer Genome Atlas database, it was found that low Egr-1 expression was associated with a poor prognosis in patients with colon cancer. Furthermore, overexpression of Egr-1 inhibited colon cancer cell proliferation, migration, and invasion, whereas knockdown of Egr-1 increased colon cancer cell proliferation, migration and invasion. Additionally, overexpression of Egr-1-induced cell proliferation, migration and invasion were reversed by overexpression of CDKL1. Furthermore, it was demonstrated that Egr-1 regulated CDKL1 expression at the transcriptional level. The present study illustrated the mechanism of Egr-1 regulating CDKL1, by which Egr-1 affected colon cancer cell proliferation, migration and invasion. The current findings suggested that Egr-1/CDKL1 may be a new promising target for the treatment of colon cancer.

Background: This study aimed to assess the effect of tissue selecting technique (TST) on low rectovaginal fistula (RVF) repair. Methods: Patients with low RVF were included in the prospective study from August 2009 and January 2013 in xx hospital. Patients assigned to the TST or control groups based on the different surgical methods. Surgical success, complications, and quality of life were evaluated. Patients were followed up for 1-3 years. Results: A total of 81 patients were included in the study. Foutry-one were in the TST group, and 40 were in the control group. Surgery was successful in 100% of patients who underwent TST, and in 95% of patients who underwent the classical perineal approach. Less patients experienced pain (72% vs 90%, p = 0.04) and edema (6% vs 25%, p < 0.001) in the TST group compared with the control group. In addition, the QOL score was significantly higher in the TST group (122 ± 21 vs 111 ± 12, p = 0.02). Conclusion:The TST stapler approach appears to be appropriate for the treatment of low RVF in adults.