Consolidation and seepage solutions in enclosure space based on non-zero-constant values boundary.

Research is ongoing to find solutions to the problem of Consolidation and seepage in saturated clay in enclosure space. Firstly, the boundary of non-zero-constant values is established, considering the seepage boundary of the clay is affected by pumping water or lowering boundary pressure on the site. Secondly, the differential equation is established to reflect the spatial and temporal variations of excess pore water pressure dissipation in the clay in enclosure space, and the solution is derived using variable separation methods. Finally, based on results of the solution derived, contour maps of the water pressure are drawn corresponding with the different inhomogeneous boundary conditions.

[Retracted] MicroRNA­877 inhibits cell proliferation and invasion in non­small cell lung cancer by directly targeting IGF­1R.

[This retracts the article DOI: 10.3892/etm.2019.7676.].

MicroRNA-877 inhibits cell proliferation and invasion in non-small cell lung cancer by directly targeting IGF-1R.

MicroRNAs (miRNAs/miRs) are frequently differentially expressed in non-small cell lung cancer (NSCLC), and differential miRNAs expression may be closely associated with NSCLC genesis and development. Therefore, an in-depth investigation of the cancer-associated miRNAs that are crucial for NSCLC pathogenesis may provide effective therapeutic targets for patients with this aggressive malignant tumor type. The expression levels and roles of miR-877 have been well studied in hepatocellular carcinoma and renal cell carcinoma. However, the expression pattern and functions of miR-877 in NSCLC as well as associated underlying mechanisms, to the best of our knowledge, have not yet been investigated. The present study revealed that miR-877 expression was downregulated in NSCLC tissues and cell lines. Low miR-877 expression was significantly associated with TNM stage and distant metastasis in patients with NSCLC. Functional experiments demonstrated that recovery of miR-877 expression restricted the proliferation and invasion of NSCLC cells. In addition, bioinformatics analysis predicted insulin-like growth factor 1 receptor (IGF-1R) as a potential target of miR-877. Luciferase reporter assays, reverse transcription-quantitative PCR and western blot analysis further validated that IGF-1R was a direct target of miR-877 in NSCLC. Furthermore, IGF-1R expression was markedly upregulated in NSCLC tissues, and exhibited an inverse correlation with miR-877 expression. Additionally, IGF-1R overexpression reversed the inhibitory effects in NSCLC cells caused by miR-877 upregulation. These findings demonstrated that miR-877 attenuated NSCLC cell proliferation and invasion, at least partly, by downregulating IGF-1R expression, thereby providing an new candidate biomarker for the diagnosis and therapy of patients with NSCLC.

Overexpression of miR-758 inhibited proliferation, migration, invasion, and promoted apoptosis of non-small cell lung cancer cells by negatively regulating HMGB.

Non-small cell lung cancer (NSCLC) is one of the most fatal types of cancer with significant mortality and morbidity worldwide. MicroRNAs (miRs) have been confirmed to have positive functions in NSCLC. In the present study, we try to explore the role of miR-758 in proliferation, migration, invasion, and apoptosis of NSCLC cells by regulating high-mobility group box (HMGB) 3 (HMGB3.) NSCLC and adjacent tissues were collected. Reverse transcription quantitative PCR (RT-qPCR) was employed to detect expression of miR-758 and HMGB3 in NSCLC and adjacent tissues, in BEAS-2B cells and NSCLC cell lines. The targetted relationship between miR-758 and HMGB3 was identified by dual luciferase reporter gene assay. The effects of miR-758 on proliferation, migration, invasion, cell cycle, and apoptosis of A549 cells. MiR-758 expression was lower in NSCLC tissues, which was opposite to HMGB3 expression. The results also demonstrated that miR-758 can target HMGB3. The cells transfected with miR-758 mimic had decreased HMGB3 expression, proliferation, migration, and invasion, with more arrested cells in G1 phase and increased apoptosis. Our results supported that the overexpression of miR-758 inhibits proliferation, migration, and invasion, and promotes apoptosis of NSCLC cells by negative regulating HMGB2. The present study may provide a novel target for NSCLC treatment.