Objective: This study explored the ability of microRNA-135a (miR-135a) to influence cell proliferation, migration, invasion, apoptosis and tumor angiogenesis through the IGF-1/PI3K/Akt signaling pathway in non-small cell lung cancer (NSCLC). Methods: NSCLC tissues and adjacent normal tissues were collected from 138 NSCLC patients. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression levels of miR-135a and IGF-1, PI3K, Akt, VEGF, bFGF and IL-8 mRNA; western blotting was used to determine the expression levels of IGF-1, PI3K and Akt protein; and enzyme-linked immunosorbent assay (ELISA) was used to analyze the expression levels of VEGF, bFGF and IL-8 protein. Human NSCLC cell lines (A549, H460, and H1299) and the human bronchial epithelial cell line (HBE) were selected. A549 cells were assigned to blank, negative control (NC), miR-135a mimics, miR-135a inhibitors, IGF-1 siRNA and miR-135a inhibitors + IGF-1 siRNA groups. The following were performed: an MTT assay to assess cell proliferation, a scratch test to detect cell migration, a Transwell assay to measure cell invasion, and a flow cytometry to analyze cell apoptosis. Results: The expression level of miR-135a was lower while those of IGF-1, PI3K and Akt mRNA were higher in NSCLC tissues than in the adjacent normal tissues. Dual-luciferase reporter assay indicated IGF-1 as a target of miR-135a. The in vitro results showed that compared with the blank group, cell proliferation, migration and invasion were suppressed, mRNA and protein levels of IGF-1, PI3K, Akt, VEGF, bFGF and IL-8 were reduced, and cell apoptosis was enhanced in the miR-135a mimics and IGF-1 siRNA groups. Compared with the IGF-1 siRNA group, cells in the miR-135a inhibitors + IGF-1 siRNA group demonstrated increased cell proliferation, migration and invasion, elevated mRNA and protein levels of IGF-1, PI3K, Akt, VEGF, bFGF and IL-8 and reduced cell apoptosis. Conclusion: These findings indicated that miR-135a promotes cell apoptosis and inhibits cell proliferation, migration, invasion and tumor angiogenesis by targeting IGF-1 gene through the IGF-1/PI3K/Akt signaling pathway in NSCLC.

Background: Previous reports have confirmed the importance of circular RNA (circRNA) in the malignant progression of non-small-cell lung cancer (NSCLC). However, the role of circRNA PRH1-PRR4 readthrough (circPRH1-PRR4) in NSCLC progression was unclear. This study was designed to reveal the mechanism behind circPRH1-PRR4 regulating NSCLC progression. Methods: Quantitative real-time polymerase chain reaction and western blot were employed to detect the expression of circPRH1-PRR4, microRNA-877-5p (miR-877-5p), the member RAS oncogene family (RAB3D), and other indicated protein markers. The positive expression rate of RAB3D was detected by immunohistochemistry assay. Cell proliferation was investigated by cell colony formation and 5-ethynyl-2 0 -deoxyuridine assays. Flow cytometry was employed to quantify apoptotic cells. Wound-healing and transwell invasion assays were used to evaluate cell metastasis. The interaction among circPRH1-PRR4, miR-877-5p, and RAB3D was identified by dual-luciferase reporter assay. In vivo assay was implemented to demonstrate the effect of circPRH1-PRR4 on tumor formation. Results: As compared with controls, NSCLC tissues and cells displayed high expression of circPRH1-PRR4 and RAB3D, and low expression of miR-877-5p. Reduced expression of circPRH1-PRR4 resulted in inhibition of cell proliferation, migration, and invasion, but promotion of cell apoptosis in vitro. In support, circPRH1-PRR4 silencing inhibited tumor formation in vivo. Knockdown of miR-877-5p, a target miRNA of circPRH1-PRR4, relieved circPRH1-PRR4 absence-mediated action. Additionally, RAB3D was identified as a target mRNA of miR-877-5p. Importantly, circPRH1-PRR4 regulated RAB3D expression by miR-877-5p. Conclusion: CircPRH1-PRR4 knockdown impeded NSCLC cell malignancy by the miR-877-5p/RAB3D pathway, providing a possible circRNA-targeted therapy for NSCLC.

In this work, high-crystalline Ga 2 O 3 nanorods with improved photoelectrochemical properties were fabricated on Ti substrates by a facile electrodeposition. The photocurrent density of oval-like Ga 2 O 3 nanorods is 122.4 uA cm À 2 at 0.6 V vs. Ag/AgCl, which is much higher than that of rectangular Ga 2 O 3 nanorods (69 uA cm À 2 ). This enhancement in performance might be ascribed to the decreased bandgap energy, which greatly promotes its oxidation ability of photogenerated hole.

A two-dimensional code was developed to simulate vortex shedding characteristic and flow-structure interaction (FSI) of plate-type structures. In the code the physical component boundary fitted coordinate (PCBFC) was used to deal with the curve boundary. The arbitrary Lagrangian Eulerian (ALE) method was used to realize the grid movement. A barrier unit idea was adopted to deal with the boundary of fluid domain and solid domain in the code. The code was validated by comparing the numerical simulation results with experimental data. It was found that the vortex shedding phenomena in case of rectangular cylinder are strongly related to the length of the rectangular cylinder in the stream line.